朱敏玲,梁贤凯,罗文才,刘文秀,张晓卉,张 博.内质网应激及自噬参与百草枯中毒所致肺损伤[J].,2018,(2):254-258 |
内质网应激及自噬参与百草枯中毒所致肺损伤 |
Endoplasmic Reticulum Stress and Autophagy are Involved in Paraquat Poisoning Induced Lung Injury |
投稿时间:2017-10-07 修订日期:2017-10-30 |
DOI:10.13241/j.cnki.pmb.2018.02.013 |
中文关键词: 百草枯中毒 内质网应激 自噬 肺损伤 |
英文关键词: Paraquat poisoning Endoplasmic reticulum stress Autophagy Pulmonary injury |
基金项目:黑龙省教育厅科研课题(12531369) |
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中文摘要: |
摘要 目的:探讨内质网应激及自噬在百草枯中毒所致大鼠肺脏损伤中的作用。方法:选取Wistar大鼠腹80只,腹腔注射百草枯(15 mg/kg)建立百草枯中毒肺脏损伤的动物模型。染毒后1、3、7、14、21 d处死动物取肺组织,采用HE染色和Van Gieson(V.G)染色观察大鼠肺脏损伤及纤维化情况,电镜观察Wistar大鼠肺脏胞浆空泡变、自噬体的形成以及肺脏损伤。Western-blot方法观察Wistar大鼠内质网应激相关蛋白(GRP94、Caspase-12和CHOP)和自噬相关蛋白(LC3-II、Beclin-1)的表达。结果:HE及V.G染色结果显示随中毒时间延长,百草枯中毒肺损伤及肺纤维化逐渐加重;电镜结果显示百草枯中毒肺脏发生胞浆空泡变、自噬体形成。与对照组比较,在百草枯中毒组内质网应激相关蛋白GRP94在3 d表达达到峰值(P<0.001),7 d表达开始降低(P<0.05),CHOP蛋白表达3 d开始增加(P<0.001),cleaved caspase-12蛋白表达7 d开始增加(P<0.001),并逐渐加强,自噬相关蛋白LC3-II和Beclin-1表达3 d开始增加(P<0.001),14 d表达最高(P<0.001)。结论:内质网应激以及细胞自噬共同参与百草枯中毒所致肺脏损伤。 |
英文摘要: |
ABSTRACT Objective: To investigate the role of endoplasmic reticulum stress and autophagy in lung injury induced by paraquat intoxication. Methods: Eighty healthy Wistar rats were randomly injected with paraquat (15 mg/kg) to establish an animal model of paraquat-induced pulmonary injury. The rats were sacrificed respectively at 1, 3, 7, 14, 21 d after injection with paraquat. The paraffin sections of lung tissue were stained with hematoxylin-eosin(HE) and Van Gieson(V.G) staining to observe the lung injury and fibrosis in Wistar rats, cytoplasmic vacuolar degeneration, autophagosome formation and pulmonary injury were examined in rat pulmonary cells by electron microscopy. Endoplasmic reticulum-related protein (GRP94, Caspase-12 and CHOP) and autophagy-related protein (LC3-II, Beclin-1) expressions in Wistar rats were assessed by Western blot analyses. Results: HE and V.G staining demonstrated injury in the lung after paraquat injection with a tendency of exaggeration with time, and finally resulted in fibrosis. The results of electron microscopy showed that the cytoplasmic vacuolar degeneration and autophagosome formation. Compared with the control group, The expression of endoplasmic reticulum stress associated protein GRP94 get the highest expression in 3 d (P < 0.001), and the expression of 7 d were decreased (P<0.05). CHOP expression began to increase from 3 d (P < 0.001). The expression of cleaved Caspase-12 began to increase from 7 d (P < 0.001) and gradually strengthened. The expression of autophagy associated protein LC3-II and Becline-1 began to increase from 3 d (P<0.001). The expression of 14 d was highest (P < 0.001). Conclusion: Endoplasmic reticulum stress and cell autophagy pathways are both involved in paraquat-treated pulmonary injury. |
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