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Cryptotanshinone Attenuates Oxidative Stress and Inflammation through the Regulation of Nrf‐2 and NF ‐κB in Mice with Unilateral Ureteral Obstruction
Author(s) -
Wang Wei,
Wang Xiao,
Zhang Xiansheng,
Liang Chaozhao
Publication year - 2018
Publication title -
basic and clinical pharmacology and toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.805
H-Index - 90
eISSN - 1742-7843
pISSN - 1742-7835
DOI - 10.1111/bcpt.13091
Subject(s) - oxidative stress , inflammation , malondialdehyde , fibrosis , medicine , superoxide dismutase , kidney , cd68 , sod2 , pathology , immunohistochemistry , pharmacology , endocrinology
Oxidative stress and inflammatory responses are closely implicated in the progression of renal interstitial fibrosis, thereby leading to chronic kidney disease. Cryptotanshinone ( CTS ) is a natural compound involved in antioxidant and anti‐inflammatory activities. We evaluated the effects of CTS on inflammation and oxidative stress in obstructed kidneys. Mice received gastric gavage of CTS from 7 days before unilateral ureteral obstruction operation to 1 week after surgery. Administration of CTS at 50 and 100 mg/kg/day significantly decreased collagen production, as shown by Masson staining. Immunohistochemistry staining and RT ‐ PCR confirmed that CTS reduced extracellular matrix proteins, such as fibronectin and collagen‐1, in the obstructed kidneys in a dose‐dependent manner. Furthermore, immunohistochemistry staining indicated that CTS inhibited infiltration of the macrophage ( CD 68‐positive) and lymphocyte ( CD 3‐positive) cells, which were associated with the suppression of the nuclear factor‐κB signalling activation. CTS increased superoxide dismutase, catalase and glutathione while decreased malondialdehyde production. More importantly, CTS activated Nrf‐2 and HO ‐1 in the obstructed kidneys for 7 days. CTS could protect renal interstitial fibrosis by ameliorating inflammation and oxidative stress, which might be through the regulation of NF ‐κB and Nrf‐2/ HO ‐1 signalling pathways.