Hemolytic anemia animal model, is the use of chemical, mechanical or other methods to construct animal models for disease research. Hemolytic anemia (hemolytic anemia) is an anemia caused when the rate of red blood cell destruction exceeds the compensatory function of bone marrow hematopoiesis, which occurs through intrinsic defects such as defects in red blood cell membranes, defects in hemoglobin structure or production, defects in red blood cell enzymes, or defects in red blood cell enzymes, or when an O-type female gives birth to an O-type non-O-type male; as well as through the influence of external factors, such as chemical, mechanical, and physical, biological, and immunological factors. exogenous factors. Currently, there are 2 main approaches to animal models of hemolytic anemia: the β-thalassemia mouse model and the sickle cell disease transgenic mouse model.
Principle
Depending on the experimental method, the corresponding principle is different:
The basic principle of the murine model of β-thalassemia is to cause β-thalassemia symptoms in mice by genetic recombination.
The basic principle of the transgenic mouse model of sickle cell disease is that the dominant control region sequence (DCR) is located flanking the human β-beadlein locus and directs the high-level, copy number-dependent expression of the β-beadlein gene in the erythrocytes of human and transgenic mice. When the bar β-bead protein DCR sequence is linked to the human α1-bead protein gene in transgenic mice, high levels of expression are obtained. Thus, it is possible to obtain transgenic mouse lines with greater expression of human hemoglobin (HbA) than endogenous mouse hemoglobin expression by using a construct containing the β-bead protein DCR, and the human β- and α1-bead protein genes, resulting in an imbalance in α- and β-bead protein synthesis.
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