Effects of PKC activation on apoptosis during ischemia/reperfusion in L-6TG rat skeletal myoblasts.
- Author:
Hong-Jie LI
1
;
Xiao-Yan KONG
;
Lian-Yuan ZHANG
;
Shu-Yun DONG
;
Xiu-Li MEN
;
Li-Jun ZHAO
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Apoptosis; Calcium; metabolism; Caspase 3; metabolism; Cells, Cultured; Mitochondria; metabolism; Myoblasts, Skeletal; cytology; metabolism; Oxidative Stress; Protein Kinase C; metabolism; Rats; Reperfusion Injury; metabolism; pathology
- From: Chinese Journal of Applied Physiology 2005;21(4):437-440
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo study the effects of PKC activation on apoptosis during ischemia/reperfusion in L-6TG rat skeletal myoblasts.
METHODSCultured L-6TG cells were divided into 3 groups: control group (C), ischemia/reperfusion group (I/R), PMA + ischemia/ reperfusion group (PMA), SOD, XOD and free calcium and mitochondrial respiration in L-6TG cell were evaluated in each group. Apoptosis was detected by flow cytometer with PI staining method and agarose gel electrophoresis, the immunohistochemical method was used to determine the expression of caspase-3.
RESULTSCompared with I/R group, in PMA group, XOD , free calcium in L-6TG cell and apoptotic percentage all decreased significantly, while SOD and mitochondrial respiration in L-6TG cell increased. DNA fragmentation analysis of L-6TG cell showed no laddering pattern. The expression of caspase-3 was down regulated significantly.
CONCLUSIONActivation of PKC can lessen ischemia/reperfusion injury and apoptosis through lessening oxidative injury and mitochondrial injury, adjusting calcium dyshomeostasis and down expression of caspase-3.
