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Int. J. Mol. Sci. 2016, 17(8), 1327; doi:10.3390/ijms17081327

Protective Effects of Berberine on Renal Injury in Streptozotocin (STZ)-Induced Diabetic Mice

Department of Nephrology, Benxi Center Hospital, 29 Victory Road, Benxi 117000, Liaoning, China
Science Experiment Center, Benxi Center Hospital, Benxi 117000, Liaoning, China
Key Laboratory of Medical Cell Biology of Ministry of Education, China Medical University, Shenyang 110001, Liaoning, China
Troops of 95935 Unit, Haerbin 150111, Heilongjiang, China
Department of pathophysiology, China Medical University, Shenyang 110001, Liaoning, China
Department of Nephrology, the First Affiliated Hospital, China Medical University, Shenyang 110001, Liaoning, China
Authors to whom correspondence should be addressed.
Academic Editors: Lu Cai and Yuehui Wang
Received: 19 April 2016 / Revised: 3 July 2016 / Accepted: 1 August 2016 / Published: 12 August 2016
(This article belongs to the Special Issue Diabetic Complications: Pathophysiology, Mechanisms, and Therapies)
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Diabetic nephropathy (DN) is a serious diabetic complication with renal hypertrophy and expansion of extracellular matrices in renal fibrosis. Epithelial-to-mesenchymal transition (EMT) of renal tubular epithelial cells may be involved in the main mechanism. Berberine (BBR) has been shown to have antifibrotic effects in liver, kidney and lung. However, the mechanism of cytoprotective effects of BBR in DN is still unclear. In this study, we investigated the curative effects of BBR on tubulointerstitial fibrosis in streptozotocin (STZ)-induced diabetic mice and the high glucose (HG)-induced EMT in NRK 52E cells. We found that BBR treatment attenuated renal fibrosis by activating the nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling pathway in the diabetic kidneys. Further revealed that BBR abrogated HG-induced EMT and oxidative stress in relation not only with the activation of Nrf2 and two Nrf2-targeted antioxidative genes (NQO-1 and HO-1), but also with the suppressing the activation of TGF-β/Smad signaling pathway. Importantly, knockdown Nrf2 with siRNA not only abolished the BBR-induced expression of HO-1 and NQO-1 but also removed the inhibitory effect of BBR on HG-induced activation of TGF-β/Smad signaling as well as the anti-fibrosis effects. The data from present study suggest that BBR can ameliorate tubulointerstitial fibrosis in DN by activating Nrf2 pathway and inhibiting TGF-β/Smad/EMT signaling activity. View Full-Text
Keywords: renal tubular epithelial cells; berberbine; EMT; diabetic nephropathy; Nrf2 pathway; TGF-β/Smad signaling pathway renal tubular epithelial cells; berberbine; EMT; diabetic nephropathy; Nrf2 pathway; TGF-β/Smad signaling pathway

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Zhang, X.; He, H.; Liang, D.; Jiang, Y.; Liang, W.; Chi, Z.-H.; Ma, J. Protective Effects of Berberine on Renal Injury in Streptozotocin (STZ)-Induced Diabetic Mice. Int. J. Mol. Sci. 2016, 17, 1327.

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