冠心病气虚血瘀证病证结合大鼠模型 z-bo 2020-12-10 321

　　Objective To analyze the relationship between CHD Qi deficiency and blood stasis syndrome combined with pathology, etiology, and tongue manifestations of the compound model in rats and the relationship with prostacyclin (PGI2) and thromboxane A2 (TXA2). The blood stasis syndrome combined with the modeling method of the rat model. Methods Thirty-two rats were randomly divided into 4 groups: Group K: normal diet and water (n=8); Group L: normal rearing for 21 days and simply ligate the left anterior descending coronary artery (n=8); Group Y: food control Compound fatigue exercise for 21 days (n = 8); Group F: food control compound fatigue exercise for 21 days + ligation of the left anterior descending coronary artery (n = 8). After modeling, use Photoshop 6.0 to analyze the RGB value of the tongue surface and use the "RGB data distribution range table" to evaluate the tongue color of each model; HE staining detects the filamentous papillary epithelial layer, keratinized layer, lamina propria height and lamina propria microvessels Quantity; immunohistochemical analysis of the positive expression rate of PGI2 and TXA2 and calculation of the T/P ratio. Results (1) The tongue quality of rats in group K was attributed to "light red tongue"; the R value of the tongue surface of rats in group L was significantly lower than that of group K, belonging to "dark red tongue"; the R value of tongue surface of rats in group Y was higher than that of K Group significantly decreased, belonging to "light white tongue"; R, G, and B values of the tongue surface of rats in group F were significantly lower than those of group K and L, and belonged to "purple tongue"; (2) rat tongue surface silk in group L There was no difference in the height of each layer of the papillae and the number of microvessels between group K; group Y compared with group K, the height of the filiform papillary keratinization layer was significantly reduced; the height of the filiform papillary epithelium and keratinization layer of group F were significantly lower than that of group K The number of microvessels in group L and group L was significantly higher than that in group K and group L; there was no difference in the height of the lamina propria of the filamentous papilla in each group; (3) PGI2 changes in group L, group Y, and group F were not significant compared with group K; group L The TXA2 level and T/P ratio was significantly higher than that of group K; the TXA2 level and T/P ratio of group F was significantly higher than that of group K and group L. Conclusion The RGB value characteristics of tongue color of CHD Qi deficiency and blood stasis syndrome are related to the decrease in the height of the filamentous papillary epithelium and keratinization layer, and the increase in the number of capillaries in the lamina propria. The molecular biological mechanism may be related to the TXA2/PGI2 imbalance; the pathological causes are compounded The model is more in line with the characteristics of a CHD model combining Qi deficiency and blood stasis syndrome.