Lipid Regulatory Mechanisms in Inflammation and Immune Responses

Lipids in inflammation and immune responses do not merely serve structural roles in membrane assembly and energy storage, but instead constitute a critical regulatory layer spanning the entire course of inflammatory initiation, signal amplification, immune cell differentiation, effector execution, and inflammatory resolution. Fatty acids, phospholipids, cholesterol, sphingolipids, and their derived lipid mediators collectively form a dynamically changing lipid network. Through regulation of membrane microdomain organization, lipid mediator biosynthesis, organelle interactions, and metabolic program reconfiguration, this network continuously shapes the activation threshold, migratory capacity, phagocytic efficiency, and inflammatory output intensity of immune cells.

Keywords: lipid metabolism; inflammatory response; immune regulation; arachidonic acid; prostaglandins; leukotrienes; cholesterol; sphingolipids; lipid droplets; inflammation resolution

I. Why Lipids Have Become a Critical Layer in Inflammation and Immune Regulation

1.1 Lipids are not merely structural molecules

(1) Membrane lipids determine the spatial organization of immune receptors

The initiation of inflammatory and immune responses generally begins with the recognition of pathogen-associated molecules, damage-associated molecules, or cytokines by membrane receptors. Whether receptors can efficiently cluster, internalize, and sustain signal transduction depends not only on receptor expression levels, but also on the membrane microenvironment in which they reside. Phospholipids, cholesterol, and sphingolipids together determine membrane fluidity, membrane curvature, and membrane microdomain stability, thereby influencing the signaling efficiency of Toll-like receptors, T-cell receptors, B-cell receptors, Fc receptors, and various adhesion molecules.

(2) Lipid metabolism is an essential basis for immune cell functional remodeling

Following immune cell activation, fatty acid uptake, lipid synthesis, cholesterol flux, and lipid droplet formation are often rapidly reprogrammed. This process is not solely intended to meet the demands of membrane expansion or energy supply, but rather to support inflammatory mediator generation, cell migration, phagocytosis, antigen presentation, and effector differentiation. Accordingly, changes in lipid metabolism themselves constitute an integral component of immune cell functional conversion.

1.2 Lipid regulation exhibits pronounced temporal phasing

(1) The initiation phase of inflammation is dominated by pro-inflammatory lipids

After tissue injury or infection occurs, polyunsaturated fatty acids in membrane phospholipids are rapidly mobilized, particularly with increased release of arachidonic acid, which is subsequently metabolized through multiple pathways into prostaglandins, leukotrienes, thromboxanes, and other pro-inflammatory lipid mediators. These molecules promote vasodilation, increased vascular permeability, leukocyte recruitment, and amplification of local inflammatory signaling.

(2) The resolution phase of inflammation requires a switch in lipid programs

Inflammation does not terminate automatically, but instead depends on an active resolution program. As the response progresses, the lipid mediator profile must gradually shift from a pro-inflammatory pattern to a pro-resolving pattern, generating lipoxins, resolvins, protectins, maresins, and other specialized pro-resolving mediators, thereby promoting neutrophil clearance, macrophage engulfment of apoptotic cells, and tissue repair. If this switch fails, inflammation is more likely to persist and develop into a chronic pathological state.

II. Key Enzymes Related to Lipid Regulation Constitute the Enzymatic Basis of the Inflammatory Response

2.1 Lipid regulation is not determined by a single enzyme

(1) From substrate release to lipid mediator generation, all steps depend on multistage enzymatic reactions

The generation of lipid signals during inflammation usually begins with membrane phospholipid cleavage, followed by oxidation, transfer, re-esterification, degradation, and reutilization. Different enzymes vary in temporal sequence, substrate preference, and cellular localization. Therefore, lipid regulation is fundamentally a multienzyme system composed of serial and branching coupling reactions.

(2) The same lipid substrate can enter distinct fate pathways

For example, arachidonic acid can enter the cyclooxygenase pathway to generate prostaglandins, the lipoxygenase pathway to produce leukotrienes or lipoxins, or cytochrome P450-related pathways to form other oxidized lipids. Thus, the key determinant of inflammatory direction is not merely whether the substrate is present, but rather which set of enzymes preferentially utilizes it.

(3) Different phospholipid cleavage sites alter downstream signaling trajectories

During the initial stage of membrane phospholipid mobilization, phospholipase A1, phospholipase A2, phospholipase C, and phospholipase D act on different bonds and generate different classes of lipid intermediates. For this reason, membrane phospholipid cleavage is not a singular process of arachidonic acid release, but rather a branching node that determines lysophospholipid profiles, second messenger generation, and subsequent directions of lipid remodeling.

2.2 Key enzymes related to lipid regulation and their functional positioning

Enzyme/Protein	Major substrate or pathway	Major product or function	Functional positioning in inflammation and immunity
Phospholipase A1 (PLA1/PLA1A)	Membrane phospholipids, especially selected substrates such as phosphatidylserine	2-acyl lysophospholipids, free fatty acids	Participates in membrane phospholipid remodeling, lysophospholipid generation, and regulation of specific immune-inflammatory signaling
Phospholipase A2 (PLA2)	Membrane phospholipids	Arachidonic acid, lysophospholipids	Initiates lipid mediator generation and serves as a key upstream enzyme in pro-inflammatory lipid pathways
Cyclooxygenase-1/2 (COX-1/COX-2)	Arachidonic acid	Prostaglandins, thromboxane precursors	Regulates fever, pain, vascular responses, and inflammatory amplification
5-Lipoxygenase (5-LOX)	Arachidonic acid	Leukotriene precursors	Promotes granulocyte recruitment, airway inflammation, and acute inflammatory responses
12/15-Lipoxygenase (12/15-LOX)	Polyunsaturated fatty acids	Lipoxins, precursors of selected pro-resolving mediators	Participates in inflammation resolution and tissue repair-associated lipid generation
Leukotriene A4 hydrolase (LTA4H)	LTA4	LTB4	Promotes neutrophil chemotaxis and inflammatory amplification
Leukotriene C4 synthase (LTC4S)	LTA4	LTC4	Participates in allergic inflammation, vascular permeability changes, and airway responses
Prostaglandin E synthase (PTGES)	PGH2	PGE2	Regulates fever, pain, blood flow, and immune cell function
Soluble epoxide hydrolase (EPHX2)	Epoxy lipids	Dihydroxylated lipids	Regulates the duration of inflammatory lipid activity and vascular responses
Fatty acid synthase (FASN)	Acetyl-CoA, malonyl-CoA	Long-chain fatty acids	Supports membrane biogenesis and metabolic reprogramming in inflammatory cells
Acetyl-CoA carboxylase (ACC)	Acetyl-CoA	Malonyl-CoA	Controls de novo fatty acid synthesis and the direction of lipid metabolism
Carnitine palmitoyltransferase 1A (CPT1A)	Long-chain acyl-CoA	Promotes mitochondrial fatty acid oxidation	Influences immune cell energy metabolism and functional differentiation
Long-chain acyl-CoA synthetase family (ACSL)	Long-chain fatty acids	Acyl-CoA	Determines whether fatty acids enter synthesis, oxidation, or remodeling pathways
Diacylglycerol acyltransferase (DGAT1/2)	Diacylglycerol	Triglycerides, lipid droplet formation	Regulates lipid droplet biogenesis and storage of inflammatory lipids
Adipose triglyceride lipase (ATGL)	Triglycerides	Free fatty acids	Mobilizes lipid droplet lipids and affects inflammatory substrate supply
Sphingomyelinase (SMase)	Sphingomyelin	Ceramide	Participates in stress responses, inflammasome activation, and cell death-related processes
Sphingosine kinase 1/2 (SPHK1/2)	Sphingosine	S1P	Regulates migration, barrier function, and immune cell distribution
S1P lyase (SGPL1)	S1P	Terminal degradation products	Terminates S1P signaling and affects lymphocyte circulation
Serine palmitoyltransferase (SPT)	Serine, palmitoyl-CoA	Initial products of sphingolipid synthesis	Determines sphingolipid biosynthetic flux
SOAT1/ACAT1	Cholesterol	Cholesteryl esters	Regulates cholesterol storage, foam cell formation, and inflammatory states
Neutral cholesterol ester hydrolase (NCEH1)	Cholesteryl esters	Free cholesterol	Affects cholesterol mobilization and lipid homeostasis in macrophages
Cholesterol 25-hydroxylase (CH25H)	Cholesterol	25-hydroxycholesterol	Links interferon responses, cholesterol metabolism, and anti-infective regulation
Phosphatidylinositol 3-kinase (PI3K)	Phosphatidylinositol lipids	PIP3 and related signaling lipids	Regulates phagocytosis, migration, survival, and inflammatory signaling pathways
Phospholipase C (PLC)	PIP2	DAG, IP3	Participates in receptor signal transduction and Ca2+ mobilization
Diacylglycerol kinase (DGK)	DAG	Phosphatidic acid	Controls receptor signal duration and the balance of lipid second messengers

III. The Arachidonic Acid Metabolic Network Constitutes the Central Axis of the Transition Between Pro-Inflammatory and Resolving States

3.1 Arachidonic acid release is the starting point of inflammatory lipid generation

(1) Membrane phospholipid mobilization determines response intensity

In most inflammatory cells, activation of PLA2 rapidly cleaves membrane phospholipids and releases arachidonic acid. This step determines not only the initial rate of lipid mediator production, but also whether downstream metabolism proceeds toward prostaglandin pathways, leukotriene pathways, or resolution-associated pathways. Therefore, PLA2 is not simply an upstream enzyme, but a major branching node in temporal control of inflammation.

(2) Different cellular sources influence metabolic direction

Neutrophils, macrophages, mast cells, and epithelial cells differ in their metabolic preference for arachidonic acid. Some cells preferentially generate leukotrienes, whereas others more readily form prostaglandins or pro-resolving lipids. As a result, the lipid profile within inflammatory microenvironments exhibits pronounced dependence on cellular origin.

3.2 Prostaglandins and leukotrienes jointly amplify acute inflammation

(1) Prostaglandins participate in regulation of blood flow and inflammatory thresholds

Prostaglandins are not a uniform group of molecules, but rather comprise different family members with distinct roles in vasodilation, pain sensitization, fever, and immune regulation. PGE2 is particularly complex, as it can both enhance selected inflammatory processes and, at specific stages, limit excessive immune activation.

(2) Leukotrienes are more strongly associated with cell recruitment and local effector enhancement

LTB4 is a potent chemotactic lipid that promotes neutrophil migration and activation, whereas cysteinyl leukotrienes are more deeply involved in changes in vascular permeability, mucosal edema, and airway hyperresponsiveness. Accordingly, leukotriene pathways have particularly prominent pathological significance in acute inflammation, allergy, and airway inflammation.

3.3 Inflammation resolution depends on a switch in lipid mediator classes

(1) Resolution is not a natural passive decline of inflammation

The resolution of inflammation requires an active switch in lipid mediators from pro-inflammatory to pro-resolving classes. Enzymes such as 12/15-LOX are especially important in this process, as they promote the generation of lipoxins and other resolution-associated molecules.

(2) Pro-resolving lipids promote clearance and repair

Lipoxins, resolvins, protectins, maresins, and related molecules suppress excessive granulocyte infiltration, promote macrophage engulfment of apoptotic cells, and support tissue repair. If this system is insufficient, inflammation may remain in a state of persistent low-grade activation even when its intensity has declined.

IV. Membrane Lipid Remodeling and Phospholipid Signaling Determine the Efficiency of Immune Receptor Activation

4.1 Membrane lipid composition alters receptor nanostructure

(1) Lipid rafts and microdomain organization influence signal clustering

Cholesterol- and sphingolipid-enriched regions can form relatively ordered membrane microdomains, allowing specific receptors and downstream signaling proteins to cluster more efficiently. Following inflammatory stimulation, whether receptors can rapidly form high-density signaling clusters often determines whether downstream signaling is transiently triggered or persistently amplified.

(2) Membrane curvature and membrane tension affect phagocytosis and endocytosis

During phagocytosis, migration, and immune synapse formation, immune cells require extensive membrane remodeling. Phospholipid classes, fatty acid saturation, and local lipid compositional changes influence membrane extensibility and bending capacity, thereby determining the efficiency of phagosome formation, endosome maturation, and vesicular trafficking.

4.2 The phosphatidylinositol signaling pathway is a central hub of membrane dynamic control

(1) Different phosphatidylinositol species represent distinct membrane identities

PI, PI4P, PI(4,5)P2, and PI(3,4,5)P3 are not merely metabolic intermediates, but important signaling lipids that define the functional identity of membrane compartments. Different molecular species recruit different effector proteins and thereby regulate cell polarity, receptor endocytosis, and cytoskeletal rearrangement.

(2) Migration, phagocytosis, and inflammasome activation all depend on PI signaling

Directed migration of neutrophils, phagocytosis by macrophages, antigen uptake by dendritic cells, and selected inflammasome-related events all require rapid local remodeling of PI signaling. Thus, phosphatidylinositol metabolism is a major pathway through which external inflammatory stimuli are converted into membrane dynamic responses.

V. Cholesterol and Oxysterols Determine the Activation Threshold of Immune Cells

5.1 Cholesterol homeostasis is not merely a metabolic issue

(1) Cholesterol influences the stability of receptor signaling platforms

Cholesterol enhances membrane order and promotes the clustering efficiency of selected receptors and signaling proteins on the membrane. When cholesterol content becomes abnormal, receptor activation thresholds change, such that stimuli of equivalent strength can induce different degrees of inflammatory output.

(2) Cholesterol imbalance can drive chronic inflammation

When macrophage cholesterol uptake increases, cholesterol efflux becomes insufficient, or cholesterol esterification becomes abnormal, foam cell-like phenotypes readily develop. This process is not merely lipid deposition, but also feeds back to amplify inflammatory transcriptional programs and tissue injury responses, especially in chronic inflammatory diseases such as atherosclerosis.

5.2 Intermediates of cholesterol metabolism possess immunoregulatory functions

(1) Oxysterols are not passive by-products

Oxysterols such as 25-hydroxycholesterol can directly participate in anti-infective and immunoregulatory processes, influencing membrane cholesterol distribution, viral entry, receptor signaling, and inflammatory gene expression.

(2) Cholesterol flux is linked to antigen presentation and phagocytic clearance

The movement of cholesterol among lysosomes, the endoplasmic reticulum, and the plasma membrane directly affects post-phagocytic membrane recycling, antigen processing, and organelle stress levels. Therefore, cholesterol homeostasis is deeply embedded in the structural and functional logic of immune cells.

VI. The Sphingolipid System Plays Bidirectional Roles in Inflammatory Amplification and Immune Homeostasis

6.1 Ceramide and S1P form a functionally antagonistic axis

(1) Ceramide is more strongly associated with stress responses and inflammatory amplification

Ceramide is generated following sphingomyelin cleavage by sphingomyelinases. Ceramide promotes membrane platform reorganization, cell death-associated programs, inflammasome activation, and enhancement of stress signaling, and is therefore commonly associated with tissue injury and inflammatory expansion.

(2) S1P is more strongly associated with migration, survival, and barrier regulation

S1P is generated by phosphorylation of sphingosine through SPHK1/2. Through receptor-mediated pathways, S1P regulates lymphocyte egress, vascular endothelial barrier stability, and inflammatory cell distribution, making it an important molecule linking local inflammation with systemic immune circulation.

6.2 The balance of sphingolipid metabolism determines inflammatory direction

(1) Upstream synthesis and downstream degradation jointly determine output

Multiple enzymes, including SPT, SMase, SPHK, and S1P lyase, collectively determine sphingolipid profiles. What truly determines whether a cell is biased toward stress-associated death, migratory survival, or maintenance of homeostasis is not the concentration of a single molecule, but rather the balance of the entire sphingolipid metabolic axis.

(2) Sphingolipid abnormalities are associated with multiple immune diseases

Rearrangement of sphingolipid profiles has been observed in infection, autoimmunity, metabolic inflammation, allergy, and tumor microenvironments. This indicates that sphingolipid pathways can serve not only as pathological marker layers, but also as interventional target layers.

VII. Fatty Acid Metabolic Reprogramming Determines Immune Cell Functional States

7.1 Fatty acid synthesis and oxidation shape distinct immune programs

(1) Pro-inflammatory states are often accompanied by enhanced lipogenesis

Activated macrophages, dendritic cells, and effector T cells frequently enhance fatty acid synthesis in order to support membrane expansion, organelle remodeling, and inflammatory mediator synthesis. Under these conditions, enzymes such as ACC, FASN, and ACSL play major roles in metabolic reprogramming.

(2) Fatty acid oxidation is often associated with persistent survival and reparative phenotypes

Certain regulatory T cells, memory T cells, and reparative macrophages rely more strongly on fatty acid oxidation to maintain long-term survival and sustained functional activity. Enzymes such as CPT1A have important regulatory significance in this direction. However, this relationship is not absolute, as different tissues and microenvironments can shift this pattern.

7.2 Lipids in immunometabolism do not operate independently

(1) Lipid metabolism is coupled with glucose metabolism and amino acid metabolism

Metabolic reprogramming of inflammatory cells is generally the result of coordinated changes across multiple pathways. Enhanced fatty acid synthesis often coincides with active glycolysis, whereas increased fatty acid oxidation is frequently associated with maintenance of mitochondrial function and oxidative metabolism.

(2) Metabolic reprogramming fundamentally alters cellular decision-making logic

Immune cells do not first determine function and then alter metabolism; rather, the metabolic program itself participates in determining effector differentiation, survival duration, and the type of inflammatory output.

VIII. Lipid Droplets Have Transitioned From Lipid Storage Structures to Inflammatory Effector Platforms

8.1 Lipid droplets are active organelles in inflammation

(1) Lipid droplets are not static lipid storage depots

In inflammatory cells, lipid droplets can recruit multiple lipid metabolic enzymes and inflammation-associated proteins, thereby serving as important platforms for lipid mediator synthesis and substrate buffering. Their formation generally indicates that the cell has entered a highly reprogrammed lipid metabolic state.

(2) Lipid droplets participate in substrate storage and toxicity buffering

When free fatty acid and cholesterol loads become excessive, lipid droplets can temporarily sequester them, thereby reducing lipotoxicity and membrane injury. However, this buffering function is not universally beneficial. Persistent lipid droplet accumulation can also provide a substrate basis for lipid mediator production and maintenance of chronic inflammation.

8.2 Lipid droplets are directly linked to immune cell function

(1) Lipid droplet burden in macrophages affects inflammatory transcriptional states

Macrophages with increased lipid droplets are often accompanied by abnormal cholesterol handling, enhanced generation of pro-inflammatory lipid mediators, and increased metabolic burden after phagocytosis. Their functional state may therefore shift from clearance and repair toward maintenance of inflammation.

(2) Lipid droplets are also important in dendritic cells and granulocytes

Changes in lipid droplets can affect the cross-presentation capacity of dendritic cells and also influence lipid mediator release and local response intensity in neutrophils. Thus, lipid droplets should be regarded as immunoregulatory platforms rather than simple metabolic by-products.

IX. How Lipid Imbalance Drives Chronic Inflammation and Immune Disease

9.1 Chronic inflammation is frequently accompanied by misaligned lipid programs

(1) Persistent presence of pro-inflammatory lipids with insufficient pro-resolving lipids

In chronic airway inflammation, atherosclerosis, autoimmune diseases, and metabolic inflammation, sustained elevation of pro-inflammatory lipid mediators is often observed together with insufficient generation of resolution-associated lipids. This indicates that disease involves not only increased inflammatory intensity, but also failure to correctly establish inflammatory termination programs.

(2) Cholesterol, sphingolipid, and lipid droplet abnormalities jointly drive disease persistence

Imbalanced cholesterol flux, shifted sphingolipid metabolism, and abnormal lipid droplet accumulation can each amplify inflammation from the levels of membrane signaling, cell fate control, and metabolic buffering, ultimately forming a stable pathological lipid microenvironment.

9.2 Lipid-targeted intervention cannot remain at the level of simple inhibition

(1) Cell specificity and stage specificity must be considered

The same lipid pathway does not have the same biological meaning during the initiation, amplification, and resolution phases of inflammation. Therapeutic strategies should not simply suppress all lipid signaling, but instead should precisely regulate lipid mediator classes, cholesterol flux, or sphingolipid balance according to disease stage and cell type.

(2) Lipidomics and functional stratification will become key tools

Measurement of cholesterol, triglycerides, or total fatty acid content alone is insufficient to explain the true immune-lipid state. More informative future strategies will integrate lipidomics approaches with molecular-species resolution, cell-subset resolution, and spatial-distribution resolution to establish higher-resolution inflammatory lipid maps.

X. Aladdin-Related Products

10.1 Phospholipase-Related Products

Product Type	Catalog No.	Product Name	Grade and Purity	Applicable Research Direction / Use
Inhibitor	M304853	ML348	≥98%	Lysophospholipid metabolism and membrane phospholipid remodeling studies
ELISA Kit	EJ1514434	Human Phospholipase A1 (PL-A1) ELISA Kit	BioReagent	PLA1 expression analysis; membrane lipid remodeling studies
Enzyme	P757681	Phospholipase A1	EnzymoPure™, 75 PLA-L/g	Phospholipid hydrolysis studies; PLA1 enzymology analysis
Enzyme	P299005	Phospholipase A1 from Aspergillus oryzae	EnzymoPure™, ≥10 KLU/G	Phospholipase A1 enzymology; membrane lipid degradation studies
Inhibitor	A286909	ASB 14780	≥98%(HPLC)	Upstream regulation of arachidonic acid release; studies of pro-inflammatory lipid generation
Inhibitor	M288686	ML 349	≥98%	Regulation of lysophospholipid metabolism; membrane lipid turnover studies
Inhibitor	O288799	OBAA	≥98%	PLA2 inhibition; studies of inflammatory lipid precursor release
Inhibitor	O275137	ONO-RS-082	≥98%	PLA2 pathway inhibition; membrane phospholipid mobilization studies
Inhibitor	Y288422	YM 26734	≥95%(HPLC)	Studies of secretory PLA2-related inflammatory pathways
ELISA Kit	EJ1513719	Human Phospholipase A2, Group IID (PLA2G2D) ELISA Kit	BioReagent	PLA2 subtype expression analysis; stratification of inflammatory models
ELISA Kit	EJ1513733	Human Calcium-dependent Phospholipase A2 (PLA2G5) ELISA Kit	BioReagent	PLA2 subtype expression analysis; lipid signaling profiling
ELISA Kit	EJ1513734	Human Phospholipase A2, Group X (PLA2G10) ELISA Kit	BioReagent	PLA2 subtype expression analysis; studies of inflammatory lipid release
ELISA Kit	EJ1514436	Human Phospholipase A2, Membrane Associated (PLA2G2A) ELISA Kit	BioReagent	Evaluation of pro-inflammatory PLA2 expression; acute inflammation studies
ELISA Kit	EJ1514755	Human Phospholipase A2, LipoProtein Associated (LpPLA2) ELISA Kit	BioReagent	Evaluation of lipoprotein-associated inflammatory phospholipid metabolism
ELISA Kit	H1509864	Human Lp-PLA2 ELISA Kit	BioReagent	Lp-PLA2 level determination; lipid-inflammatory risk assessment
ELISA Kit	EJ1511943	Rat Phospholipase A2, Membrane Associated (PLA2G2A) ELISA Kit	BioReagent	PLA2 expression analysis in rat inflammatory models
ELISA Kit	EJ1512283	Rat Phospholipase A2, LipoProtein Associated (LpPLA2) ELISA Kit	BioReagent	Evaluation of lipoprotein inflammatory pathways in rats
ELISA Kit	EJ1512597	Mouse Phospholipase A2, Membrane Associated (PLA2G2A) ELISA Kit	BioReagent	PLA2 expression analysis in mouse inflammatory models
ELISA Kit	EJ1513140	Mouse Phospholipase A2, LipoProtein Associated (LpPLA2) ELISA Kit	BioReagent	Studies of Lp-PLA2-related inflammation in mice
Enzyme	P1501339	Phospholipase A2 (PLA2) from Porcine pancreas	ActiBioPure™, Bioactive, High Performance, EnzymoPure™, ≥200LeU/mg powder	Phospholipase A2 enzymology; construction of arachidonic acid release models
Inhibitor	U302223	U73122	Moligand™, ≥97%	PLC signaling inhibition; receptor-mediated phospholipid signaling studies
Activator	M287045	m-3M3FBS	Moligand™, ≥98%	PLC activation; studies of Ca2+ mobilization and receptor signaling
Enzyme	P757679	Phospholipase C	EnzymoPure™, ≥5000 PLC-S/g	Phospholipase C enzymology; membrane phospholipid cleavage studies
Enzyme	P1434805	Phosphatidylinositol phosphodiesterase		PI-specific phospholipid cleavage; membrane signal transduction studies
Inhibitor	F288161	FIPI	≥98%(HPLC)	Phospholipase D inhibition; membrane lipid remodeling and vesicular signaling studies

10.2 Arachidonic Acid Metabolism-Related Products

Product Type	Catalog No.	Product Name	Grade and Purity	Applicable Research Direction / Use
Inhibitor	C336912	COX-1 Inhibitor II	≥95%	COX-1 pathway inhibition; studies of basal prostaglandin generation
Inhibitor	C135780	SC-560	Moligand™, ≥98%(HPLC)	Selective COX-1 inhibition; studies of cyclooxygenase functional division
ELISA Kit	EJ1514286	Human Cyclooxygenase 1 (COX-1) ELISA Kit	BioReagent	COX-1 expression analysis; evaluation of prostaglandin synthesis pathways
ELISA Kit	EJ1512116	Rat Cyclooxygenase 1 (COX-1) ELISA Kit	BioReagent	Rat COX-1 expression analysis; inflammatory model studies
ELISA Kit	EJ1512869	Mouse Cyclooxygenase 1 (COX-1) ELISA Kit	BioReagent	Mouse COX-1 expression analysis; evaluation of arachidonic acid metabolism
Inhibitor	D287247	DuP 697	≥98%	COX-2 inhibition; studies of inflammation-amplifying pathways
Inhibitor	F287097	FK 3311	≥98%(HPLC)	Selective COX-2 inhibition; studies of pro-inflammatory prostaglandin generation
Inhibitor	N274713	NS 398	Moligand™, ≥98%	COX-2 inhibition; studies of acute inflammation and fever-related pathways
Inhibitor	N288651	NCX 466	≥98%(HPLC)	Studies of combined COX inhibition and nitric oxide donor effects
ELISA Kit	EJ1514287	Human Cyclooxygenase-2 (COX-2) ELISA Kit	BioReagent	COX-2 expression analysis; evaluation of inflammatory severity
Inhibitor	B288165	BAY-X 1005	Moligand™, ≥98%(HPLC)	Upstream inhibition of the leukotriene pathway; studies of the 5-LOX accessory complex
Inhibitor	B288192	BW-B 70C	Moligand™, ≥98%(HPLC)	5-LOX inhibition; studies of leukotriene generation
Inhibitor	L607227	5-LOX inhibitor 2m	Moligand™	5-LOX inhibition; studies related to granulocyte recruitment
ELISA Kit	EJ1513404	Human 5-Lipoxygenase (5-LOX) ELISA Kit	BioReagent	5-LOX expression analysis; evaluation of leukotriene pathways
Inhibitor	T288932	2-TEDC	Moligand™, ≥99%(HPLC)	Multi-LOX pathway inhibition; studies of the switch between pro-inflammatory and pro-resolving programs
Inhibitor	C274883	CDC	Moligand™, ≥98%	LOX pathway inhibition; lipid oxidation metabolism studies
Inhibitor	M275434	MK886	Moligand™, ≥98%	Regulation studies of leukotriene-related LOX branches
Inhibitor	P287013	PD 146176	Moligand™, ≥98%(HPLC)	15-LOX inhibition; studies of pro-resolving precursor generation
Inhibitor	L1496742	15-LOX-1 inhibitor 1	Moligand™, 10 mM in DMSO	15-LOX-1 inhibition; studies of lipoxins and pro-resolving lipids
Inhibitor	L647840	15-LOX-1 inhibitor 1	≥98%	15-LOX-1 inhibition; analysis of resolution pathways
Inhibitor	H1440710	h15-LOX-2 inhibitor 2		15-LOX-2 inhibition; lipid oxidation branch studies
Inhibitor	H1440701	h15-LOX-2 inhibitor 3		15-LOX-2 inhibition; studies of resolution-related metabolism
ELISA Kit	EJ1514788	Human Arachidonate-12-Lipoxygenase (ALOX12) ELISA Kit	BioReagent	ALOX12 expression analysis; studies of the 12-LOX branch
ELISA Kit	EJ1513171	Mouse Arachidonate-12-Lipoxygenase (ALOX12) ELISA Kit	BioReagent	Mouse ALOX12 expression analysis; LOX pathway profiling
ELISA Kit	EJ1514333	Human Leukotriene A-4 Hydrolase (LTA4H) ELISA Kit	BioReagent	Detection of the LTB4-generating pathway; studies of neutrophil chemotaxis
ELISA Kit	EJ1512135	Rat Leukotriene A4 Hydrolase (LTA4H) ELISA Kit	BioReagent	Rat LTA4H expression analysis; evaluation of leukotriene pathways
Inhibitor	C287028	C3	Moligand™, ≥98%(HPLC)	Inhibition of downstream PGE2 synthesis; studies of the prostaglandin E pathway
Inhibitor	T287865	TPPU	≥98%(HPLC)	EPHX2/sEH inhibition; studies of epoxy-lipid homeostasis
Enzyme	E1429656	Epoxide hydrolase		Enzymology studies of epoxy-lipid metabolism; studies of oxidized lipid conversion
ELISA Kit	EJ1515603	Human Prostaglandin E2 (PGE2) ELISA Kit	BioReagent	PGE2 level determination; evaluation of inflammation-amplifying effects
ELISA Kit	EJ1515384	Rat Prostaglandin E2 (PGE2) ELISA Kit	BioReagent	Rat PGE2 determination; pharmacodynamic evaluation studies
ELISA Kit	EJ1515486	Mouse Prostaglandin E2 (PGE2) ELISA Kit	BioReagent	Mouse PGE2 determination; inflammatory model monitoring
ELISA Kit	EJ1515325	Lipoxin A4 (LXA4) ELISA Kit	BioReagent	Detection of pro-resolving lipids during inflammation resolution; evaluation of resolution programs

10.3 Cholesterol- and Sphingolipid Metabolism-Related Products

Product Type	Catalog No.	Product Name	Grade and Purity	Applicable Research Direction / Use
Inhibitor	A129742	Avasimibe	≥98%	Inhibition of cholesterol esterification; studies of foam cell formation
Inhibitor	C276393	CI 976 (PD 128042)	≥98%	Inhibition of the ACAT/SOAT pathway; studies of cholesterol storage
Inhibitor	T275108	TMP-153	≥95%	Inhibition of cholesterol ester formation; cholesterol homeostasis studies
Inhibitor	V286658	VULM 1457	≥98%	Regulation of cholesterol esterification; studies of inflammatory lipid accumulation
Inhibitor	Y287168	YM 750	≥98%(HPLC)	ACAT inhibition; studies related to cholesterol loading
siRNA	S1476297	SOAT1 Human Pre-designed siRNA Set A		SOAT1 gene silencing; functional validation of cholesterol esterification
siRNA	N1482130	NCEH1 Human Pre-designed siRNA Set A		NCEH1 gene silencing; studies of cholesteryl ester hydrolysis
siRNA	C1488055	CH25H Human Pre-designed siRNA Set A		CH25H gene silencing; studies of oxysterols and anti-infective regulation
Detection Kit	T1505557	Total Cholesterol (TC) Content Assay Kit (Single-Reagent COD-PAP, Micro Method)	BioReagent	Quantification of total cholesterol in cells/tissues
Detection Kit	T1505558	Total Cholesterol (TC) Content Assay Kit (Double-Reagent COD-PAP, Micro Method)	BioReagent	Total cholesterol determination; evaluation of cholesterol homeostasis
Detection Kit	T1515864	Total Cholesterol (TC) Content Assay Kit (Single-Reagent COD-PAP, Colorimetric Method)	BioReagent	Measurement of cholesterol loading; cholesterol metabolism studies
Detection Kit	F1505559	Free Cholesterol (FC) Content Assay Kit (COD-PAP, Micro Method)	BioReagent	Quantification of free cholesterol; cholesterol flux analysis
Detection Kit	F1515865	Free Cholesterol (FC) Content Assay Kit (Single Reagent COD-PAP, Colorimetric Method)	BioReagent	Free cholesterol determination; analysis of esterification/de-esterification balance
Detection Kit	F1515866	Free Cholesterol (FC) Content Assay Kit (Dual Reagent COD-PAP, Colorimetric Method)	BioReagent	Studies of cholesterol flux and mobilization
ELISA Kit	EJ1511959	Rat Sphingomyelin Phosphodiesterase 2 (NSMASE) ELISA Kit	BioReagent	Detection of the sphingomyelin-ceramide axis; rat model studies
ELISA Kit	EJ1512612	Mouse Sphingomyelin Phosphodiesterase 2 (NSMASE) ELISA Kit	BioReagent	nSMase expression analysis; studies of sphingolipid metabolism in mice
Inhibitor	D286815	DPTIP	≥98%(HPLC)	nSMase2 inhibition; studies of ceramide generation
Inhibitor	N1441174	nSMase2-IN-1	≥98%	Inhibition of neutral sphingomyelinase 2; studies of sphingolipid stress pathways
Inhibitor	S129855	SKI II	Moligand™, ≥98%	SPHK1/2 inhibition; studies of S1P generation
Inhibitor	S275155	SKI-I	≥90%	Sphingosine kinase inhibition; studies of migration and barrier signaling
Inhibitor	C276256	CAY10621 (SKI 5C)	≥98%	Selective SPHK1 inhibition; studies of S1P signaling regulation
Inhibitor	M288047	MP A08	Moligand™, ≥97%	Dual SPHK1/2 inhibition; studies of sphingolipid homeostasis
siRNA	S1490203	SGPL1 Human Pre-designed siRNA Set A		SGPL1 gene silencing; studies of terminal S1P degradation
Substrate	S1452349	SGPL1 fluorogenic substrate		SGPL1 activity assay; functional analysis of S1P lyase
ELISA Kit	EJ1513355	Mouse Sphingosine 1 Phosphate Lyase 1 (SGPL1) ELISA Kit	BioReagent	Mouse SGPL1 expression analysis; evaluation of S1P metabolism

10.4 Fatty Acid Metabolism, Lipid Droplet, and Phospholipid Signaling-Related Products

Product Type	Catalog No.	Product Name	Grade and Purity	Applicable Research Direction / Use
ELISA Kit	EJ1514752	Human Fatty Acid Synthase (FASN) ELISA Kit	BioReagent	FASN expression analysis; fatty acid synthesis studies
ELISA Kit	EJ1513138	Mouse Fatty Acid Synthase (FASN) ELISA Kit	BioReagent	Mouse FASN expression analysis; immune metabolic reprogramming studies
Activity Assay Kit	F1516011	Fatty Acid Synthase (FAS) Activity Assay Kit (UV Micro Method)	BioReagent	FASN activity assay; evaluation of lipid synthesis capacity
Activity Assay Kit	F1516012	Fatty Acid Synthase (FAS) Activity Assay Kit (UV Colorimetric Method)	BioReagent	Assessment of fatty acid synthesis flux; pharmacodynamic studies
Inhibitor	A1440171	ACC1-IN-2		ACC1 inhibition; studies of fatty acid synthesis regulation
Inhibitor	A1440172	ACC1/2-IN-1		Dual ACC1/2 inhibition; studies of the balance between synthesis and oxidation
Inhibitor	A1440169	ACC1/2-IN-2		ACC1/2 inhibition; studies of lipid metabolic directionality control
Inhibitor	A275993	ACC2 Inhibitor	≥98%	ACC2 inhibition; studies favoring fatty acid oxidation
Inhibitor	P288592	PF 05175157	≥98%(HPLC)	ACC1/2 inhibition; immune metabolic reprogramming studies
Activity Assay Kit	A1515852	Acetyl CoA Carboxylase (ACC) Activity Assay Kit (AHM, Micro Method)	BioReagent	ACC activity assay; studies of precursor generation for fatty acid synthesis
Activity Assay Kit	A1515969	Acetyl-CoA Carboxylase (ACC) Activity Assay Kit (AHM, Colorimetric Method)	BioReagent	ACC activity assay; evaluation of pharmacological intervention
ELISA Kit	EJ1515058	Human Long-chain-fatty-acid—CoA Ligase 4 (ACSL4) ELISA Kit	BioReagent	ACSL4 expression analysis; studies of long-chain fatty acid activation
Enzyme	A774049	Acyl-CoA Synthetase (ACS)	Bioactive, ActiBioPure™, High Performance, EnzymoPure™, ≥85%(SDS-PAGE), ≥5 U/mg protein	Fatty acid activation; studies of acyl-CoA generation
Enzyme	R1506902	Acyl-CoA Synthetase (ACS)	Bioactive,Recombinant,ActiBioPure™,High Performance,EnzymoPure™,≥1 U/mg enzyme powder	Construction of recombinant fatty acid activation systems; metabolic pathway analysis
Inhibitor	A129800	A922500	≥98%	DGAT1 inhibition; studies of lipid droplet formation
Inhibitor	A286752	AZD 3988	≥98%(HPLC)	DGAT1 inhibition; studies of triglyceride synthesis
Inhibitor	A128057	AZD7687	Moligand™, ≥98%	DGAT1 inhibition; studies of lipid droplet burden regulation
Inhibitor	D649195	DGAT-1 inhibitor 2	≥95%	DGAT1 inhibition; studies of lipid droplet biogenesis
Inhibitor	D651790	DGAT1-IN-1	≥95%	DGAT1 inhibition; studies of lipid droplet storage
Inhibitor	D647241	DGAT1-IN-3	≥99%	DGAT1 inhibition; studies of triglyceride storage
Inhibitor	D1439626	DGAT2-IN-3		DGAT2 inhibition; studies of lipid droplet maturation and lipid storage
Inhibitor	J287704	JNJ DGAT2-A	≥98%	DGAT2 inhibition; studies of late-stage lipid droplet formation
Inhibitor	P286969	PF 06424439	≥98%(HPLC)	DGAT2 inhibition; studies of triglyceride synthesis
ELISA Kit	EJ1514750	Human Adipose Triglyceride Lipase (ATGL) ELISA Kit	BioReagent	ATGL expression analysis; studies of lipid droplet mobilization
Inhibitor	A129503	AS-252424	Moligand™, ≥98%	PI3Kγ inhibition; studies of migration and inflammatory membrane signaling
Inhibitor	A129517	AS-604850	Moligand™, ≥98%	PI3Kγ inhibition; studies of receptor-downstream phospholipid signaling
Inhibitor	A127765	AS-605240	Moligand™, ≥98%	Studies of PI3Kγ-dependent phagocytosis/migration pathways
Inhibitor	I126757	IC-87114	Moligand™, ≥98%	PI3Kδ inhibition; studies of immune cell signaling regulation
Inhibitor	S414119	Selective PI3Kδ Inhibitor 1 (compound 7n)	≥98%	Selective PI3Kδ inhibition; inflammatory signaling studies
Inhibitor	T127783	TG100-115	Moligand™, ≥98%	Dual PI3Kγ/δ inhibition; studies of membrane dynamics and migration
Inhibitor	G126357	GDC-0941	Moligand™, ≥98%	Broad PI3K pathway inhibition; studies of phagocytosis and survival signaling
Inhibitor	X129499	XL147	Moligand™, ≥98%	PI3K inhibition; studies of phosphatidylinositol signaling
Inhibitor	Z126804	ZSTK474	Moligand™, ≥98%	PI3K inhibition; studies of membrane identity and inflammatory signaling
Inhibitor	R288294	R 59-022	≥98%(HPLC)	DGK inhibition; studies of DAG/phosphatidic acid balance and receptor signaling

Lipid regulation in inflammation and immune responses is, in essence, a multilayered network jointly composed of membrane lipid remodeling, lipid mediator generation, metabolic program switching, and organelle interactions. Lipids participate not only in the initiation of inflammation, but also determine whether inflammation can be resolved in a timely manner; they not only shape the effector output of immune cells, but also define their metabolic boundaries and tissue adaptability. Only by understanding pro-inflammatory lipids, pro-resolving lipids, cholesterol flux, sphingolipid signaling, and lipid droplet dynamics within a unified framework can the true regulatory logic of inflammation and immune responses be more accurately captured, thereby providing a stronger theoretical foundation for subsequent mechanistic investigation and precision intervention.

For more related articles, please see below:

[1] How to Map the NF-κB Pathway and Choose Inhibitors: Bringing Inflammatory Transcriptional Output into a “Controllable Range” (Tables A–F)