Protective Effects of Armillaria mellea Polysaccharides against Ethanol-Induced Vascular Endothelial Cell Injury in Rats

The aim of this study is to evaluate the protective effect of Armillaria mellea polysaccharides (AMP) against ethanol-induced vascular endothelial cell injury in rats. Altogether 40 SD rats were randomly divided into 4 groups: normal control, injury, low-and high-dose AMP. The rats from all groups except the normal control group were gavaged with 40% ethanol at 10 mL/kg m_b to induce endothelial cell injury. The rats in the low-and high-dose groups were gavaged with AMP at 100 and 400 mg/kg m_b, respectively, while the remaining groups were given an equal volume of physiological saline. The administration period lasted for 4 weeks. The histopathological changes of carotid arteries were observed by hematoxylin-eosin (HE) staining. Serum triglycerides (TG), total cholesterol (T-CHO), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), nitric oxide (NO), endothelin 1 (ET-1), superoxide dismutase (SOD), and malondialdehyde (MDA) levels were detected. In addition, the effects of different doses (100 and 400 μg/mL) of AMP on the levels of reactive oxygen species (ROS), mitochondrial transmembrane potential, apoptosis, and the expression of apoptosis-associated proteins such as B cell lymphoma 2 (Bcl-2), Bcl-2 associated X protein (Bax), and caspase-3 in human umbilical vein endothelial cell injured by 600 μmol/mL ethanol were investigated. Results: AMP attenuated ethanol-induced endothelial cell injury, decreased T-CHO, TG, LDL-C, iNOS, NO, ET-1, and MDA levels, and increased HDL-C and SOD activity. In vitro, AMP reduced cellular ROS levels, inhibited the ethanol-induced decrease in mitochondrial transmembrane potential and apoptosis, increased Bcl-2/Bax ratio and down-regulated the expression of cleaved caspase-3. Conclusion: AMP have a protective effect against ethanol-induced endothelial cell injury in rats, and the mechanism may be related to their lipid-lowering, antioxidant, and anti-apoptotic effects.