目的 探討金絲桃苷對代謝相關(guān)脂肪性肝?。∕AFLD）的保護(hù)作用。方法 將36只ApoE^-/-小鼠，隨機(jī)分為模型組、金絲桃苷（200 mg/kg）組和辛伐他?。栃詫φ账?，5.2 mg/kg）組，每組12只；另將12只C57BL/6小鼠作為對照組。對照組給予普通飼料，其他3組均給予高脂飼料構(gòu)建MAFLD模型，同時每天ig給藥2次，對照組和模型組ig 0.5% CMC-Na溶液，連續(xù)給藥12周。HE染色法觀察小鼠肝臟組織病理變化；油紅O染色法觀察小鼠肝臟組織內(nèi)脂肪沉積情況；全血項(xiàng)分析儀檢測小鼠血清總膽固醇（TC）、三酰甘油（TG）、高密度脂蛋白膽固醇（HDL-C）、低密度脂蛋白膽固醇（LDL-C）、天冬氨酸氨基轉(zhuǎn)移酶（AST）和丙氨酸氨基轉(zhuǎn)移酶（ALT）含量；ELISA法檢測小鼠肝組織丙二醛（MDA）、超氧化物歧化酶（SOD）、谷胱甘肽過氧化物酶（GSH-Px）、白細(xì)胞介素-6（IL-6）和腫瘤壞死因子-α（TNF-α）水平。結(jié)果 與模型組比較，金絲桃苷可以減小模型小鼠肝臟細(xì)胞空洞和炎癥浸潤；顯著改善脂質(zhì)沉積（P<0.01）；顯著降低血清LDL-C、AST、ALT水平（P<0.01）；顯著降低肝臟MDA、IL-6和TNF-α水平（P<0.01），顯著升高肝臟SOD和GSH-Px水平（P<0.05、0.01）。結(jié)論 金絲桃苷通過減少脂質(zhì)囤積、減輕氧化應(yīng)激、抑制炎癥反應(yīng)發(fā)揮對MAFLD的保護(hù)作用。

Objective To explore the protective effect of hyperoside on non-alcoholic fatty liver disease. Methods Thirty-six ApoE-/- mice were randomly divided into model group, hyperin (200 mg/kg) group and simvastatin (positive control drug, 5.2 mg/kg) group, with 12 mice in each group. Another 12 C57BL/6 mice were used as control group. The control group was given ordinary diet, and the other three groups were given high-fat diet to construct the MAFLD model, and the control group and the model group were given 0.5% CMC-Na solution intragaally twice a day, for 12 weeks. HE staining method was used to observe the pathological changes of mouse liver. Oil red O staining method to observe the fat content in mouse liver tissue. Whole blood analyzer to detect total cholesterol (TC), triglyceride (TG) and high-density lipoprotein cholesterol (HDL-C) in mouse serum , Low-density lipoprotein cholesterol (LDL-C), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) content. ELISA method was used to detect malondialdehyde (MDA) and superoxide dismutase (SOD) in mouse liver tissue, glutathione peroxidase (GSH-Px), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) content. Results Hyperoside can reduce the area of cavities and inflammatory infiltration of mouse liver cells and improve the condition of lipid deposition (P < 0.01). Hyperin significantly decreased the serum levels of TC, LDL-C, HDL-C, AST and ALT (P < 0.01), decreased the levels of MDA, IL-6 and TNF-α in liversignificantly (P < 0.01), and increased the levels of SOD and GSH-Px in liver significantly (P < 0.05, 0.01). Conclusion Hyperin can slow down the pathological process of non-alcoholic fatty liver disease, and its protective effect may be achieved by reducing lipid accumulation, reducing oxidative stress, and inhibiting inflammation.

R285.5

遼寧省自然科學(xué)基金面上項(xiàng)目（2015010708）