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[摘要]
目的 研究葛根素对链脲佐菌素诱导妊娠期糖尿病大鼠氧化应激损伤的保护作用.方法 通过ip 链脲佐菌素35mg/kg 制备妊娠期糖尿病大鼠模型.选取64 只模型大鼠并根据血糖水平随机分为模型组、葛根素40、80、160 mg/kg 组,另选取16 只同期妊娠的大鼠作为妊娠对照组,并取16 只同龄非妊娠雌性大鼠作为非妊娠对照组.ig 给药治疗,1 次/d,给药容积为20 mL/kg,连续给药2 周.分别于给药前和给药第7、14 天测定空腹血糖水平.给药治疗2 周后,测定丙氨酸转氨酶(ALT)、天门冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)活性,检测血清中丙二醛(MDA)含量及总抗氧化能力(T-AOC)水平;测定肝脏组织中超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性和MDA 含量.给药2 周后,通过HE 染色观察肝脏组织病理形态学改变.结果 葛根素160 mg/kg 组大鼠空腹血糖水平较模型组显著降低(P< 0.05、0.01).与模型组比较,葛根素80、160 mg/kg 组大鼠血清中ALT、AST 活性和MDA 含量均显著降低(P< 0.05、0.01),葛根素160 mg/kg 组ALP 活性显著降低(P< 0.01)、T-AOC 水平显著升高(P< 0.05).与模型组比较,葛根素80、160 mg/kg 组肝脏组织中SOD活性显著升高(P< 0.05、0.01),MDA 含量显著降低(P< 0.05、0.01);葛根素160 mg/kg 组CAT 活性显著升高(P< 0.01).葛根素组大鼠肝脏组织病理形态学改变明显改善.结论 葛根素对链脲佐菌素诱导妊娠期糖尿病大鼠氧化应激损伤具有保护作用,其作用机制可能与葛根素能够有效改善抗氧化酶活性、降低氧化应激损伤有关.
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[Abstract]
Objective To investigate protective effects of puerarin against oxidative stress injury in gestational diabetic rats induced by streptozocin. Methods Gestational diabetic model rats were made by ip administration with streptozocin (35 mg/kg). According to blood glucose levels, a total of 64 gestational diabetic rats were randomly divided into model group and puerarin (40, 80, and 160 mg/kg) groups. And other 16 pregnant rats in the same period were selected into the gestation control group, and 16 non-gestation female rats of the same age also were selected into the non-gestation control group. Rats were ig administered with dosage of 20 mL/kg, and the treatment was adopted once daily and lasted for 2 weeks. The level of fasting blood sugar in gestational diabetic rats were determined before treatment and treated for 7 and 14 d. After treatment for 2 weeks, the activities of ALT, AST, and ALP in serum were determined. Also the content of MDA and the level of T-AOC in serum were determined. The activity of SOD, CAT, and the content of MDA in hepatic tissue were determined. Histopathological changes of hepatic tissue were observed by HE staining. Results Compared with model group, the level of fasting blood sugar of puerarin 160 mg/kg group was significantly decreased (P < 0.05, 0.01). Compared with model group, the activities of ALT, AST, and the content of MDA of puerarin 80 and 160 mg/kg groups were significantly decreased (P < 0.05, 0.01), and the activity of ALP in serum of puerarin 160 mg/kg group was significantly decreased (P <0.01), while the level of T-AOC in serum was significantly increased (P < 0.05). Compared with model group, the activity of SOD in hepatic tissue of puerarin 80 and 160 mg/kg groups were significantly increased (P < 0.05, 0.01), but the content of MDA was significantly decreased (P < 0.05, 0.01), and the activity of CAT in hepatic tissue of puerarin 160 mg/kg group was significantly increased (P < 0.01). Histopathological changes of hepatic tissue in puerarin groups were significantly improved. Conclusion Puerarin has protection against oxidative stress injury in gestational diabetic rats induced by streptozocin, which perhaps is related to improvement of the anti-oxidant enzyme activity and depression of oxidative stress.
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