Renoprotective effect of berberine on type 2 diabetic nephropathy in rats |
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| Authors: | Si‐Fan Sun Ting‐Ting Zhao Hao‐Jun Zhang Xiao‐Ru Huang Wei‐Ku Zhang Lei Zhang Mei‐Hua Yan Xi Dong Hua Wang Yu‐Min Wen Xin‐Ping Pan Hui Yao Lan Ping Li |
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| Affiliation: | 1. Graduate School of Peking Union Medical College, Chinese Academy of Medical Science, Peking Union Medical College, Beijing, China;2. Institute of Clinical Medical Sciences, China‐Japan Friendship Hospital, Beijing, China;3. Department of Medicine and Therapeutics, Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Hong Kong, China;4. National Innovation Center of TCM Modernization in Shanghai, Shanghai, China;5. Shanghai Innovative Research Center of Traditional Chinese Medicine, Shanghai, China;6. Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen, China |
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| Abstract: | 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‐1β, 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. |
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| Keywords: | berberine diabetic nephropathy fibrosis inflammation NF‐κ B TGF‐β /Smad signalling |
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