摘要
目的研究甘草酸二铵脂质配位体(DGLL)对非酒精性脂肪肝(NAFLD)大鼠肿瘤坏死因子-α(TNF-α)表达的影响及分子机制。方法用高脂乳剂灌胃诱导大鼠NAFLD模型,并给予DGLL干预,6周后检测肝脏组织及血清TNF-α的变化。Western blot法检测肝脏组织核因子-κB p65(NF-κB p65)和NF-κB抑制蛋白α(I-κBα)表达水平。结果与高脂模型组相比,DGLL能明显降低NAFLD大鼠肝脏组织和血清中TNF-α的表达,下调大鼠肝脏组织NF-κB p65蛋白表达,同时显著地抑制肝脏组织I-κBα蛋白的降解。结论 DGLL能显著降低高脂饮食诱导的NAFLD大鼠TNF-α水平,这种作用与抑制NF-κB p65的表达相关。
Objective To study the therapeutic effects and molecular mechanism of diammonium glycyrrhizinate lipid ligand（DGLL） on tumor necrosis factor-α（TNF-α） expression with nonalcoholic fatty liver disease（NAFLD）.Methods The rats of the model group were fed with high fat forage.At the same time,the rats of DGLL groups were administrated with relative dose of medicine.After six weeks,the TNF-α level in liver tissues and in plasma were measured by immunohistochemistry and ELISA,respectively.The expressions of NF-κB p65 and I-κBα in liver were determined by Western blot.Results Compared with model groups,the expression of TNF-α in liver tissues and plasma were both ameliorated remarkably by administration of DGLL.Meanwhile,the up-regulation of NF-κB p65 expression and degradation of I-κBα were reversed by DGLL treatment.Conclusion DGLL could ameliorat rat TNF-α expression with NAFLD,which was related to NF-κB p65 down-regulation.
出处
《安徽医科大学学报》
CAS
北大核心
2011年第8期725-728,共4页
Acta Universitatis Medicinalis Anhui
基金
安徽省教育厅自然科学研究项目(编号:KJ2010A183)
安徽医科大学七年制临床医学专业学生“早期接触科研”训练计划项目(编号:2009-ZQKY-04)
