Esculin Inhibits Lipoplysaccharide-induced Myocardial Injury by Regulating TLR/NF-κB Pathway

OBJECTIVE To investigate the effects of esculin on lipopolysaccharide(LPS)-induced myocardialinjury and TLR/NF-κB pathway in rats. METHODS The myocardial injury model induced by LPS was established. Rats were randomly divided into control group, LPS group, esculin low dose group(20 mg·kg^-1), esculin middle dose group(40 mg·kg^-1), esculin high dose group (80 mg·kg^-1) and positive control group(dexamethasone, 2 mg·kg^-1). Cardiac function was detected by echocardiography, and the degree of cardiac histological damage was detected by HE staining. The content of cardiactroponin I(cTnI), creatine kinase(CK)-MB(CK-MB), myoglobin(Mb), tumor necrosis factor-α(TNF-α), interleukin-6 (IL-6), IL-1β, malondialdehyde(MDA), superoxide dismutase(SOD) and myeloperoxidase(MPO) in blood were detected by ELISA. The proteinexpressive levels of Toll-like receptor 2(TLR2), TLR4, myeloid differentiation factor 88(MyD88), interleukin-1 receptor-associated kinases(IRAK1) and phosphorylated-nuclear factor-κB(p-NF-κB) were detected by Western blotting in cardiac tissue. RESULTS Compared with the LPS group, the levels of heart rate, left ventricular wall thickness and left ventricular ejection fraction were significantly increased after esculin treatment(P<0.05), while left ventricular end systolic volume was significantly decreased(P<0.05). The expression of myocardial enzymes cTnI, CK-MB and Mb was significantly down-regulated(P<0.05). The expression of pro-inflammatory cytokines IL-6, TNF-α and IL-1β were down-regulated(P<0.05). The oxidative stress markers SOD content was increased significantly(P<0.05), while MDA and MPO content was decreased significantly(P<0.05). Protein expression levels TLR2, TLR4, MyD88, IRAK1 and p-NF-κB were significantly reduced(P<0.05). CONCLUSION Esculin has a protective effect on LPS-induced myocardial injury and inhibits TLR/NF-κB signaling pathway.