DUAN Yanhua
1. School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, China. 2. Center for Drug Safety Evaluation, Hangzhou Medical College, Hangzhou 310053. 3. Key Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Hangzhou Medical College, Hangzhou 310053CHEN Yunxiang
2. Center for Drug Safety Evaluation, Hangzhou Medical College, Hangzhou 310053. 3. Key Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Hangzhou Medical College, Hangzhou 310053ZHENG Gaoli
2. Center for Drug Safety Evaluation, Hangzhou Medical College, Hangzhou 310053. 3. Key Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Hangzhou Medical College, Hangzhou 310053WEN Lei
2. Center for Drug Safety Evaluation, Hangzhou Medical College, Hangzhou 310053. 3. Key Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Hangzhou Medical College, Hangzhou 310053CHEN Hao
2. Center for Drug Safety Evaluation, Hangzhou Medical College, Hangzhou 310053. 3. Key Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Hangzhou Medical College, Hangzhou 310053ZHANG Lili
2. Center for Drug Safety Evaluation, Hangzhou Medical College, Hangzhou 310053. 3. Key Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Hangzhou Medical College, Hangzhou 310053QIN Li
2. Center for Drug Safety Evaluation, Hangzhou Medical College, Hangzhou 310053. 3. Key Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Hangzhou Medical College, Hangzhou 310053WANG Jiahong
2. Center for Drug Safety Evaluation, Hangzhou Medical College, Hangzhou 310053. 3. Key Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Hangzhou Medical College, Hangzhou 310053LIU Fang
2. Center for Drug Safety Evaluation, Hangzhou Medical College, Hangzhou 310053. 3. Key Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Hangzhou Medical College, Hangzhou 310053XIA Daozong
1. School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, China.ZHANG Lijiang
2. Center for Drug Safety Evaluation, Hangzhou Medical College, Hangzhou 310053. 3. Key Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Hangzhou Medical College, Hangzhou 3100531. School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, China. 2. Center for Drug Safety Evaluation, Hangzhou Medical College, Hangzhou 310053. 3. Key Laboratory of Drug Safety Evaluation and Research of Zhejiang Province, Hangzhou Medical College, Hangzhou 310053
Objective This study aimed to test the efficacy of an ethanolic extract of Polygonum cuspidatum(PCE) against adenine-induced renal interstitial fibrosis (RIF) in C57BL/6N mice and reveal its underlying molecular mechanisms of action. Methods An RIF model was induced by gavaging C57BL/6N mice with adenine. Fifty male C57BL/6N mice were randomly divided into five groups (n=10 per group): normal control group, model group, PCE-L, PCE-M and PCE-H (75, 150, 300 mg/ kg, respectively) groups. After treatment for 42 consecutive days, serum creatinine (Scr) and blood urea nitrogen (BUN) levels were measured with commercially purchased kits. Histopathological changes to the kidneys were assessed by HE and Masson staining. The protein expression levels of TGF-β1, Smad6, α-SMA, and type I collagen (Collagen I) in kidney tissue were detected by Western Blot. Results Compared with the normal control group, the model group had significantly increased BUN and Scr (P<0. 01). The protein expression level of TGF-β1 was significantly increased (P< 0. 01), while Smad6, a negative regulator of the TGF-β/ Smad pathway, was significantly downregulated (P< 0. 01). The expression of the epithelial-mesenchymal transformation (EMT) marker protein α-SMA and the extracellular matrix (ECM) protein Collagen I were significantly increased (P< 0. 01). Compared with the model group, the drug intervention groups showed decreased levels of BUN and Scr; declining protein expression levels of TGF-β1, α-SMA and Collagen I; increased levels of Smad6 protein; and the alleviation of pathological changes. Conclusions PCE treatment attenuated adenine-induced renal impairment and ameliorated renal interstitial fibrosis in mice. The mechanism of action may be related to changes to the TGF-β1/ Smad signaling pathway and the suppression of EMT and ECM protein deposition.
