Du Lifen, Lei Yongfang, Chen Jinglou, Song Hongping, Wu Xinying
Department of Pharmacy, Puai Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department of Pharmacy, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Cell Physiol Biochem. 2017;43(4):1359-1368. doi: 10.1159/000481847. Epub 2017 Oct 9.
BACKGROUND/AIMS: Cadmium (Cd) is an environmental pollutant with reproductive toxicity. Swertia mileensis is used in Chinese medicine for the treatment of prostatic deficits and named as Qing Ye Dan (QYD). This study was undertaken to investigate the potential protective effects of QYD against Cd-induced prostatic deficits.
Rat model of prostatic deficits was induced by 0.2 mg/kg/d CdCl2 subcutaneous injection for 15 days. The prostatic oxidative stress was evaluated by detecting the levels of malondialdehyde, nitric oxide, reduced/ oxidized glutathione, total sulfhydryl groups and enzymatic antioxidant status. The prostatic inflammation was estimated by testing the levels of pro-inflammatory cytokines. The levels of epithelial-mesenchymal transition (EMT) markers E-cadherin, fibronectin, vimentin and α-smooth muscle actin were measured by qPCR analysis. Additionally, the prostatic expressions of transforming growth factor-β1 (TGF-β1), type I TGF-β receptor (TGF-βRI), Smad2, phosphorylation-Smad2 (p-Smad2), Smad3, p-Smad3, Smad7, nuclear related factor-2 (Nrf-2), heme oxygenase-1 (HO-1), B-cell CLL/lymphoma (Bcl)-2 and Bcl-2-associated X protein (Bax) were measured by western blot assay.
It was found that QYD ameliorated the Cd-induced prostatic oxidative stress and inflammation, attenuated prostatic EMT, inhibited the TGF-β1/Smad pathway, increased Bcl-2/Bax ratio and enhanced the activity of Nrf-2/HO-1 pathway.
These results showed that QYD could ameliorate Cd-induced prostatic deficits via modulating Nrf-2/HO-1 and TGF-β1/Smad pathways.
背景/目的：镉（Cd）是一种具有生殖毒性的环境污染物。青叶胆在中药中用于治疗前列腺亏虚，名为青叶胆片（QYD）。本研究旨在探讨青叶胆片对镉诱导的前列腺亏虚的潜在保护作用。
通过皮下注射0.2 mg/kg/d氯化镉15天诱导大鼠前列腺亏虚模型。通过检测丙二醛、一氧化氮、还原型/氧化型谷胱甘肽、总巯基水平和酶促抗氧化状态来评估前列腺氧化应激。通过检测促炎细胞因子水平来评估前列腺炎症。通过qPCR分析测量上皮-间质转化（EMT）标志物E-钙黏蛋白、纤连蛋白、波形蛋白和α-平滑肌肌动蛋白的水平。此外，通过蛋白质印迹法检测前列腺中转化生长因子-β1（TGF-β1）、I型TGF-β受体（TGF-βRI）、Smad2、磷酸化Smad2（p-Smad2）、Smad3、p-Smad3、Smad7、核相关因子-2（Nrf-2）、血红素加氧酶-1（HO-1）、B细胞淋巴瘤/白血病-2（Bcl-2）和Bcl-2相关X蛋白（Bax）的表达。
发现青叶胆片改善了镉诱导的前列腺氧化应激和炎症，减轻了前列腺EMT，抑制了TGF-β1/Smad通路，增加了Bcl-2/Bax比值，并增强了Nrf-2/HO-1通路的活性。
这些结果表明，青叶胆片可通过调节Nrf-2/HO-1和TGF-β1/Smad通路改善镉诱导的前列腺亏虚。
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