Kan Baotian, Jian Xiangdong, Zhou Qian, Wang Jieru, Yu Guangcai, Sun Jing, Gao Yikai
Department of Poisoning and Occupational Disease, Qilu Hospital of Shandong University, Jinan, Shandong 250012, P.R. China.
Mol Med Rep. 2014 Apr;9(4):1232-6. doi: 10.3892/mmr.2014.1938. Epub 2014 Feb 7.
In China, and other Asian countries, numerous patients have succumbed to pulmonary fibrosis induced by paquarat poisoning, but the early pathogenesis remains unclear. In this study the effect of cytokine transforming growth factor (TGF)-β1 was observed in early acute paraquat poisoning and examined the mechanism by which paraquat caused early acute lung injury. It was discovered that the rat serum TGF-β1 levels in the paraquat groups were significant higher than that in the control group (P<0.05) and the rat pulmonary TGF-β1 mRNA expression levels were also higher than that in the control group (P<0.05). Histological examination indicated that the rat lung tissue was broad and congested, and had been infiltrated by inflammatory cells. Masson's trichrome staining for collagen showed that the lung tissue appeared fibrotic following paraquat poisoning. Ultramicrostructure observation found that macrophages, red blood cells, lymphocytes and granulocytes infiltrated the alveolar space and there were cytolysosomes in the macrophages. The shape of the type II alveolar epithelial cell nuclei were irregular with karyopyknosis. The heterochromatin migrated to the cell edge and lamellar body vacuolization was also observed. Type I alveolar epithelial cells shrank. In conclusion, the effect of cytokine TGF-β1 on paraquat-induced acute lung tissue injury may be important.
在中国及其他亚洲国家，众多患者死于百草枯中毒所致的肺纤维化，但早期发病机制仍不清楚。本研究观察了细胞因子转化生长因子（TGF）-β1在早期急性百草枯中毒中的作用，并探讨了百草枯导致早期急性肺损伤的机制。研究发现，百草枯组大鼠血清TGF-β1水平显著高于对照组（P<0.05），大鼠肺组织TGF-β1 mRNA表达水平也高于对照组（P<0.05）。组织学检查表明，大鼠肺组织广泛充血，有炎性细胞浸润。Masson三色胶原染色显示，百草枯中毒后肺组织出现纤维化。超微结构观察发现，巨噬细胞、红细胞、淋巴细胞和粒细胞浸润肺泡腔，巨噬细胞内有溶酶体。Ⅱ型肺泡上皮细胞核形态不规则，核固缩。异染色质迁移至细胞边缘，还观察到板层小体空泡化。Ⅰ型肺泡上皮细胞萎缩。总之，细胞因子TGF-β1对百草枯诱导的急性肺组织损伤可能具有重要作用。
