ANGPTL8 knockout reduces lipopolysaccharide-induced hepatic lipid deposition
10.3969/j.issn.1006-5725.2024.09.004
- VernacularTitle:血管生成素样蛋白8敲除减轻脂多糖诱导的肝脏脂质沉积
- Author:
Shan LUO
1
,
2
;
Ying FENG
;
Dandan FAN
;
Wenxin ZHENG
;
Xingrong GUO
;
Xuzhi RUAN
Author Information
1. 湖北医药学院基础医学院附属太和医院,胚胎干细胞研究湖北省重点实验室,脐带血造血干细胞治疗临床医学研究中心(湖北十堰 442000)
2. 湖北省十堰市太和医院内分泌风湿免疫科(湖北十堰 442000)
- Keywords:
ANGPTL8;
LPS;
CAV1;
lipid deposition;
apoptosis
- From:
The Journal of Practical Medicine
2024;40(9):1197-1203
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the influence of ANGPTL8 in lipopolysaccharide(LPS)-induced hepatic lipid deposition.Methods Male wild-type(WT)and ANGPTL8 knockout mice at 6-8 weeks were used to induce sepsis models by intrabitoneal injection of LPS(10 mg/kg).qPCR and immunofluorescence were used to detected the mRNA and protein expression of ANGPTL8 in liver tissue and HepG2 cells respectively;The contents of alanine aminotransferase(ALT),aspartate aminotransferase(AST)in serum and the triglyceride(TG)and malondialdehyde(MDA)in liver homogenate were detected by kits;the histopathological changes of liver tissue were analyzed through HE staining.Lipids accumulation in liver were detected by oil red O staining.The apoptosis of liver was determinated by TUNEL staining.RNA-seq was used to analyzing the differentially expressed genes in the liver tissue of WT and ANGPTL8 KO mice,and the qPCR and Western Blot were used to verify the differential expressed genes.Results The expression of ANGPTL8 in the liver was significantly upregulated at 48 hours after LPS stimulation.Compared with WT mice,the hepatic lipid deposition,steatosis,and apoptosis were significantly alleviated in liver of ANGPTL8 KO mice,the ALT and AST levels in serum and the TG and MDA content in liver homogenate of ANGPTL8 KO mice were also reduced significantly.The expression of caveolin-1(CAV1)in liver of ANGPTL8 KO mice was significantly higher than that of WT mice.Conclusions LPS promoted the expression and secretion of ANGPTL8 in liver tissue,and ANGPTL8 increased hepatic lipid deposition and peroxidation by inhibiting the expression of CAV1.
