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KS‐370G ameliorates renal fibrosis, oxidative stress and inflammation induced by unilateral ureteral obstruction
Author(s) -
Chuang Sung-Ting,
Su Ming-Jai
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1051.12
Subject(s) - oxidative stress , medicine , kidney , janus kinase 2 , fibrosis , endocrinology , inflammation , ampk , chemistry , protein kinase a , pharmacology , kinase , biochemistry , receptor
Renal fibrosis is a common morphological feature of progressive chronic renal diseases including unilateral ureteral obstruction (UUO). In this study, we evaluated the role of KS‐370G, a caffeamide derivative, in the kidney fibrosis induced by UUO. Adult ICR mice were subjected to UUO and then administered with either KS‐370G (10mg/kg/day, gavage) or vehicle from 1day after UUO. UUO was maintained for 14 days. KS‐370G administration daily for 13 days significantly decreased the UUO‐induced kidney fibrotic changes including collagen deposition and fibronectin protein expression. KS‐370G also attenuated renal weight loss which result from UUO. KS‐370G reduced iNOS expression that contribute to renal inflammation. KS‐370G attenuated the increases of oxidative stress by the prevention of UUO‐induced decreases of manganese superoxide dismutase (MnSOD). Furthermore, UUO‐induced AMP‐activated protein kinase (AMPK), p42/p44 mitogen‐activated protein kinase (MAPK), Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (stat3) phosphorylation was markedly blocked by KS‐370G. In conclusion, KS‐370G prevented renal fibrosis following UUO by the inhibition of inflammation, oxidative stress and JAK2/Stat3 signaling pathway. The source of research support: National Science Council.