动物造模,冠心病气虚血瘀证病证结合 z-bio 2022-11-02 375

　　Objective To explore the modeling method of CHD model with syndrome of Qi deficiency and blood stasis by analyzing the pathology, etiology, tongue manifestation of the compound model and the relationship with prostacyclin and thromboxane A2.

　　Methods Thirty two rats were randomly divided into four groups: group K: normal diet and drinking water (n=8); Group L: after 21 days of normal feeding, the anterior descending branch of left coronary artery was ligated (n=8); Group Y: diet control combined with fatigue exercise for 21 days (n=8); Group F: diet control combined with fatigue exercise for 21 days+ligation of left anterior descending coronary artery (n=8). After modeling, use Photoshop 6.0 to analyze the RGB value of tongue surface and use "RGB data distribution range table" to evaluate the tongue color of each model; HE staining was used to detect the height of the superior cortex, cornification layer, lamina propria and the number of microvessels in lamina propria of filamentous papilla; The positive expression rates of PGI2 and TXA2 were analyzed by immunohistochemistry and the T/P ratio was calculated.

　　Results (1) The tongue of group K rats belonged to "light red tongue"; The R value of the tongue surface in group L was significantly lower than that in group K, which belonged to "dark red tongue"; The R value of tongue surface in group Y was significantly lower than that in group K, which belonged to "light white tongue"; The R, G, B values of the tongue surface of rats in group F were significantly lower than those in group K and group L, belonging to "purple tongue"; (2) There was no difference in the height of each layer of lingual filamentous papilla and the number of microvessels between group L and group K; Compared with group K, the height of filamentous papillary keratoderma in group Y decreased significantly; The heights of the upper cortex and cornification layer of filamentous papilla in group F were significantly lower than those in group K and L, and the number of microvessels in group F was significantly higher than that in group K and L; There was no difference in the height of lamina propria of filamentous papilla in each group; (3) The change of PGI2 in group L, Y, F was not significant compared with that in group K; TXA2 level and T/P ratio in group L were significantly higher than those in group K; TXA2 level and T/P ratio in group F were significantly higher than those in group K and group L.

　　Conclusion The RGB numerical characteristics of tongue color in CHD with Qi deficiency and blood stasis syndrome are related to the reduction of the height of the upper cortex and cornification layer of the filamentous papilla and the increase of the number of capillaries in the lamina propria, and its molecular biological mechanism may be related to the imbalance of TXA2/PGI2; The combined model of pathology and etiology is more in line with the characteristics of CHD model of Qi deficiency and blood stasis syndrome.