Molecular Network of the Kinin System in Pain and Neural Regulation

The kinin system is a major molecular network linking tissue injury, inflammatory responses, vascular reactivity, and regulation of neural excitability. Through coordinated control of kinin generation, receptor stratification, ion-channel sensitization, and amplification of neuroinflammation, this system participates in the initiation of acute pain, the maintenance of persistent hypersensitivity, and the development of central sensitization. Systematic analysis of this network helps clarify the key molecular basis of inflammatory pain, neuropathic pain, and visceral pain.

Keywords: kinin system; bradykinin; B1 receptor; B2 receptor; pain; neural regulation; TRPV1; TRPA1; neuroinflammation; central sensitization

1. Composition and Functional Framework of the Kinin System

1.1 Basic composition of the kinin system

(1) The kinin system consists of precursors, generating enzymes, active peptides, and degradative enzymes

Upstream components of the kinin system include high-molecular-weight kininogen and low-molecular-weight kininogen. Intermediate components include plasma kallikrein and tissue kallikrein, whereas downstream components include bradykinin, kallidin, and their metabolic peptide derivatives. In parallel, degradative systems such as angiotensin-converting enzyme, aminopeptidases, and neutral endopeptidases continuously restrict the duration and spatial spread of kinin signaling. Accordingly, the kinin system is not a simple ligand-receptor axis, but rather a short-lived signaling network characterized by high turnover, strong temporal dynamics, and marked local specificity.

(2) The kinin system integrates inflammatory, vascular, and neural regulatory properties

Bradykinin was initially recognized for its vasodilatory and permeability-enhancing effects. In pain research, however, its greater significance lies in its ability to directly act on nociceptive neurons and further promote neuronal hyperresponsiveness, inflammatory mediator release, and local neuroimmune remodeling. For this reason, under pathological conditions, the kinin system should not be regarded merely as an accessory inflammatory pathway, but as an important organizer within the pain network.

1.2 Functional division between B1 and B2 receptors provides the temporal basis of the kinin system

(1) B2 receptors are more closely associated with constitutive expression and acute responses

B2 receptors are typically constitutively expressed in normal tissues and serve as the principal receptors for bradykinin and kallidin. Their activation rapidly induces vasodilation, local edema, sensitization of peripheral nerve endings, and immediate pain responses. They are therefore more commonly associated with early post-injury nociception and neural excitation during the acute inflammatory phase.

(2) B1 receptors are more closely associated with inducible expression and persistent pathological states

B1 receptors are commonly induced and upregulated in the context of inflammatory cytokines, tissue injury, infection, and nerve damage, and they primarily recognize des-Arg kinin metabolites. Compared with B2 receptors, B1 receptors are more often involved in persistent hypersensitivity, neuropathic pain, and long-term pain maintenance during chronic inflammation.

1.3 The balance between kinin generation and inactivation determines the amplification threshold of the pain network

(1) Enhanced kinin generation rapidly converts local injury into neural input

When local tissue injury occurs, the contact system is activated, the proteolytic environment changes, or inflammatory responses intensify, conversion of kininogens into active kinins is markedly increased. The pathological significance of this change lies not simply in increased mediator abundance, but in its ability to rapidly translate tissue-level injury information into input signals that can be recognized and amplified by the nervous system.

(2) Insufficient degradation prolongs the pronociceptive window of kinins

Degradative enzymes such as ACE are involved not only in vasoactive peptide metabolism but also in determining how long kinin signaling persists. When degradative efficiency declines, or generation exceeds clearance, the duration of action of bradykinin and its metabolic peptides is extended. Under these conditions, local nociceptors more readily remain in a hyperexcitable state, thereby driving peripheral sensitization toward persistence.

Table 1. Key components and functional hierarchy of the kinin system in the pain network

Component	Functional level	Primary role	Significance in the pain network
High-molecular-weight kininogen	Precursor level	Provides substrate for bradykinin generation	Determines humoral kinin-releasing potential
Low-molecular-weight kininogen	Precursor level	Provides substrate for local kinin generation	Participates in tissue inflammation and local nociception
Plasma kallikrein	Generation level	Cleaves precursors to generate bradykinin	Links vascular responses with acute nociception
Tissue kallikrein	Generation level	Generates active peptides such as kallidin	Participates in local tissue responses and neuroinflammation
Bradykinin	Active peptide level	Activates B2 receptors	Initiates acute pain and peripheral sensitization
Des-Arg kinin metabolites	Active peptide level	Activates B1 receptors	Participates in chronic inflammation and persistent hypersensitivity
B2 receptor	Receptor level	Mediates rapid vascular and neural responses	More closely associated with the pain-initiation phase
B1 receptor	Receptor level	Mediates inducible chronic amplification responses	More closely associated with the pain-maintenance phase
ACE and related degrading enzymes	Termination level	Restrict duration of kinin signaling	Determine the intensity and spatial range of kinin action

2. Pronociceptive Kinin Network in Peripheral Nociceptors

2.1 The kinin system is one of the earliest amplifiers of pain after tissue injury

(1) Kinin release rapidly transforms injury information into neural excitatory signals

When local tissues are exposed to mechanical injury, inflammatory stimulation, infection, or ischemia-reperfusion, the kinin system is often activated at a very early stage. Once generated, bradykinin can rapidly act on peripheral nociceptive nerve endings, making sensory neurons that were previously in a resting or low-sensitivity state more prone to firing. The critical issue here is not merely whether pain is produced, but whether nerve endings have been shifted into a state in which they are more readily co-activated by mechanical, thermal, and chemical stimuli.

(2) The core pronociceptive significance of kinins lies in threshold reduction rather than simple stimulus addition

From the perspective of molecular networks, kinins do not simply add another pronociceptive ligand. Rather, they globally lower the response threshold of the local neural system. For this reason, the kinin system rarely acts in complete isolation; instead, it interacts with prostaglandins, cytokines, ATP, protons, nerve growth factor, and other mediators to establish a rapidly formed hyperresponsive microenvironment after injury.

2.2 Kinin receptors remodel neuronal excitability through ion-channel sensitization

(1) B2 receptor activation first alters the intracellular signaling environment of neurons

Following binding of bradykinin to the B2 receptor, G protein-coupled signaling pathways including PLC, PKC, PKA, and MAPK are activated. These pathways enhance intracellular Ca2+ mobilization, alter membrane protein phosphorylation states, and ultimately increase the probability of opening of multiple pain-related ion channels. Thus, the true function of kinin receptors is not merely signal reception, but rapid reconfiguration of the electrophysiological background of sensory neurons.

(2) TRPV1 and TRPA1 are among the most important downstream amplifiers of the kinin system

In pain research, TRPV1 and TRPA1 are often regarded as key executors of inflammatory hypersensitivity, and the kinin system is one of their critical upstream regulators. Through PKC-related pathways and related signaling cascades, bradykinin can enhance the thermal and chemical sensitivity of TRPV1 and can also promote TRPA1-mediated responses to inflammatory stimulation. In other words, the kinin system translates local inflammatory signals into a state in which ion channels are more easily activated, thereby amplifying pain signaling.

(3) Voltage-gated sodium and calcium channels are also incorporated into the kinin-sensitization network

In addition to TRP channels, kinin signaling can influence the opening probability and expression status of NaV and CaV channels, making action potentials easier to initiate and sustain. This level of regulation is particularly important, because it determines that excitation of local nociceptors does not remain confined to receptor activation alone, but is further converted into higher-frequency and more persistent neural discharge.

2.3 The kinin system further expands nociceptive signaling through vascular and immune environments

(1) Changes in vascular permeability reshape the local pronociceptive microenvironment

Bradykinin promotes vasodilation and increased vascular permeability, enabling plasma protein extravasation, local edema formation, and recruitment of inflammatory cells. In the context of pain, the significance of this vascular effect does not lie merely in swelling itself, but in the creation of a tissue microenvironment that favors accumulation of prostaglandins, cytokines, and proteases, thereby continuously exposing local nerve endings to pronociceptive stimuli.

(2) Peripheral sensory neurons are not passive recipients, but active participants in neurogenic inflammation

Once nociceptors are activated by the kinin system, sensory neurons themselves can participate in amplification of local neurogenic inflammation, thereby further enhancing vascular responses, immune-cell migration, and inflammatory mediator release. Consequently, the kinin system forms not a single receptor-mediated effect, but a peripheral amplification loop involving vascular, immune, and neural terminal components.

3. Kinin Network in Spinal and Brain Pain Regulation

3.1 The kinin system participates in amplification of excitability in the spinal dorsal horn

(1) Kinin-related signaling enhances synaptic transmission in the spinal dorsal horn

Persistent peripheral kinin input does not remain restricted to sensory endings, but instead drives enhanced excitability in nociceptive circuits of the spinal dorsal horn. The kinin system can facilitate glutamatergic transmission and increase the responsiveness of dorsal horn neurons to peripheral input, thereby further amplifying otherwise limited stimuli into persistent pain output at the spinal level.

(2) This indicates that the kinin system serves as a bridge between peripheral and central sensitization

If the kinin system is viewed only as a peripheral inflammatory mediator, its role in chronic pain development will be underestimated. More accurately, the kinin system continuously transmits local injury information into the spinal cord and drives the spinal network into a hyperresponsive state through synaptic amplification. It therefore functions as a transitional node linking local injury to central amplification.

3.2 Receptor remodeling in dorsal root ganglia determines the input background of persistent hypersensitivity

(1) After nerve injury, B1 receptors are more readily upregulated in dorsal root ganglia

In the context of nerve injury, chronic inflammation, and diabetes-related metabolic disturbances, dorsal root ganglion neurons often undergo reprogramming of their sensitivity to the kinin system, particularly through inducible upregulation of B1 receptors. As a result, peripheral kinin stimulation of the same intensity can evoke stronger neuronal responses and more readily generate spontaneous pain, ectopic discharges, and mechanical hypersensitivity.

(2) In this context, B1 receptors function more as maintainers than initiators

Unlike B2 receptors, which are biased toward acute initiation, remodeling of B1 receptors in dorsal root ganglia is more closely related to the maintenance of persistent abnormal input. This distinction helps explain why early inflammatory pain and chronic neuropathic pain stages do not depend on kinin receptors in exactly the same manner.

3.3 In brain-level neural regulation, the kinin system is more closely associated with inflammation- and stress-related effects

(1) Kinin signaling can influence neuroinflammation and neural network plasticity in the brain

At higher levels of neural regulation, the kinin system does not correspond to direct nociception as prominently as it does in the periphery and spinal cord. Instead, it is more closely involved in neuroinflammation, blood-brain barrier status changes, and local rearrangement of network excitability. Accordingly, in headache, post-brain-injury hypersensitivity, and inflammation-related central discomfort states, the kinin system retains substantial mechanistic relevance.

(2) Its significance lies in linking pain regulation to broader central stress networks

This suggests that the kinin system is not merely a local pain-amplifying factor, but may also exert broader neuromodulatory effects in states shaped jointly by emotional stress, autonomic fluctuations, and neuroinflammation.

4. Coupling Between the Kinin System, Glial Cells, and Neuroinflammation

4.1 The impact of the kinin system on glial cells determines the depth of pain chronification

(1) Astrocytes and microglia can be recruited into the kinin-amplification network

Once kinin receptor-related signaling extends to the glial-cell level, its significance is no longer limited to transient nociception. Activation of glial cells can induce Ca2+ changes, MAPK cascades, and inflammatory cytokine release, thereby providing sustained support for neuronal excitability. This converts the pain state from a condition of neuronal hyperresponsiveness alone into an abnormal network jointly maintained by neurons and glia.

(2) Glial involvement shifts pain from a reversible response to a maintainable state

Acute pain may diminish as injury resolves, but once glial cells are engaged, the spinal and central microenvironment may remain under chronic inflammatory and hyperexcitable conditions. This is one of the major reasons why chronic pain is difficult to reverse through a single peripheral analgesic strategy.

4.2 The kinin system forms a positive-feedback loop with inflammatory cytokines

(1) Inflammatory cytokines can further induce B1 receptor expression

Inflammatory cytokines such as TNF-alpha and IL-1beta can promote upregulation of B1 receptors, thereby strengthening the persistent signaling capacity of the kinin system. In other words, the immune system first amplifies the kinin network, and the kinin network in turn further enhances pain and neuroinflammation.

(2) This positive-feedback loop is an important pathological basis of chronic hypersensitivity

Once kinin release, B1 receptor induction, TRP-channel sensitization, glial activation, and enhanced spinal excitability form a closed loop, pain is no longer merely a passive consequence of injury, but evolves into a self-sustaining pathological network state.

Table 2. Network shifts of the kinin system across different pain stages

Pain stage or type	Major feature of the kinin system	Key molecular focus	Major network consequence
Acute inflammatory pain	Rapid kinin generation and immediate B2 receptor activation	Bradykinin, B2 receptor, TRPV1	Pain initiation, thermal hyperalgesia, local edema
Persistent inflammatory hypersensitivity	Progressive induction and upregulation of B1 receptors	Des-Arg kinin metabolites, B1 receptor	Mechanical hypersensitivity, allodynia, maintenance of inflammation
Neuropathic pain	Receptor remodeling in DRG and spinal cord	B1 receptor, TRPA1, NaV channels	Spontaneous pain, ectopic discharge, persistent hypersensitivity
Central sensitization stage	Spinal glutamatergic amplification and glial participation	B1/B2 receptors, MAPK, glial cells	Dorsal horn hyperexcitability, formation of chronic pain networks
Neuroinflammation-related state	Receptor induction and positive feedback with inflammatory cytokines	B1 receptor, IL-1beta, TNF-alpha	Difficult-to-reverse hypersensitivity, network chronification

5. Differences in Kinin Networks Across Pain Types

5.1 Inflammatory pain

(1) In inflammatory pain, acute sensitization is more prominently dominated by B2 receptors

In inflammatory pain, rapid bradykinin release and B2 receptor activation typically constitute the earliest pronociceptive axis. This stage is characterized by rapid onset, strong locality, and close association with vascular responses and tissue edema.

(2) As inflammation persists, the importance of B1 receptors gradually increases

With accumulation of inflammatory cytokines and metabolic kinin products, B1 receptor expression rises, shifting pain from an acute stimulus response toward a persistent hypersensitive state. Thus, even within inflammatory pain itself, receptor dominance shifts from B2 toward B1 over time.

5.2 Neuropathic pain

(1) In neuropathic pain, the kinin system is more strongly associated with maintenance-type abnormalities

In neuropathic pain, the importance of the kinin system lies less in initiating stimuli and more in maintaining persistent sensitization and abnormal discharge. In particular, coupling among B1 receptors, TRPA1, NaV channels, and neuroinflammation jointly determines whether pain abnormalities persist after nerve injury.

(2) This also explains the difficulty of intervention

Neuropathic pain does not depend solely on kinin receptors themselves, but also involves ion-channel remodeling, glial activation, and central plasticity. Consequently, blockade of a single kinin receptor is unlikely to achieve sufficient efficacy across all chronic pain models.

5.3 Visceral pain and vascular pain-related abnormalities

(1) In visceral pain, the kinin system carries simultaneous smooth-muscle, vascular, and neural significance

Visceral pain is not equivalent to superficial inflammatory pain, and its development commonly involves distension, spasm, local ischemia, and permeability changes. The kinin system is well positioned to participate in all three processes and therefore has strong explanatory value in intestinal, bladder, and vascular pain conditions.

(2) Its distinctive role lies in directly translating tissue microenvironmental changes into sensory abnormalities

In these forms of pain, the kinin system often serves as the molecular bridge that translates changes in the tissue chemical environment into neural excitation. Its significance therefore extends beyond that of a conventional inflammatory mediator and includes a central role in abnormal visceral sensation.

6.Commonly Used Research Products

Table 3. Common small molecules and functional compounds used in research on the kinin system in pain and neural regulation

Name	CAS No.	Experimental stage	Key use	Use notes
Bradykinin	58-82-2	B2 receptor activation	Construction of acute pronociceptive and peripheral sensitization models	Suitable for cell stimulation, local injection, and ex vivo neuronal response experiments
des-Arg9-Bradykinin	15958-92-6	B1 receptor activation	Simulation of chronic inflammation and persistent hypersensitivity	More suitable for persistent inflammatory and nerve-injury models
Kallidin	342-10-9	Tissue kinin-system activation	Simulation of tissue kallikrein-related pathways	Suitable for local tissue inflammation and visceral pain studies
Icatibant	130308-48-4	B2 receptor blockade	Validation of the role of B2 receptors in acute nociception and vascular responses	Suitable as a classical B2 receptor antagonist control
R715	185052-09-9	B1 receptor blockade	Validation of the contribution of B1 receptors to chronic hypersensitivity	More suitable for neuropathic pain and persistent inflammation models
B9430	180981-09-3	Dual B1/B2 receptor blockade	Simultaneous assessment of B1 and B2 receptor functions in the overall kinin network	Suitable for parallel dual-receptor antagonism studies
Aprotinin	9087-70-1	Upstream generation inhibition	Inhibition of kallikrein activity to reduce kinin generation	Suitable for verifying the contribution of upstream kinin generation to pain phenotypes
HC-030031	349085-38-7	TRPA1 blockade	Validation of whether kinin-mediated pain depends on TRPA1 participation	Suitable for combination with B1 receptor or inflammatory models
A-967079	1170613-55-4	TRPA1 blockade	More selective TRPA1 inhibitory tool compound	Suitable for TRPA1-specific validation
Capsazepine	138977-28-3	TRPV1 blockade	Validation of whether bradykinin-B2 receptor signaling is amplified through TRPV1	Suitable for thermal hyperalgesia and neuronal Ca2+ studies
AMG9810	545395-94-6	TRPV1 blockade	Validation of the role of TRPV1 in acute inflammatory pain	Suitable as a TRPV1 pharmacological control
SB-366791	472981-92-3	TRPV1 blockade	Validation of thermal pain and inflammatory hypersensitivity pathways	Suitable for joint analysis with bradykinin stimulation
Allyl isothiocyanate	57-06-7	TRPA1 activation	Construction of chemical pain and TRPA1-response models	Suitable for validation of kinin-TRPA1 coupling
Cinnamaldehyde	104-55-2	TRPA1 activation	Construction of irritant chemical pain models	Suitable for behavioral validation of downstream TRPA1 signaling
Capsaicin	404-86-4	TRPV1 activation	Construction of TRPV1-dependent nociceptive models	Suitable for upstream-downstream analysis relative to B2 receptor signaling
Resiniferatoxin	57444-62-9	Strong TRPV1 activation	Construction of high-intensity TRPV1 stimulation or sensory-neuron ablation-related models	Suitable for high-intensity TRPV1 functional validation
Ruthenium red	11103-72-3	Broad cation-channel inhibition	Early validation tool for TRP-related channels	More suitable for preliminary screening than for replacement of selective inhibitors
Formaldehyde	50-00-0	Chemical pain model	Construction of formalin-like persistent pain and inflammatory responses	Suitable for behavioral and spinal amplification studies
Carrageenan	9000-07-1	Inflammation induction	Construction of classical inflammatory hypersensitivity models	Suitable for observing initiation and maintenance roles of the kinin system in inflammatory pain
U-73122	112648-68-7	PLC inhibition	Validation of whether downstream PLC signaling of B2 receptors participates in channel sensitization	Suitable for cell-signaling and electrophysiology studies
GF109203X	133052-90-1	PKC inhibition	Validation of whether bradykinin-induced TRPV1 sensitization depends on PKC	Suitable for receptor-channel coupling studies
U0126	109511-58-2	MEK/ERK inhibition	Evaluation of whether the kinin system has entered an ERK-dependent persistent amplification stage	Suitable for spinal-cord- and glia-related studies
Prostaglandin E2	363-24-6	Inflammatory synergy validation	Construction of cooperative pain models involving kinins and prostaglandins	Suitable for analysis of synergistic amplification among inflammatory mediators
Indometacin	53-86-1	COX inhibition	Validation of the degree of prostaglandin-pathway participation in kinin effects	Suitable for combined use with carrageenan or bradykinin models
N-Methylmaleimide	930-88-1	Reactive electrophilic stimulation	Construction of TRPA1-related chemical stimulation models	Suitable as a complementary TRPA1-dependent validation tool
Tunicamycin	11089-65-9	Stress and neuroinflammation coupling	Induction of stress states to assist analysis of coupling between the kinin system and neuroinflammation	Suitable for expansion into stress-pain coupling models

Table 4. Common enzyme and protein tools used in kinin-system research

Catalog No.	Name	Grade and Purity	Research level	Research direction / intended use
H1443249	Human Kallikrein		Kinin generation layer	Suitable for direct construction of in vitro systems related to kinin generation and for validating the contribution of kinin release to pain initiation and local inflammatory amplification
rp167404	Recombinant Human Plasma Kallikrein/KLKB1 Protein	Animal Free,Carrier Free,Bioactive,ActiBioPure™,His Tag,≥90%(SDS-PAGE)	Kinin generation layer	Suitable for direct study of human plasma kallikrein activity in recombinant systems, validation of the role of KLKB1 in kinin generation, initiation of peripheral sensitization, and pain amplification, and screening of upstream inhibitors and in vitro mechanistic reconstruction
np001049	Kallikrein, Human Plasma (lyophilized)	≥95%(SDS-PAGE), Extinction Coefficient: 1.06	Kinin generation layer	Suitable for in vitro reconstruction of human plasma kinin-generation systems and for validating the relationship between bradykinin generation and peripheral sensitization
np001050	Kallikrein from Human Plasma	Bioactive,ActiBioPure™,Native,High Performance,EnzymoPure™,≥95%(SDS-PAGE),≥15 U/mg protein; Protein concentration: See COA	Kinin generation layer	Suitable for construction of human kinin-release systems under natural-source conditions, analysis of kininogen cleavage, bradykinin generation, and their effects on downstream pain- and inflammation-related signaling, and use as a function-validation tool closer to physiological conditions
EJ1514276	Human Kallikrein 1 (KLK1) ELISA Kit	BioReagent	Kinin generation layer	Suitable for detection of KLK1 levels in human samples and analysis of the relationship between tissue-type kinin-generation activity and pain or inflammatory status
EJ1514278	Human Prekallikrein (PK) ELISA Kit	BioReagent	Kinin generation precursor layer	Suitable for evaluation of prekallikrein reserves and kinin-system activation potential in human samples
EJ1514279	Human Kallistatin (KAL) ELISA Kit	BioReagent	Kinin regulatory layer	Suitable for investigation of inhibitory roles of kallikrein-regulatory proteins in inflammation, vascular permeability, and neural regulation
EJ1512000	Rat Prekallikarein (PK) ELISA Kit	BioReagent	Kinin generation precursor layer	Suitable for monitoring prekallikrein levels in rat models of inflammatory pain, neuropathic pain, and local injury
EJ1512867	Mouse Prekallikrein (PK) ELISA Kit	BioReagent	Kinin generation precursor layer	Suitable for analysis of kinin-system initiation capacity and pathological temporal changes in mouse models
np001051	Kallikrein, Cynomolgus Monkey Plasma	≥95%(SDS-PAGE)	Kinin generation layer	Suitable for comparative studies of kinin generation in primate-related settings and for in vitro validation with greater translational relevance
EJ1514275	Human Kininogen 1 (KNG1) ELISA Kit	BioReagent	Kinin precursor layer	Suitable for detection of kininogen reserves in human samples and analysis of the association between precursor supply and pain or inflammatory responses
EJ1512112	Rat Kininogen 1 (KNG1) ELISA Kit	BioReagent	Kinin precursor layer	Suitable for analysis of the relationship between kininogen changes and inflammatory hypersensitivity in rat models
EJ1512866	Mouse Kininogen 1 (KNG1) ELISA Kit	BioReagent	Kinin precursor layer	Suitable for assessment of kinin precursor levels and system activation status in mouse pain models
np001046	Kininogen, low molecular weight from Human Plasma	BioReagent,Native,≥95%(SDS-PAGE),Pre-lyophilization Protein Concentration: See COA	Kinin precursor layer	Suitable for construction of low-molecular-weight kininogen-related systems and study of local tissue-type kinin release and inflammatory responses
np001047	Kininogen, HMW, Human Plasma	BioReagent,Native,≥95%(SDS-PAGE),Protein concentration: See COA	Kinin precursor layer	Suitable for comparative studies of high- and low-molecular-weight kininogens and analysis of the influence of different precursor pools on kinin generation
T1488747	TRPV1 Human Pre-designed siRNA Set A		Downstream channel layer	Suitable for TRPV1 gene silencing to validate whether bradykinin-B2 receptor signaling depends on TRPV1 for amplification of thermal pain and inflammatory hypersensitivity
EJ1514987	Human Transient Receptor Potential Cation Channel Subfamily V, Member 1 (TRPV1) ELISA Kit	BioReagent	Downstream channel layer	Suitable for detection of TRPV1 levels in human samples and analysis of coupling between the kinin system and pain-executing channels
EJ1513278	Mouse Transient Receptor Potential Cation Channel Subfamily V, Member 1 (TRPV1) ELISA Kit	BioReagent	Downstream channel layer	Suitable for monitoring TRPV1 changes in mouse inflammatory pain and nerve-injury models
G1488399	GFAP Human Pre-designed siRNA Set A		Glial layer	Suitable for GFAP silencing studies of the role of astrocytes in kinin-system-mediated central amplification and chronification
Ab156546	GFAP Mouse mAb	ExactAb™, Validated, Carrier Free, Azide Free, High performance, 1.0 mg/mL	Glial layer	Suitable for detecting astrocyte activation levels and evaluating whether the kinin system has entered a glial-amplification stage
EJ1514471	Human Glial Fibrillary Acidic Protein (GFAP) ELISA Kit	BioReagent	Glial layer	Suitable for detecting GFAP levels in human samples and assessing the degree of neuroinflammation and glial responses
EJ1512977	Mouse Glial Fibrillary Acidic Protein (GFAP) ELISA Kit	BioReagent	Glial layer	Suitable for obtaining astrocyte activation readouts in mouse models
Ab156545	Iba1 Mouse mAb	ExactAb™, Validated, Animal Free, Carrier Free, Azide Free, High Performance, ≥95%(SDS-PAGE), 1.0 mg/mL	Glial layer	Suitable for detecting microglial activation and analyzing whether the kinin system drives neuroimmune amplification
Ab109181	Recombinant Iba1 Antibody	Recombinant, ExactAb™, Validated, See COA	Glial layer	Suitable for Iba1 immunodetection and for complementing evidence of microglial activation
rp156641	Recombinant Human AIF-1/Iba1 Protein	Carrier Free,Azide Free,His Tag,≥90%(SDS-PAGE)	Glial layer	Suitable as a standard protein tool for Iba1-related detection and methodological validation
Ab156213	c-Fos Mouse mAb	ExactAb™, Carrier Free, Validated, Azide Free, High performance, ≥95%(SDS-PAGE), 1.0 mg/mL	Neuronal activation layer	Suitable for detecting c-Fos expression in the spinal dorsal horn or related central regions and assessing kinin-system-induced amplification of neuronal excitability
rp170130	Recombinant Human c-Fos Protein	Carrier Free,Azide Free,His Tag,≥90%(SDS-PAGE)	Neuronal activation layer	Suitable as a standard protein tool for establishment of c-Fos-related detection and quantification systems

The role of the kinin system in pain and neural regulation is fundamentally reflected in a continuous process involving peripheral generation, receptor stratification, ion-channel sensitization, amplification of neuroinflammation, and remodeling of central networks. Its research value lies in revealing how local injury signals are transformed into persistent neural hypersensitivity and chronic pain networks.

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