[Intervention effect of apocynin on silicosis induced by silica in rats].

Objective: To investigate the intervention effect and its mechanism of apocynin, an inhibitor of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) on silicosis induced by silica (SiO(2)) in rats. Methods: In October 2021, 24 SPF SD male rats were divided into control group, silicosis model group and apocynin intervention group according to random number table method, with 8 rats in each group. SiO(2) was exposed by one-time intratracheal instillation. The rats in the apocynin intervention group were intraperitoneally injected with apocynin 50 mg/kg, 3 times a week, on the second day after treatment. The rats were sacrificed 28 days later, and lung coefficients were calculated after lung tissues were weighed. Hematoxylin-eosin staining and Masson staining were used to observe the lung histopathological changes in each group, respectively. The levels of NOX, reactive oxygen species (ROS), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in lung tissue were detected. The expressions of interleukin-1 beta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were determined by Enzyme-Linked Immunosorbent Assay (ELISA). The level of hydroxyproline (HYP) was detected by alkaline hydrolysate. The expressions of transforming growth factor beta 1 (TGF-β1), E-cadherin (E-cad) and α-smooth muscle actin (α-SMA) in lung tissue were detected by Western blotting. Results: Compared with the control group, the body weight of silicosis model group was decreased, the lung tissue showed obvious inflammatory infiltration and fibrosis, and the levels of lung coefficient, IL-1β, IL-6, TNF-α and TGF-β1 were significantly increased (P<0.05). Compared with the silicosis model group, the lung tissue injury in the apocynin intervention group was significantly improved, the lung coefficient, NOX, ROS, MDA, IL-1β, IL-6, TNF-α and TGF-β1 levels were decreased, and the activity of GSH-Px was increased (P<0.05). Compared with the silicosis model group, the expressions of HYP and α-SMA were decreased and the level of E-cad was increased in the apocynin intervention group (P<0.05) . Conclusion: Apocynin may alleviate SiO(2)-induced fibrosis in silicosis rats by reducing oxidative stress, the release of inflammatory factors and inhibiting the process of epithelial-mesenchymal transition.目的： 探讨烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶（NOX）抑制剂罗布麻宁对二氧化硅（SiO(2)）诱导的大鼠矽肺模型的干预作用，并探讨其作用机制。 方法： 于2021年10月，将24只SPF级SD雄性大鼠按随机数字表法分为对照组、矽肺模型组、罗布麻宁干预组，每组8只。采用一次性气管滴注SiO(2)的方法染尘，罗布麻宁干预组大鼠于处理后第2天开始腹腔注射罗布麻宁50 mg/kg，3次/周。于28 d后处死大鼠，取肺组织称重后计算肺系数，苏木精-伊红染色和Masson染色分别观察各组大鼠肺组织病理学变化。检测肺组织NOX、活性氧（ROS）、谷胱甘肽过氧化物酶（GSH-Px）活力及丙二醛（MDA）水平；酶联免疫吸附试验法测定肺组织白细胞介素1β（IL-1β）、白细胞介素6（IL-6）及肿瘤坏死因子α（TNF-α）表达；碱水解法检测羟脯氨酸（HYP）水平；蛋白免疫印迹法检测肺组织转化生长因子β1（TGF-β1）、E-钙黏蛋白（E-cad）及α-平滑肌蛋白（α-SMA）的表达。 结果： 与对照组相比，矽肺模型组大鼠体重降低，肺组织出现明显的炎性浸润及纤维化，肺系数、IL-1β、IL-6、TNF-α及TGF-β1水平均明显升高（P<0.05）；与矽肺模型组比较，罗布麻宁干预组大鼠肺组织损伤明显改善，肺系数、NOX、ROS、MDA、IL-1β、IL-6、TNF-α及TGF-β1水平均降低，GSH-Px活力增加（P<0.05）；与矽肺模型组比较，罗布麻宁干预组大鼠肺组织HYP和α-SMA表达均降低，E-cad水平增加（P<0.05）。 结论： 罗布麻宁可能通过减少矽肺大鼠氧化应激、炎性因子释放及抑制上皮-间质转化，缓解SiO(2)诱导的大鼠纤维化作用。.