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Renoprotective effect of berberine on type 2 diabetic nephropathy in rats
Author(s) -
Sun SiFan,
Zhao TingTing,
Zhang HaoJun,
Huang XiaoRu,
Zhang WeiKu,
Zhang Lei,
Yan MeiHua,
Dong Xi,
Wang Hua,
Wen YuMin,
Pan XinPing,
Lan Hui Yao,
Li Ping
Publication year - 2015
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12402
Subject(s) - diabetic nephropathy , medicine , streptozotocin , inflammation , endocrinology , fibrosis , kidney , glomerulosclerosis , diabetes mellitus , pharmacology , proteinuria
Summary Inflammation, fibrosis, and lipid disorder are essential promoters in the pathogenesis of diabetic kidney injury in diabetes mellitus type 2. Berberine ( BBR ) has been reported to have beneficial effects on diabetic nephropathy, but its action mechanism is still unclear. The present study was designed to elucidate the therapeutic mechanism of BBR in a type 2 diabetic nephropathy rat model induced by a high‐fat diet and low‐dose streptozotocin injection. The diabetic rats were treated with or without BBR by gavage for 20 weeks and examined by serology, 24‐h albuminuria, histology, immunohistochemistry, and molecular analyses. Results showed that treatment with BBR significantly reduced serum levels of blood glucose and lipids, inhibited urinary excretion of albumin, and attenuated renal histological injuries in diabetic rats. Berberine treatment also inhibited renal inflammation, which was associated with inactivation of nuclear factor kappa‐light‐chain‐enhancer of activated B‐cell signalling. As a result, the upregulation of pro‐inflammatory cytokines (interleukin‐1 β , tumour necrosis factor‐ α ) and chemokine (monocyte chemotactic protein‐1) was blocked. In addition, BBR treatment also inactivated transforming growth factor‐ β /Smad3 signalling and suppressed renal fibrosis, including expression of fibronectin, collagen I, and collagen IV . The present study reveals that BBR is a therapeutic agent for attenuating type 2 diabetic nephropathy by inhibiting nuclear factor kappa‐light‐chain‐enhancer of activated B cell‐driven renal inflammation and transforming growth factor‐ β /Smad3 signalling pathway.