摘要
为研究TLR4通路在油酸(oleic acid,OA)致BRL 3A细胞脂肪变性中的作用,用不同浓度的OA(0、1.2、1.8、2.4 mmol/L)处理BRL 3A细胞24 h,再用显微镜观察细胞损伤状况,DAPI染色观察细胞核形态,油红O染色观察脂滴生成量,甘油三脂(TG)试剂盒测定TG含量,Western-blot检测TLR4通路蛋白TLR4、My D88、TBK1的表达量。结果显示:与对照组相比,随着OA浓度增加,细胞损伤增加,细胞核变形、破碎、皱缩,呈一定的浓度梯度依赖性;细胞内脂滴生成量增加,TG含量显著增加(P<0.05);与对照组相比,TLR4、My D88及TBK1的表达量随着OA浓度增加呈显著或极显著增加(P<0.05或P<0.01)。这表明油酸可能通过TLR4/My D88途径促进BRL 3A细胞发生脂肪变性。
In order to investigate the effect of TLR4 pathway in steatosis of BRL 3A cells induced by oleic acid(OA),BRL 3A cells were treated with different concentrations of OA(0,1.2,1.8,2.4 mmol/L)for 24 h,and the cell damage was observed by microscope.The nuclear morphology was observed by DAPI staining.Oil red O staining was used to observe lipid droplets.The amount of triglyceride(TG) was determined by TG kit.The expressions of TLR4 pathway proteins TLR4,MyD88,and TBK1 were detected by Western-blot.The results showed that compared with the control group,cell damage increased with the increase of OA concentration.The nucleus of BRL 3A cell showed deformation,fragmentation and shrinkage in a concentration-dependent manner.Intracellular lipid droplet increased,and intracellular TG content increased significantly(P<0.05).Compared with the control group,the relative expression levels of TLR4,MyD88 and TBK1 showed a significant or extremely significant increase with the increase of OA concentration(P<0.05 or P<0.01).These results indicate that OA may accelerates steatosis of BRL 3A cells through TLR4/MyD88 pathway.
作者
王玲
赵健亚
刘宗平
WANG Ling;ZHAO Jian-ya;LIU Zong-ping(College of Veterinary Medicine,Yangzhou University,Yangzhou 225009,China;Jiangsu Co-innovation Center for Prevention and Control of Important Animal Infectious Diseases and Zoonoses,Yangzhou 225009,China)
出处
《中国兽医科学》
CAS
CSCD
北大核心
2020年第1期112-117,共6页
Chinese Veterinary Science
基金
国家自然科学基金项目(31872533)
江苏高校优势学科建设工程资助项目(2018)
作者简介
王玲(1994-),女,江苏南通人,硕士生,主要从事动物营养代谢病研究,Tel:0514-87991448,E-mail:934872739@qq.com;通信作者:刘宗平(1964-),教授,主要从事动物营养代谢病与中毒病研究,Tel:0514-87991448,E-mail:liuzongping@yzu.edu.cn。
