コンテンツメニュー

村田 智昭

所属 山口大学

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.
作成者 : 岡本 匡史 梅本 誠治 吉村 耕一 作村 俊浩 村田 智昭 深井 透 矢野 雅文 松﨑 益徳 出版者 : Yamaguchi University School of Medicine
European journal of cardio-thoracic surgery 45 巻 6 号 pp. 976 - 982
2014-02 発行
作成者 : 藏澄 宏之 Li Tao-Sheng 竹本 圭宏 Suzuki Ryo 美甘 章仁 Guo Changying 村田 智昭 濱野 公一 出版者 : Elsevier Science Publishers
PloS one 7 巻 11 号 pp. e48052 -
2012-11-14 発行
作成者 : 竹本 圭宏 Li Tao-Sheng Kubo Masayuki 大島 真子 藏澄 宏之 上田 和弘 榎 忠彦 村田 智昭 濱野 公一 出版者 : Public Library of Science