Study on the Mechanism by Which Tiaopihuxin Recipe Improves Myocardial Injury in Rats with Chronic Heart Failure by Regulating TLR4/MyD88/NF-κB Pathway to Mediate Inflammatory Factors
Objective: To observe the mechanism by which Tiaopihuxin Recipe improves myocardial damage in rats with chronic heart failure by regulating the TLR4/MyD88/NF-κB signaling pathway to mediate inflammatory factors. Methods: 30 healthy SD rats were randomly divided into normal group, model group, Western medicine group, Chinese medicine group and Chinese medicine + Western medicine group, with 6 rats in each group. Twenty-four SD rats ex-cept the normal group were subjected to coronary artery ligation to create a heart failure rat model. After success, the normal group and the model group were given normal saline 20ml/(kg·d) by gavage, and the Western medicine group was given Sacuba. Trivalsartan sodium 10 mg/(kg·d) was given by intragastric administration, the Chinese medicine group was given Tiaopihuxin prescription granules 23.40mg/(kg·d), and the Chinese medicine + western medicine group was given Tiaopihuxin prescription 23.40mg/(kg·d) combined with sacubitril/valsartan sodium 10 mg/(kg·d) by intragastric administration. After 4 weeks of continuous intragastric treatment, the mental state, diet, drinking water, activity level, fur color and other general conditions of the rats in each group were observed. Western blotting was used to detect the protein expression levels of TLR4, MyD88 and NF-κB in myocardial tissue. RT-qPCR was used to detect the gene transcription levels of TLR4, MyD88 and NF-κB in myocardial tissue. Enzyme-linked immunosorbent assay was used to detect NT-proBNP, TNF-α and IL-6. IL-10 expression level, LVEF level and changes in cardiomyocytes of rats in each group under light microscope were detected by ultrasound system. Results: Compared with the normal group, the TLR4, MyD88, NF-κB gene transcription and protein expression levels, and the expression levels of NT-proBNP, TNF-α, IL-6, and IL-10 in the model group were significantly increased (P<0.05); Compared with the model group, the gene transcription and protein expression levels of TLR4, MyD88, NF-κB, and the expression levels of NT-proBNP, TNF-α, IL-6, and IL-10 in each administration group were significantly reduced (P<0.05); Compared with the traditional Chinese medicine group, the TLR4, MyD88, NF-κB gene transcription and protein expression levels, and the expression levels of NT-proBNP, TNF-α, IL-6, and IL-10 in the western medicine group were relatively sim-ilar (P>0.05); compared with the western medicine group , the TLR4, MyD88, NF-κB gene transcription and protein expression levels, and the expression levels of NT-proBNP, TNF-α, IL-6, and IL-10 were significantly reduced in the traditional Chinese medicine + western medicine group (P<0.05). Conclusion: Tiaopihuxin Recipe can mediate inflam-matory factors by regulating the TLR4/MyD88/NF-κB pathway, slow down myocardial damage and alleviate clini-cal symptoms in rats with chronic heart failure. The combined application of Tiaopihuxin prescription and sacubitril-valsartan sodium can achieve more significant therapeutic effects.
Heart failureratsTiaopihuxin prescriptionTLR4/MyD88/NF-κB pathwayExperimental research
万方数据
维普
