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人参皂苷CK对2型糖尿病大鼠肝损伤的保护机制 被引量:5

Protective Mechanism of Ginsenoside CK on Liver Injury in Type 2 Diabetic Rats
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摘要 目的:探究人参皂苷CK对2型糖尿病(T2DM)大鼠肝损伤的保护机制。方法:本试验通过建立T2DM大鼠模型,记录大鼠空腹血糖值(FBG),灌胃8周后进行口服糖耐量(OGTT)测试,检测血清中相关指标,肝组织匀浆中相关指标以及四种炎性因子的水平,苏木精-伊红(HE)染色法检测肝组织病变情况,Western Blot法检测TLR/Myd88/NF-κB信号通路蛋白的表达。结果:人参皂苷CK组能够显著的降低T2DM大鼠的FBG水平(P<0.05),恢复其糖耐量水平,显著提高总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)、谷丙转氨酶(ALT)、谷草转氨酶(AST)、超氧化物歧化酶(SOD)、谷胱甘肽(GSH)、过氧化氢酶(CAT)水平(P<0.05),显著降低高密度脂蛋白(HDL-C),丙二醛(MDA),四种炎性因子以及Toll样受体4(TLR4)、髓样分化因子(Myd88)、细胞核因子(p65)和大鼠核因子κB抑制蛋白α(p-IκB-α)蛋白的表达水平(P<0.05),恢复肝组织形态结构。结论:人参皂苷CK能够通过降低炎症以及氧化应激反应从而保护T2DM大鼠的肝损伤情况,并调控TLR/Myd88/NF-κB信号通路。 Objective:To explore the protective mechanism of ginsenoside CK on liver injury in type 2 diabetes(T2DM)rats.Methods:In this experiment,the T2DM rat model was established,the FBG of the rats was recorded,and OGTT test after 8 weeks of gavage.Detection of relevant indicators in serum,related indicators and levels of four inflammatory factors in liver tissue homogenate.Detection of liver tissue lesions by HE staining.Western Blot method was used to detect the expression of TLR/Myd88/NF-κB signaling pathway protein.Results:The group of ginsenoside CK could significantly reduced FBG levels in T2DM rats(P<0.05),restored its glucose tolerance level,increased the levels of TC,TG,LDL-C,ALT,AST,SOD,GSH,CAT significantly(P<0.05),reduced the expression levels of HDL-C,MDA,four inflammatory factors and TLR4,Myd88,p65 and p-IKB-αprotein significantly(P<0.05),liver tissue morphology was restored.Conclusion:Ginsenoside CK could protect the liver injury of T2DM rats by reducing inflammation and oxidative stress,and regulate TLR/Myd88/NF-κB signaling pathway.
作者 闫爽 李光耀 戴丛书 崔昊震 柳振宇 林长青 YAN Shuang;LI Guangyao;DAI Congshu;CUI Haozhen;LIU Zhenyu;LIN Changqing(Department of Traditional Chinese Medicine,School of Medicine,Yanbian University,Yanji 133000,China)
出处 《食品工业科技》 CAS 北大核心 2021年第2期310-315,共6页 Science and Technology of Food Industry
关键词 人参皂苷CK 2型糖尿病 肝损伤 炎症 TLR/Myd88/NF-κB ginsenoside CK type 2 diabetes liver injury inflammation TLR/Myd88/NF-κB
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