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Sodium butyrate protects against lipopolysaccharideinduced liver injury partially via the GPR43/b-arrestin-2/NF-кb network

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Gastroenterology Report 2021年第2期9卷 154-165,I0002页

作者： Qian-Jiang Luo Mei-Xing Sun Yun-Wei Guo Si-Wei Tan Xiao-Ying Wu Kodjo-Kunale Abassa Li Lin Hui-Ling Liu Jie Jiang Xiu-Qing Wei Department of Gastroenterology The Third Affiliated Hospital of Sun Yat-sen UniversityGuangzhouGuangdongP.R.China Department of Gastroenterology The Eighth Affiliated Hospital of Sun Yat-sen University(Shenzhen Futian Hospital)ShenzhenGuangdongP.R.China

background butyrate acts as a regulator in multiple inflammatory organ ***,the role of butyrate in acute liver injury has not yet been fully *** the present study,we aimed to investigate the association between butyrate and lipopolysaccharide(LPS)-induced acute liver injury and the signaling pathways *** LPS-induced acute liver injury was induced by intraperitoneal injection of LPS(5 mg/kg)in G-protein-coupled receptor 43(GPR43)-knockout(KO)and wild-type female C57bL/6 *** butyrate(500mg/kg)was administered intraperitoneally 30min prior to LPS *** injury was detected by serum markers,tissue morphology,and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL).Pro-inflammatory-factor levels were detected by enzyme-linked immunosorbent assay and real-time polymerase chain reaction(RT-PCR).Cell models were first treated with sodium butyrate(4μmol/mL),followed by LPS(1μg/mL)half an hour later in GPR43 small interfering RNA(siRNA)-transfected or control RAW264.7 ***-inflammation status was evaluated through detecting pro-inflammatory-factor expression by RT-PCR and also through checking toll-like receptor 4/nuclear factor-кb(TLR4/NF-кb)-element levels including TLR4,TRAF6,IKKb,Iкbα,phospho-Iкbα,p65,and phospho-p65 by Western *** interaction between GPR43 and barrestin-2 was tested by *** Sodium butyrate reversed the LPS-induced tissue-morphology changes and high levels of serum alanine aminotransferase,aspartate transaminase,myeloperoxidase,TUNEL,and pro-inflammatory cytokines such as tumor necrosis factor-a and *** ameliorating effect of sodium butyrate was weakened in GPR43-KO mice and GPR43 siRNA RAW264.7 cells,compared with those of GPR43-positive *** butyrate downregulated some elements of the TLR4/NF-кb pathway,including phospho-Iкbαand phospho-p65,in RAW264.7 *** interactions between GPR43 and b-arrestin-2,and betw

关键词： sodium butyrate short-chain fatty acids lipopolysaccharide-induced liver injury G-protein-coupled receptor 43 b-arrestin-2 NF-кb

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