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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:

27卷

期数:

2021年03期

页码:

239-242,251

栏目:

基础医学

出版日期:

2021-05-30

文章信息/Info

Title:

Research the role of AMPKα2 in palmitic acid-induced lipid deposition and inflammation in hepatocyte

文章编号:

1006-8147(2021)03-0239-04

作者:

郭蓓; 牛文彦

天津医科大学基础医学院免疫学系，天津300070；天津医科大学朱宪彝纪念医院检验科，天津300134

Author(s):

GUO Bei; NIU Wen-yan

Department of Immunology，School of Basic Medical Sciences，Tianjin Medical University，Tianjin 300070，China；Department of Clinical Laboratory，Chu Hsien-Ⅰ Memorial Hospital，Tianjin Medical University，Tianjin 300134，China

关键词:

原代肝细胞; AMPKα2; 脂质沉积; 炎症

Keywords:

primary hepatocytes;  AMPKα2;  lipid deposition;  inflammation

分类号:

R392.6

DOI:

-

文献标志码:

A

摘要:

目的：探讨AMP活化蛋白激酶（AMPK）α2在棕榈酸（PA）诱发的肝细胞脂质沉积和脂多糖（LPS）诱导的炎症中的作用和机制。方法：分离小鼠原代肝细胞，将一部分细胞分为非特异性小干扰RNA（siRNA）对照组（siNR）和敲除AMPKα2 （siAMPKα2）组，每组细胞再分别用10%牛血清白蛋白（BSA）、200 μmol/L PA、磷酸盐缓冲液（PBS）、10 μg/mL LPS孵育16 h或6 h。油红O染色检测细胞中的脂质，Western 印迹检测核因子κB抑制蛋白（IκB）激酶（IKK）和激活c-Jun氨基末端激酶（JNK）的磷酸化。将另一部分肝细胞分为转染对照腺病毒组（Ad-GPF）和AMPKα2腺病毒组（Ad-AMPKα2），每组再分别用10% BSA、200 μmol/L PA、PBS、10 μg/mL LPS孵育16 h或6 h，Western 印迹检测JNK和IKKα/β的磷酸化。结果：与对照组相比，siAMPKα2组 PA诱导的细胞内脂质积累增加（t=2.133，P<0.05），PA和LPS磷酸化JNK（1.51±0.08，t=2.701，P<0.05）和IKKα/β（1.35±0.03，t=1.657，P<0.05）的作用加强，而AMPKα2腺病毒组PA和LPS升高JNK和IKKα/β磷酸化的作用显著受抑制。结论：AMPKα2可能通过抑制JNK及核因子-κB信号通路，改善PA诱导的肝细胞脂质沉积以及和PA和LPS诱导的肝细胞炎症。

Abstract:

Objective: To investigate the role and mechanism of AMP-activated kinase（AMPK） α2 in palmitic acid-induced lipid deposition and lipopolysaccharide（LPS） induced inflammation in hepatocytes. Methods: Primary mouse hepatocytes were isolated and divided into non-specific small interfering RNA（siRNA） control group（siNR） and AMPKα2 knock down group（siAMPKα2）. The hepatocytes were incubated with 10% bovine serum albumin（BSA），200 μmol/L palmitic acid，PBS，10 μg/mL LPS for 16 h or 6 h to induce lipid deposition. The lipid in cells were detected by oil red O staining，and the phosphorylation of IKK and JNK were detected by Western blotting. Another part of hepatocytes were divided into control adenovirus group（Ad-GPF） and AMPKα2 adenovirus group （Ad-AMPKα2），and each group was incubated with 10% BSA，200 μmol/L PA，PBS and 10 μg/ml LPS for 16 h or 6 h respectively. The phosphorylation of JNK and IKKα/β were detected by Western blotting. Results: Compared with the control group，in siAMPKα2 group PA induced intracellular lipid accumulation was increased（t=2.133，P <0.05），the phosphorylation of JNK（1.51±0.08，t=2.701，P <0.05） and IKKα/β（1.35±0.03，t=1.657，P <0.05） by PA and LPS were enhanced，while the increased phosphorylation of JNK and IKKα/β by PA and LPS was significantly inhibited in AMPKα2 adenovirus group. Conclusion: AMPKα2 may improve PA induced lipid deposition as well as PA and LPS induced inflammation in hepatocytes by inhibiting JNK and NF-κB signaling pathway.

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相似文献/References:

备注/Memo

备注/Memo:

作者简介 郭蓓（1977-），女，主管技师，硕士在读，研究方向：内分泌免疫学；
通信作者：牛文彦，E-mail：wyniu@163.com。

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更新日期/Last Update: 2021-05-30