摘要
目的研究Adip/CaMKKβ/AMPK通路是否参与丹皮酚(paeonol,Pae)治疗小鼠酒精性脂肪肝的过程。方法在小鼠酒精性脂肪肝模型的基础上给予丹皮酚治疗后,通过ELISA法检测小鼠血清中各炎症因子和TG、TC,同时用ELISA法检测小鼠血清中Adip和ACC表达水平,用qPCR法及Westren blot法检测小鼠肝组织Adip、CaMKKβ、AMPKα和SREBP1c核酸和蛋白水平。 结果 Adip表达水平在各处理组无显著变化;酒精诱导增加炎症因子和TG、TC表达,降低了CaMKKβ和AMPKα在核酸和蛋白磷酸化水平上的表达,水飞蓟宾与丹皮酚降低了炎症因子和TG、TC表达,提高了CaMKKβ和AMPKα在核酸和蛋白磷酸化水平上的表达;酒精诱导增加了SREBP1c在核酸和蛋白水平上的表达,水飞蓟宾与丹皮酚降低了SREBP1c的表达。 结论 从Adip/CaMKKβ/AMPK信号传导的变化验证了丹皮酚可通过此信号转导来减轻酒精性脂肪肝的脂肪变性损伤和炎症水平。
Aim To investigate whether the Adip/CaMKKβ/AMPK pathway is involved in the treatment of alcoholic fatty liver in mice treated with paeonol.Methods After administration of paeonol on the basis of the mouse alcoholic fatty liver model,the inflammatory factors and TG and TC were detected by Elisa method to verify the validity of the model and drug treatment;meanwhile,the expression levels of Adip and ACC were detected by Elisa,and the nucleic acid and protein levels of Adip,CaMKKβand AMPKαby PCR and WB.Results Adip expression levels did not change significantly in each treatment group.Compared with control group,as for the expression of CaMKKβand AMPKαat the nucleic acid and proteinphosphorylation levels,the EtOH group was down-regulated to varying degrees,and the Sil and Pae groups improved the phenomenon to varying degrees.Compared with control group,as for the expression of SREBP1c at the nucleic acid and protein levels,the EtOH group was up-regulated to varying degrees,and the Sil and Pae groups improved the phenomenon to varying degrees.Conclusions The changes of theAdip/CaMKKβ/AMPK signaling pathway confirm that paeonol reduces steatosis injury of alcoholic fatty liver and inflammatory level in mice via this pathway.
作者
司远青
颜贵明
SI Yuan-qing;YAN Gui-ming(Dept of Pathogenic Biology and Immunology,College of Integrated Chinese and Western Medicine,Anhui University of Chinese Medicine,Hefei 230012,China)
出处
《中国药理学通报》
CAS
CSCD
北大核心
2020年第1期80-86,共7页
Chinese Pharmacological Bulletin
基金
安徽省高校省级自然科学研究重点项目(KJ2018A0280)
