Deficiency of p38 in macrophage ameliorates d-galactosamine/TNF--induced acute liver injury in mice
文献类型：期刊论文
| 作者 | Liu, Jiao4; Zhang, Shengjie4; Cao, Hongchao4; Wang, Hui4; Sun, Chao4; Liu, Shengnan4; Yu, Shuxian4; Li, Yan4; Liu, Wei4; Ying, Hao4 |
| 刊名 | FEBS JOURNAL
 |
| 出版日期 | 2017 |
| 卷号 | 284期号:24页码:4200-4215 |
| 关键词 | liver injury macrophage polarization p38 |
| ISSN号 | 1742-464X |
| DOI | 10.1111/febs.14294 |
| 文献子类 | Article |
| 英文摘要 | Growing evidence suggests that hepatic macrophages play an important role in tissue repair after liver injury by coordinating the induction and resolution of inflammation, removing apoptotic cells, and promoting hepatocyte proliferation. Understanding the role of macrophages in the pathogenesis of liver injury will help pave the way to future therapeutics. Here, we investigated whether macrophage p38 plays a regulatory role in the tissue repair following d-galactosamine (GalN)/tumor necrosis factor- (TNF-)-induced acute liver injury. We found that macrophage p38-deficient mice displayed decreased mortality and relieved liver injury as evident from less apoptosis, accelerated regeneration, decreased granulocytes recruitment, monocytes infiltration, and cytokine production after GalN/TNF- treatment. Mechanistically, we found that p38 signaling was activated by lipopolysaccharide/interferon- treatment but not by inteleukin-4 stimulation, while pharmaceutical inhibition of p38 induced a shift in polarization from M1 macrophages to M2 macrophages. Together, our results indicated that macrophage p38 signaling is involved in the pathogenesis of liver injury induced by GalN/TNF-, and inhibition of p38 signaling in macrophage could ameliorate liver injury and accelerate regeneration, probably by promoting the polarization of macrophages from the M1 phenotype to the M2 phenotype. |
| 学科主题 | Biochemistry & Molecular Biology |
| WOS关键词 | TUMOR-NECROSIS-FACTOR ; TNF-ALPHA ; PARTIAL-HEPATECTOMY ; CELL-PROLIFERATION ; OXIDATIVE STRESS ; GENE-EXPRESSION ; MAP KINASE ; RAT-LIVER ; ACTIVATION ; APOPTOSIS |
| 语种 | 英语 |
| WOS记录号 | WOS:000418246000005 |
| 出版者 | WILEY |
| 版本 | 出版稿 |
| 源URL | [http://202.127.25.144/handle/331004/941]  |
| 专题 | 中国科学院上海生命科学研究院营养科学研究所 |
| 作者单位 | 1.Shanghai Jiao Tong Univ, Sch Med, Sch Publ Hlth, Shanghai, Peoples R China; 2.Minist Hlth, Key Lab food safety risk Assessment, Beijing, Peoples R China, 3.Fudan Univ, Zhongshan Hosp, Dept Endocrinol & Metab, Shanghai, Peoples R China; 4.Univ Chinese Acad Sci, Key Lab food safety Res, Inst Nutr Sci, Shanghai Inst Biol Sci,Chinese Acad Sci, 320 Yueyang Rd, Shanghai 200031, Peoples R China; |
| 推荐引用方式 GB/T 7714 | Liu, Jiao,Zhang, Shengjie,Cao, Hongchao,et al. Deficiency of p38 in macrophage ameliorates d-galactosamine/TNF--induced acute liver injury in mice[J]. FEBS JOURNAL,2017,284(24):4200-4215. |
| APA | Liu, Jiao.,Zhang, Shengjie.,Cao, Hongchao.,Wang, Hui.,Sun, Chao.,...&,.(2017).Deficiency of p38 in macrophage ameliorates d-galactosamine/TNF--induced acute liver injury in mice.FEBS JOURNAL,284(24),4200-4215. |
| MLA | Liu, Jiao,et al."Deficiency of p38 in macrophage ameliorates d-galactosamine/TNF--induced acute liver injury in mice".FEBS JOURNAL 284.24(2017):4200-4215. |
入库方式： OAI收割
来源：上海营养与健康研究所
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