ERK1/2在缺血再灌注损伤肺细胞凋亡中的作用及缺血后处理的干预

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Abstract Objective: To investigate the role of ERK1/2 on pneumocyte apoptosis after lung ischemia/reperfusion injury and ischemic postconditioning (IPO) intervention. Methods: Forty adult male Sprague-Dawley rats were randomly divided into 5 groups based upon the intervention (n=8): control group (C), IR group (IR), IR+IPO group (IPO), IPO+solution countrol group (D), IPO+U0126 group (U). Left lung tissue was isolated after the 2 hours of reperfusion, The ultrastructure of the left lung were observed under electron transmission microscopes. Apoptosis index (AI) of lung tissue was determined by terminal deoxynuleotidyl transferase mediated dUTP nick end and labeling (TUNEL) method. The mRNA expression and protein levels of Bcl-2 and Bax were measured by RT-PCR and quantitative immunohistochemistry (IHC). Results: Compared with C group, AI and the expression of Bax of IR were significantly increased, the expression of Bcl-2 and Bcl-2/Bax were significantly decreased (P< 0.05), and ultrastructure abnormality was obviously found in lung tissue. Compared with IR group, all the indexes of IPO except for the expression of Bcl-2 and Bcl-2/Bax were obviously reduced, the expression of Bcl-2 and Bcl-2/Bax was increased (P<0.05). All the indexes between D and IPO were little or no significant (P>0.05). the expression of Bcl-2 and Bcl-2/Bax of U was significantly decreased and other indexes were increased than those of IPO (P<0.05). Conclusion: IPO may attenuate pneumocyte apoptosis in LIRI by activation of ERK1/2 MAPK, up-regulating expression of Bcl-2/Bax ratio.

Key words： ischemia/reperfusion ischemic postconditioning lung cell apoptosis ERK1/2 U0126 Bcl-2 Bax rats

Received: 22 September 2013

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	CHEN Haie
	MA Yingchun
	HUANG Linjing
	HE Jinbo
	SONG Dong
	ZHENG Mengxiao
	YING Lei
	WANG Wantie

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https://xb.wmu.edu.cn/EN/ OR https://xb.wmu.edu.cn/EN/Y2014/V44/I2/95

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