Department of Respiratory Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Department of Cardiology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
Life Sci. 2016 Nov 1;164:1-8. doi: 10.1016/j.lfs.2016.09.001. Epub 2016 Sep 4.
To investigate the effects of curcumin on alveolar epithelial injury in a rat model of chronic obstructive pulmonary disease (COPD) and its potential mechanism.
The rat COPD model was established by cigarette smoke exposure combined with intratracheal administration of lipopolysaccharide. Thirty-eight male Sprague-Dawley rats were randomly divided into four groups: control, COPD model, COPD with curcumin and COPD with solvent groups. Neutrophil and macrophage infiltration in bronchoalveolar lavage fluid (BALF) was evaluated, and the levels of IL-6, IL-8 and TNF-α in BALF and serum were determined by ELISA. Histopathological examination and TUNEL staining were used to assess the alveolar epithelial injury. The protein expression of p66Shc and p-p66Shc in the lung tissues was determined by immunohistochemistry and western blot.
Curcumin significantly decreased the numbers of total cells, neutrophils and macrophages in BALF from COPD rats. In addition, the levels of IL-6, IL-8 and TNF-α in BALF and serum of COPD rats were significantly decreased after treatment with curcumin. Moreover, curcumin ameliorated emphysema and ultrastructural damage of alveolar epithelial cells in COPD rats. The apoptosis index of alveolar epithelial cells in the COPD with curcumin group was significantly lower than that in the COPD model group. Furthermore, the protein expression of p66Shc and p-p66Shc in alveolar epithelia was significantly decreased in the COPD with curcumin group compared with COPD model group.
Curcumin attenuates alveolar epithelial injury in COPD rats, which may be partially due to the down-regulation of p66Shc.
研究姜黄素对慢性阻塞性肺疾病(COPD)大鼠模型肺泡上皮损伤的影响及其潜在机制。
采用香烟烟雾暴露联合气管内滴注脂多糖的方法建立大鼠 COPD 模型。38 只雄性 Sprague-Dawley 大鼠随机分为四组:对照组、COPD 模型组、COPD 加姜黄素组和 COPD 加溶剂组。评估支气管肺泡灌洗液(BALF)中中性粒细胞和巨噬细胞浸润情况,ELISA 法检测 BALF 和血清中白细胞介素 6(IL-6)、IL-8 和肿瘤坏死因子-α(TNF-α)水平。组织病理学检查和 TUNEL 染色评估肺泡上皮损伤。免疫组织化学和 Western blot 法检测肺组织中 p66Shc 和 p-p66Shc 的蛋白表达。
姜黄素显著降低 COPD 大鼠 BALF 中总细胞、中性粒细胞和巨噬细胞的数量。此外,姜黄素治疗后 COPD 大鼠 BALF 和血清中 IL-6、IL-8 和 TNF-α水平明显降低。而且,姜黄素改善了 COPD 大鼠肺气肿和肺泡上皮细胞超微结构损伤。COPD 加姜黄素组肺泡上皮细胞的凋亡指数明显低于 COPD 模型组。此外,与 COPD 模型组相比,COPD 加姜黄素组肺泡上皮中 p66Shc 和 p-p66Shc 的蛋白表达明显降低。
姜黄素减轻 COPD 大鼠的肺泡上皮损伤,这可能部分归因于 p66Shc 的下调。