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首页> 外文期刊>Drug Design, Development and Therapy >The Protective Role of Tanshinone IIA in Silicosis Rat Model via TGF-β1/Smad Signaling Suppression, NOX4 Inhibition and Nrf2/ARE Signaling Activation
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The Protective Role of Tanshinone IIA in Silicosis Rat Model via TGF-β1/Smad Signaling Suppression, NOX4 Inhibition and Nrf2/ARE Signaling Activation

机译：丹参酮IIA在矽肺病大鼠模型中通过TGF-β1/ Smad信号抑制，NOX4抑制和NRF2 /信号激活的保护作用

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Purpose: Silicosis is an occupational disease caused by inhalation of silica and there are no effective drugs to treat this disease. Tanshinone IIA (Tan IIA), a traditional natural component, has been reported to possess anti-inflammatory, antioxidant, and anti-fibrotic properties. The current study’s purpose was to examine Tan IIA’s protective effects against silica-induced pulmonary fibrosis and to explore the underlying mechanisms. Methods: 48 male SD rats were randomly divided into four groups (n=12): i) Control group; ii) Silicosis group; iii) Tan IIA group; iv) Silicosis +Tan IIA group. Two days after modeling, the rats of Tan IIA group and Silicosis +Tan IIA group were given intraperitoneal administration 25 mg/kg/d Tan IIA for 40 days. Then, the four groups of rats were sacrificed and the lung inflammatory responses were measured by ELISA, lung damage and fibrosis were analyzed by hematoxylin and eosin (H&E) staining and Masson staining, the expression levels of collagen I, fibronectin and α-smooth muscle actin (α-SMA) were measured by immunohistochemistry. The markers of oxidative stress were measured by commercial kits, and the activity of the TGF-β1/Smad and NOX4, Nrf2/ARE signaling pathways were measured by RT-PCR and Western blotting. Results: The silica-induced pulmonary inflammtory responses, structural damage and fibrosis were significantly attenuated by Tan IIA treatment. In addition, treatment with Tan IIA decreased collagen I, fibronectin and α-SMA expression, and inhibited TGF-β1/Smad signaling in the lung tissue. The upregulated levels of oxidative stress markers in silicosis rats were also markedly restored following Tan IIA treatment. Furthermore, treatment with Tan IIA reduced NOX4 expression and enhanced activation of the Nrf2/ARE pathway in the lung tissue of silicosis rats. Conclusion: These findings suggest that Tan IIA may protect lung from silica damage via the suppression of TGF-β1/Smad signaling, inhibition of NOX4 expression and activation of the Nrf2/ARE pathway.
机译：目的：矽肺病是吸入二氧化硅引起的职业病，没有有效的药物治疗这种疾病。据报道，丹参酮IIA（Tan Iia）是一种传统的天然组分，具有抗炎，抗氧化和抗纤维化特性。目前的研究目的是检查TAN IIA对二氧化硅诱导的肺纤维化的保护作用，并探讨潜在的机制。方法：将48只雄性SD大鼠随机分为四组（n = 12）：i）对照组; ii）矽肺组织; III）TAN IIA集团; iv）矽肺蛋白+棕褐色IIA集团。建模后两天，Tan IIA组和矽肺病+ Tan IIA组的大鼠腹腔给药25mg / kg / d Tan Iia持续40天。然后，处死四组大鼠并通过ELISA测量肺炎反应，通过苏木精和曙红（H＆E）染色和Masson染色分析肺损伤和纤维化，胶原蛋白I，纤连蛋白和α-平滑肌的表达水平通过免疫组织化学测量肌动蛋白（α-SMA）。通过商业试剂盒测量氧化应激的标志物，通过RT-PCR和Western印迹测量TGF-β1/ Smad和NOX4，NRF2 /是信号传导途径的活性。结果：Tan IIa治疗显着减弱了二氧化硅诱导的肺炎炎反应，结构损伤和纤维化。此外，用棕褐色IIa治疗减少胶原I，纤连蛋白和α-SMA表达，并抑制肺组织中的TGF-β1/ Smad信号。在Tan IIa治疗后，矽肺大鼠中氧化应激标记物的上调水平也明显恢复。此外，用Tan IIa治疗降低NOx4表达，并增强NRF2 /硅化大鼠肺组织中的NRF2 /途径的活化。结论：这些研究结果表明，TAN IIA可以通过抑制TGF-β1/ SMAD信号传导，抑制NOX4表达和NRF2 /途径的激活来保护肺免受二氧化硅损伤。

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