庞棋文,李丽华,孙振,景乐乐,邵晨,严金川,王中群.CML促进高脂诱导糖尿病ApoE-/-小鼠非酒性脂肪肝进展的研究.[J].中南医学科学杂志.,2020,(2):146-150.
CML促进高脂诱导糖尿病ApoE-/-小鼠非酒性脂肪肝进展的研究
Effects of CML on high fat diet-induced diabetic ApoE-/- mice nonalcoholic fatty liver disease
投稿时间:2019-12-02  修订日期:2019-12-28
DOI:10.15972/j.cnki.43-1509/r.2020.02.009
中文关键词:  Nε-羧甲基赖氨酸  非酒精性脂肪肝  糖尿病
英文关键词:Nε-carboxymethyl-Lysine  non-alcoholic fatty liver  diabetes
基金项目:
作者单位
庞棋文 江苏大学附属医院 心内科,江苏 镇江 212001 
李丽华 江苏大学附属医院 病理科,江苏 镇江 212001 
孙振 江苏大学附属医院 心内科,江苏 镇江 212001 
景乐乐 江苏大学附属医院 心内科,江苏 镇江 212001 
邵晨 江苏大学附属医院 心内科,江苏 镇江 212001 
严金川 江苏大学附属医院 心内科,江苏 镇江 212001 
王中群 江苏大学附属医院 心内科,江苏 镇江 212001 
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中文摘要:
      研究 Nε-羧甲基赖氨酸(CML)对非酒精性脂肪肝(NAFLD)的影响并探索其作用机制。首先通过体外实验,观察不同浓度CML对HepG2细胞脂质蓄积的影响。以6周龄雄性ApoE-/-小鼠腹腔注射链脲佐菌素40 mg/kg/day连续五天,2周后将血糖水平≥300 mg/dL的小鼠纳入实验研究;用免疫组化染色法检测CML的表达,HE染色观察肝脏形态以及检测血清总胆固醇(TC)、甘油三酯(TG)、谷丙转氨酶(ALT)、谷草转氨酶(AST)、超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)的变化。结果显示,不同浓度CML处理后,上调肝组织中CML表达。CML浓度依赖性升高小鼠血清TC、TG、AST、ALT、MDA 的含量,降低血清中 SOD、GSH-Px含量,加重肝脏脂肪变性,并增加HepG2细胞内脂质蓄积。结果表明CML促进高脂诱导糖尿病ApoE-/-小鼠非酒性脂肪肝进展。
英文摘要:
      The aim is to study the effect of Nε-carboxymethyl-Lysine (CML) on non-alcoholic fatty liver (NAFLD) and explore its mechanism. In vitro study, the effects of different concentrations of CML on lipid accumulation in HepG2 cells were observed. In vivo study, 6-week-old male ApoE-/- mice were intraperitoneally injected with streptozotocin (STZ, 40 mg / kg / day) for five days in succession. Mice with blood glucose levels ≥ 300 mg/dL are considered diabetic after two weeks. The expression of CML was detected by immunohistochemical staining, liver morphological staining was observed by HE staining, the total cholesterol (TC), triglyceride (TG), alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) were measured. The results showed that CML expression in liver tissue increased significantly after treatment with different concentrations of CML. CML concentration-dependently increased the serum TC, TG, AST, ALT, MDA levels; decreased serum SOD, GSH-Px levels and aggravated liver steatosis,and significantly increased lipid accumulation in HepG2 cells. These results showed that CML promoted the progression of non-alcoholic fatty liver in high-fat-induced diabetic ApoE-/- mice.
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