ObjectiveTo explore the mechanism by which Liqi Huoxue Dripping Pill (LQHXDP) inhibits cardiomyocyte apoptosis in rats with myocardial ischemia-reperfusion injury (MIRI).MethodsMale Sprague-Dawley (n=96) rats were randomly assigned to a normal, sham-operated, model, LQHXDP, adenovirus negative control (Ad-shNC), adenovirus-mediated HIF-1α knockdown (Ad-shHIF-1α), LQHXDP+ Ad-shNC, or LQHXDP+ Ad-shHIF-1α group using a random number table. LQHXDP was administered daily via oral gavage at 175.0 mg/(kg·d) for 10 consecutive days. On day 7, recombinant adenovirus was injected into the left ventricular wall of rats in the corresponding groups at multiple points. On day 10, the MIRI model was established by ligating the left anterior descending coronary artery. The sham-operated group underwent thoracotomy and suture placement without coronary ligation. Samples were collected after reperfusion was completed. Serum creatine kinase isoenzymes (CK-MB), cardiac troponin I (cTnI), and heart-type fatty acid binding protein (H-FABP) levels were measured using enzyme-linked immunosorbent assay. 2, 3, 5-Triphenyltetrazolium chloride staining was used to measure the volume ratio of myocardial infarction. HE staining was performed to observe the morphology of myocardial tissue. Terminal transferase uridyl nick end labeling assay was conducted to analyze the apoptosis rate of cardiomyocytes, and Western blotting was used to detect the expression of key proteins in the apoptosis (B-cell lymphoma-2 [Bcl-2], Bcl-2 associated X protein [Bax], and cleaved cysteinyl aspartate specific proteinase 3[Cleaved-Caspase-3] and HIF-1α/ Bcl-2-adenovirus E1B 19 kDa interacting protein 3 (BNIP3) signaling pathway (HIF-1α, heme oxygenase-1 [HO-1], and BNIP3).ResultsLQHXDP pretreatment significantly reduced serum CK-MB, cTnI, and H-FABP levels, as well as the myocardial infarction volume ratio in rats with MIRI. LQHXDP also improved myocardial tissue morphology, decreased cardiomyocyte apoptosis, upregulated Bcl-2 protein expression, and downregulated Bax, Cleaved-Caspase-3, HIF-1α, HO-1, and BNIP3 protein expressions (P < 0.05). However, adenovirus-mediated shRNA HIF-1α impaired the effects of LQHXDP pretreatment in attenuating myocardial injury and inhibiting apoptosis in MIRI rats (P < 0.05).ConclusionLQHXDP reduces cardiomyocyte apoptosis and protects rat myocardium from MIRI by regulating the HIF-1α/BNIP3 signaling pathway.

디칸퍼연장복 젬; 심실 근경색 후 재훈구속성; 세포 소멸; 혈종호유성-1α/B-림의미-2-염기의상호작용단백질3 신호 형랭; 대쥬