Wang Xu-Tao, Chen Si-Si, Qi Min-You
Institute of Pharmacology, College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou 310014, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2018 Feb 8;34(2):134-136. doi: 10.12047/j.cjap.5598.2018.033.
To study the effects of ursolic acid on liver injury in diabetic mice induced by high-fat diet combined with streptozotocin(STZ), and to explore its possible mechanisms.
Diabetes mellitus was induced in twenty male ICR mice by a combination of high-fat diet for 6 weeks with low-dose streptozotocin (30 mg/kg, i. p.) for 5 consecutive days. After 9 days, fasting blood glucose levels were determined. Mice with fasting blood glucose levels exceeded 11. 1 mmol/L were diagnosed as diabetic mice and selected for further experiment. These mice were randomly divided into two groups(each group of 10):diabetic group, ursolic acid group (100 mg/kg, i. g.), and another 10 mice were set as control group. After continuous administration for 8 weeks, body weight (BW) were weighed, fasting blood glucose (FBG), total cholesterol (TC), triglyceride (TG), alanine aminotransferase (ALT), aspartate transaminase (AST) in serum and superoxide dismutase (SOD), malondialdehyde (MDA) in liver were measured. HE staining was used to observe pathological changes of liver tissue.
Compared with the control group, the level of FBG, TC, TG, ALT, AST, MDA were dramatically increased (<0. 05, <0. 01) and SOD was markedly decreased (<0.01) in the diabetic group; HE staining showed that parts of liver cells swelled and had a light fatty degeneration as well as lymphocyte infiltrated around the portal area in model group. Compared with the diabetic group, the level of FBG, TC, TG, ALT, AST, MDA were significantly declined (<0.05, <0.01) and SOD was considerably increased (<0.01) in the ursolic acid group; HE staining showed that the liver cells relatively arranged in order, edema was not obvious and inflammatory cells infiltrated lightly in the ursolic acid group.
Ursolic acid has a protective effect on liver injury in diabetic mice induced by high-fat diet combined with STZ by intraperitoneal ingector, and its mechanism may be associated with lowering blood glucose, regulating the lipid metabolism, reducing oxidative stress and enhancing the ability of anti-oxidation in liver.
研究熊果酸对高脂饮食联合链脲佐菌素（STZ）诱导的糖尿病小鼠肝损伤的影响，并探讨其可能机制。
将20只雄性ICR小鼠采用高脂饮食6周并连续5天腹腔注射低剂量链脲佐菌素（30mg/kg）诱导糖尿病。9天后，测定空腹血糖水平。空腹血糖水平超过11.1mmol/L的小鼠被诊断为糖尿病小鼠并选入进一步实验。将这些小鼠随机分为两组（每组10只）：糖尿病组、熊果酸组（100mg/kg，灌胃），另设10只小鼠作为对照组。连续给药8周后，称量体重（BW），测定血清空腹血糖（FBG）、总胆固醇（TC）、甘油三酯（TG）、丙氨酸氨基转移酶（ALT）、天冬氨酸氨基转移酶（AST）以及肝脏中超氧化物歧化酶（SOD）、丙二醛（MDA）。采用HE染色观察肝组织病理变化。
与对照组相比，糖尿病组FBG、TC、TG、ALT、AST、MDA水平显著升高（<0.05，<0.01），SOD显著降低（<0.01）；HE染色显示模型组部分肝细胞肿胀，有轻度脂肪变性，门管区周围有淋巴细胞浸润。与糖尿病组相比，熊果酸组FBG、TC、TG、ALT、AST、MDA水平显著下降（<0.05，<0.01），SOD显著升高（<0.01）；HE染色显示熊果酸组肝细胞排列相对整齐，水肿不明显，炎症细胞浸润较轻。
熊果酸对高脂饮食联合STZ腹腔注射诱导的糖尿病小鼠肝损伤具有保护作用，其机制可能与降低血糖、调节脂质代谢、减轻氧化应激及增强肝脏抗氧化能力有关。
