Effect of Salvianolate on Myocardial Ischemia Reperfusion Injury and Its Mechanism

Abstract

<sec> <title>Background:</title> The paper investigated the H9c2 cardiomyocyte model induced by hypoxia. Cell viability was monitored by real-time unlabeled cell function analyzer to determine the levels of LDH, MDA and SOD in cell supernatant. </sec> <sec> <title>Material and Methods:</title> The cytoskeleton staining was labeled by phalloidin staining. WB was applied to detect the expression of myocardial cytoskeleton microtubuleassociated protein and the expression of HIF-1α protein in each group. After adding AMPK inhibitor Compound C, Hoechst 33342 was employed to detect the apoptosis rate of cardiomyocytes, and WB was applied to detect the expressions of myocardial cytoskeleton-associated protein and p-AMPK. </sec> <sec> <title>Results:</title> Salvianolate can effectively improve cell viability, reduce LDH and MDA levels, increase SOD content, improve skeletal structure damage, reduce nuclear concentration, reduce cell debris, and promote the expressions of microtubule-associated protein, α-tubulin and β-tubulin, MAP4, and microfilament-associated protein MLCK, p-MLC-2 in myocardial cytoskeleton microtubules after ischemia and hypoxia. The addition of AMPK inhibitor can inhibit the expressions of p-AMPK, tubulin MAP4, microfilament protein MLCK and p-MLC-2 up-regulated by Salvianolate. </sec> <sec> <title>Conclusion:</title> Salvianolate can promote the expressions of microtubule-associated protein α-tubulin, β-tubulin,MAP4, microfilament-associated protein MLCK and p-MLC-2 in myocardial cytoskeleton after ischemia and hypoxia, indicating that Salvianolate can protect the myocardial cytoskeleton after ischemia and hypoxia, and may protect the structure and function of microtubules and microfilaments in the myocardial cytoskeleton through the AMPK/MAP4 and AMPK/MLCK pathways. </sec>