目的 研究紅景天苷對鏈脲佐菌素所致糖尿病大鼠肝臟的保護作用。方法 一次性ip鏈脲佐菌素(60 mg/kg)制備糖尿病大鼠模型,取造模成功的糖尿病大鼠80只,按血糖水平隨機分為模型組,紅景天苷25、50、100 mg/kg組以及鹽酸二甲雙胍(25 mg/kg)組,每組16只;另取同齡正常飼養(yǎng)大鼠16只作為對照組。ip給藥治療,1次/d,療程為12周。分別于0、4、8、12周測定各組大鼠血糖水平。治療12周后,測定各組大鼠體質(zhì)量和肝臟指數(shù);檢測血清中轉(zhuǎn)氨酶(ALT、AST)、堿性磷酸酶(ALP)活性;測定肝臟組織中超氧化物歧化酶(SOD)、過氧化氫酶(CAT)活性和丙二醛(MDA)含量;并通過HE染色觀察肝臟組織病理學(xué)改變。結(jié)果 與模型組比較,紅景天苷50、100 mg/kg組大鼠血糖水平顯著降低(P < 0.05、0.01),肝臟指數(shù)顯著降低、體質(zhì)量顯著增高(P < 0.05、0.01),血清中ALP活性明顯降低(P < 0.01),肝臟組織中SOD、CAT活性顯著升高(P < 0.05、0.01);紅景天苷25、50、100 mg/kg組大鼠血清中轉(zhuǎn)氨酶(ALT、AST)活性和肝組織中MDA含量顯著降低(P < 0.05、0.01);紅景天苷組大鼠肝組織病理形態(tài)學(xué)改變程度明顯減輕。結(jié)論 紅景天苷對鏈脲佐菌素所致糖尿病大鼠肝臟具有劑量相關(guān)性的保護作用,其作用機制可能與紅景天苷能夠有效改善抗氧化酶系統(tǒng)活性、降低氧化應(yīng)激損傷,從而改善肝功能有關(guān)。

Objective To investigate protective effects of salidroside on hepatic in diabetic rats induced by streptozotocin (STZ). Methods The experimental diabetic rat models were made by ip administered with STZ, and 80 models were selected. According to blood sugar levels, rats were randomly divided into the model group, salidroside (25, 50, and 100 mg/kg) groups, metformin hydrochloride (25 mg/kg) group, and other 16 rats as the control group. The drugs were given by ig administration for 12 weeks, once daily. In 0, 4, 8, and 12th weeks after experiment, the levels of fasting blood sugar were determined. After 12 weeks, the body weight and hepatic index were detected. The activities of ALT, AST, and ALP in serum were determined, and the activities of SOD and CAT, and the content of MDA in hepatic tissue were also determined. Histopathology changes of hepatic tissues were observed by HE staining. Results Compared with the model group, the fasting blood glucose level in salidroside 50 and 100 mg/kg groups significantly decreased (P < 0.01), the hepatic index significantly decreased (P < 0.05, 0.01), the body weight significantly increased (P < 0.05, 0.01), the activity of ALP significantly decreased (P < 0.01), and the activity of SOD and CAT in the hepatic tissue significantly increased (P < 0.05, 0.01). The activities of ALT and AST in salidroside 25, 50, and 100 mg/kg groups were significantly decreased (P < 0.05, 0.01), and the content of MDA in the hepatic tissue also significantly decreased (P < 0.05, 0.01). The histopathology changes of hepatic tissue in salidroside groups were significantly improved. Conclusion Salidroside has the protective effect on hepatic in diabetic rats induced by STZ with dose-dependent relation, whose mechanism may be related to its effects of improving antioxidant ability, reducing the damage of free radical, and improving hepatic function.