紀要論文 Angiotensin II increases oxidative stress and induces glomerular sclerosis via toll-like receptor 4

Okamoto, Tadashi  ,  Umemoto, Seiji  ,  Yoshimura, Koichi  ,  Sakumura, Toshihiro  ,  Murata, Tomoaki  ,  Fukai, Tohru  ,  Yano, Masafumi  ,  Matsuzaki, Masunori

63 ( 1-2 )  , pp.25 - 34 , 2016 , Yamaguchi University School of Medicine
ISSN:0513-1812
NII書誌ID(NCID):AA00594272
内容記述
Background: Angiotensin II (AngII) increases reactive oxygen species (ROS) and induces glomerular sclerosis. Toll-like receptor 4 (TLR4)-mediated inflammation enhances the renal impairment in renal inflammatory diseases. The relationship between TLR4 and AngII-induced glomerular sclerosis is unknown.Methods: Mice lacking TLR4 function (Tlr4^{lps-d}) and wild-type (WT) mice were randomized into groups treated with AngII, norepinephrine (NE) or a sub-depressor dose of the AngII receptor blocker irbesartan along with AngII for 2 weeks. We then assessed the expressions of NADPH oxidase and monocyte chemoattractant protein-1 (MCP-1) and the inflammatory cell recruitment in the glomeruli. We also evaluated the mesangial matrix proliferation and ROS.Results: AngII and NE equally increased the systolic blood pressure compared to the control mice (p<0.05). In the WT mice treated with AngII, we observed glomerular sclerosis, an increase in NADPH oxidase, MCP-1 and the infiltration of macrophages as well as ROS content in the glomeruli compared to the control mice (p<0.05), whereas the Tlr4^{lps-d} mice showed little effects of AngII on these indices. In addition, the sub-depressor-dose irbesartan treatment reversed these changes. NE had little effects on these indices. Conclusions: TLR4 plays an important role in AngII-induced oxidative stress, inflammation and glomerular sclerosis through the AT1 receptor.
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http://petit.lib.yamaguchi-u.ac.jp/G0000006y2j2/file/26489/20160923132524/A050063000104.pdf

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