目的 研究杜仲多糖(EUP)对2型糖尿病db/db小鼠糖脂代谢的影响及相关作用机制。方法 采用db/db 2型糖尿病小鼠模型,随机分成模型组、EUP低、中、高剂量组以及阳性对照二甲双胍组,另设同周龄-+/db小鼠为正常对照组,给药9周后称量小鼠体质量,检测小鼠空腹血糖(FBG)、血脂、白细胞介素-8(IL)-8、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、超氧化物歧化酶(SOD),谷胱甘肽过氧化物酶(GSH-Px)和丙二醛(MDA)的含量变化;HE染色和油红O染色评估小鼠肝脏病理学变化及脂肪变性;Western-blot 检测小鼠肝脏组织核因子(NF)-κB p65和血红素加氧酶(HO-1)蛋白表达。结果 EUP能够减轻自发性2型糖尿病db/db小鼠的体质量,降低FBG、TG、TC、LDL-C、IL-8、IL-1β、IL-6、MDA和NF-κB p65蛋白水平,提高HDL-C、GSH-Px、SOD和HO-1蛋白水平;EUP能够减轻db/db小鼠肝脏的病理改变和脂肪变性。结论 EUP对2型糖尿病db/db小鼠表现的肥胖、高血糖、高血脂和肝损伤均有较好的改善作用,其机制跟调控炎症反应及氧化应激水平有关。
Abstract
OBJECTIVE To investigate the effect and mechanism of Eucommia ulmoides polysaccharide (EUP) on db/db diabetic mice′s glycolipid metabolism. METHODS The db/db type 2 diabetes mice model were randomly divided into model control group, EUP low, middle and high dose group and positive control metformin group,-+/db mice of the same age were set as normal control group. The mice were weighed, and the changes of fasting blood glucose (FBG), blood lipid (TG, TC, LDL-C, HDL-C), interleukin (IL-8, IL-1β, IL-6), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) were detected after drug delivery for 9 weeks. HE staining and oil red O staining were used to evaluate the pathological changes and steatosis of liver in mice. Western blot assay were used to detect the protein expressions of NF-κB p65 and HO-1 in liver tissues of mice. RESULTS EUP could reduce the body weight of db/db mice, reduce the levels of FBG, TG, TC, LDL-C, IL-8, IL-1β, IL-6, MDA, NF-κB p65 proteins and increase the levels of HDL-C and HO-1 proteins. EUP could alleviate pathological changes and steatosis of liver in db/db mice. CONCLUSION The obesity, hyperglycemia, hyperlipidemia and liver injury of db/db mice with type 2 diabetes are all improved by EUP, and the mechanism is related to the regulation of inflammatory response and oxidative stress.
关键词
杜仲多糖 /
2型糖尿病 /
炎症反应 /
氧化应激
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Key words
Eucommia ulmoides polysaccharide /
type 2 diabetes /
inflammatory response /
oxidative stress
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中图分类号：
R965
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脚注
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基金
国家自然科学基金项目资助(81703996)
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