目的 研究枸杞多糖對小鼠酒精性肝損傷的保護作用及機制。方法 將小鼠隨機分為對照組、模型組和枸杞多糖低、中、高劑量（75、150、300 mg/kg）組，第1~9天于每日13：00時分別ig給藥，模型組和對照組給予等量雙蒸水。第10~16天給藥4 h后，枸杞多糖和模型組小鼠均ig 50%酒精20 mL/kg進行造模，對照組小鼠給予等量雙蒸水。觀察小鼠一般狀態(tài)，末次ig酒精16 h后處死小鼠，檢測肝臟指數(shù)；全自動生化分析儀檢測血清中丙氨酸轉(zhuǎn)氨酶（ALT）、天冬氨酸轉(zhuǎn)氨酶（AST）、三酰甘油（TG）、總膽固醇（TC）水平；試劑盒法測定肝組織丙二醛（MDA）、還原型谷胱甘肽（GSH）、谷胱甘肽過氧化物酶（GSH-Px）、總超氧化物歧化酶（SOD）及炎性因子腫瘤壞死因子-α（TNF-α）、白介素-1β（IL-1β）的含量；HE染色觀察肝組織病理變化。結(jié)果 與模型組比較，枸杞多糖各劑量組小鼠醒酒時間短，毛色有所改善，較活躍；各劑量組肝臟指數(shù)呈下降趨勢，但不具有統(tǒng)計學意義；各劑量組血清ALT、AST、TC、TG均呈下降趨勢，其中高、中劑量組ALT顯著降低（P<0.05），3個劑量組TG濃度均差異顯著（P<0.01）；各劑量組小鼠肝臟MDA含量顯著降低（P<0.05、0.01），GSH、SOD水平顯著升高（P<0.05、0.01），GSH-Px水平升高但未表現(xiàn)出顯著性差異；高、中劑量組小鼠肝臟TNF-α和IL-1β水平顯著降低（P<0.05、0.01）。HE染色顯示，與模型組比較，枸杞多糖各組肝組織破壞程度較輕。結(jié)論 枸杞多糖對于乙醇誘導的酒精性肝損傷具有一定的保護作用，作用機制可能與通過清除體內(nèi)多余自由基、增強體內(nèi)抗氧化能力以及減輕炎癥反應(yīng)相關(guān)。

Objective To investigate the protection of lycium barbarum polysaccharide (LBP) on alcohol-induced liver injury and explore their pharmacological mechanisms.Methods 60 male mice were randomly divided into five groups, normal control group, model group and LBP different concentrations (75, 150, 300 mg/kg) groups. Drugs was ig administered at 13:00 a day on the 1st to 9th day. The model group and the control group were given the same amount of double steamed water. After 4 hours of administration from 10th to 16th day, alcoholic liver injury model was induced by 50% ethanol for 7 days. The general state of mice was observed. After 16 h of the last administration, serum and liver were obtained and related markers were determined. The liver tissue injury situation was assessed by HE staining. The levels of serum alanine transaminase (ALT), serum aspartate transaminase (AST), serum triglyceride (TG) and serum total cholesterol (TC), and the liver levels of malondialdehyde (MDA), glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and inflammatory factor TNF-α, IL-1β were measured. Results Compared with model group, LBP group had shorter sobering time, better hair color and more active; liver index of each dose group showed a downward trend, but not statistically significant; ALT, AST, TC and TG in serum of each dose group showed a downward trend, and ALT in high and middle dose groups decreased significantly (P<0.05), and TG concentration in three dose groups had significant difference (P<0.01); MDA content in liver of rats decreased significantly (P<0.05, 0.01), GSH and SOD levels increased significantly (P<0.05, 0.01), GSH-Px levels increased but there was no significant difference; TNF-α and IL-1β levels in liver of mice in high and medium dose groups decreased significantly (P<0.05, 0.01). HE staining showed that compared with the model group, LBP groups had less damage to liver tissue. Conclusion LBP have protective effect on alcohol-induced acute alcoholic liver injury, the mechanism may be related to the elimination of excess free radicals, the enhancement of antioxidant capacity and the alleviation of inflammation.