Effects of cyclosporine A on pneumocyte apoptosis with lung ischemia/reperfusion injury in rats.
- Author:
Yong-Yue DAI
1
;
Ren-Wu ZHU
;
Shi-Rong NI
;
Mao-Lin HAO
Author Information
- Publication Type:Journal Article
- MeSH: Alveolar Epithelial Cells; cytology; drug effects; Animals; Apoptosis; drug effects; Caspase 3; metabolism; Cyclosporine; pharmacology; Cytochromes c; metabolism; Lung; blood supply; pathology; Male; Rats; Rats, Sprague-Dawley; Reperfusion Injury; metabolism; pathology
- From: Chinese Journal of Applied Physiology 2010;26(4):493-496
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of cyclosporine A (CsA), a powerful inhibitor of mitochondrial permeability transition pore (MPTP), on pneumocyte apoptosis, the release of cytochrome C and the activity of caspase-3 after lung ischemia/reperfusion, and explore the mechanisms.
METHODSSingle lung in situ ischemia/reperfusion animal model was used. 30 SD rats were randomly divided into three groups (n = 10): sham (S) group, ischemia/reperfusion (I/R) group and cyclosporine A (CsA) group. Apoptosis of pneumocyte was assessed by TUNEL method, cytochrome C (CytC) in cytoplasm was detected by immunohistochemistry techniques, and the activity of caspase-3 was measured with spectrophotometer.
RESULTSThe content of CytC in cytoplasm, the activity of caspase-3, and the value of apoptosis index (AI) in ischemia/reperfusion group were evidently higher than that in S group (P < 0.01). CsA suppressed apoptosis as well as CytC release and caspase-3 activity (P < 0.01).
CONCLUSIONCsA can prevent the release of cytochrome C, block the apoptosis of pneumocyte accordingly maybe by closing the MPTP.
