Department of Pulmonary Medicine, Inonu University Faculty of Medicine, Malatya, Turkey,
Inflammation. 2015;38(3):1166-80. doi: 10.1007/s10753-014-0081-1.
We aimed to investigate the preventive and therapeutic effect of apocynin (APO) on bleomycin (BLC)-induced lung injury in rats. Rats were assigned into groups as follows: control group; APO group, 20 mg/kg APO was given intraperitoneal for 29 days; BLC-1 and BLC-2 groups, a single intratracheal injection of BLC (2.5 mg/kg); APO+BLC-preventive group, 20 mg/kg APO was administered 12 h before the intratracheal BLC injection and continued for 14 days; BLC+APO-treatment group, 20 mg/kg APO was given on the 14th day after the intratracheal BLC injection and continued to sacrifice. The BLC-1 group was sacrificed on the 14th day of BLC administration to validate BLC-induced lung inflammation and fibrosis on the 14th of study initiation. All other groups were sacrificed on the 29th day after BLC administration. The semiquantitative histopathological assessment, tissue levels of malondialdehyde (MDA), superoxide dismutase, catalase (CAT), glutathione peroxidase (GPx), reduced glutathione (GSH), total antioxidant capacity, total oxidant status (TOS), and oxidative stress index (OSI) were measured. An addition to the serum myeloperoxidase (MPO), the cell count and cytokines (IL-1β, IL-6, and IL-8) of bronchoalveolar lavage (BAL) fluid were assayed. BLC-provoked histological changes were significantly detected compared to the control group. APO restored these histological damages in different quantity in the treatment and prevention groups. BLC caused a significant decrease in GSH, CAT, and GPX, which were accompanied with significantly the increased MDA, TOS levels, and OSI in the lung tissue concomitant with increased levels of the cellular account and proinflammatory cytokines in the BAL fluid. Otherwise, APO administration, both before and after BLC, reversed all biochemical markers and cytokine as well as histopathological changes induced by BLC. Interestingly, APO treatment reversed MPO activity in serum increased by BLC. In this study, both protective and therapeutic effects of APO against BLC-induced lung fibrosis were demonstrated for the first time.
我们旨在研究白杨素（APO）对博来霉素（BLC）诱导的大鼠肺损伤的预防和治疗作用。将大鼠分为以下几组：对照组；APO 组，腹腔内给予 20mg/kgAPO，共 29 天；BLC-1 和 BLC-2 组，单次气管内注射 BLC（2.5mg/kg）；APO+BLC-预防组，在气管内注射 BLC 前 12 小时给予 20mg/kgAPO，并持续 14 天；BLC+APO-治疗组，在气管内注射 BLC 后第 14 天给予 20mg/kgAPO，并继续处死。BLC-1 组于 BLC 给药的第 14 天处死，以验证研究开始第 14 天 BLC 诱导的肺炎症和纤维化。所有其他组均于 BLC 给药后第 29 天处死。半定量组织病理学评估、丙二醛（MDA）、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GPx）、还原型谷胱甘肽（GSH）、总抗氧化能力、总氧化状态（TOS）和氧化应激指数（OSI）的组织水平进行了测定。除了血清髓过氧化物酶（MPO）外，还测定了支气管肺泡灌洗液（BAL）中的细胞计数和细胞因子（IL-1β、IL-6 和 IL-8）。与对照组相比，BLC 引起的组织学变化明显。APO 在治疗和预防组中以不同的量恢复了这些组织损伤。BLC 导致 GSH、CAT 和 GPX 显著减少，同时肺组织中 MDA、TOS 水平和 OSI 显著增加，BAL 液中的细胞计数和促炎细胞因子水平也显著增加。相反，APO 给药，无论是在 BLC 之前还是之后，都逆转了 BLC 诱导的所有生化标志物、细胞因子和组织病理学变化。有趣的是，APO 治疗逆转了 BLC 引起的血清 MPO 活性增加。在这项研究中，首次证明了 APO 对 BLC 诱导的肺纤维化具有保护和治疗作用。
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