Effects of Salvia miltiorrhiza Bunge.f.alba. on mitochondrial damage and apoptosis induced by cerebral ischemia and reperfusion / 中国病理生理杂志
Chinese Journal of Pathophysiology
;
(12): 725-729, 2010.
Article
in Chinese
| WPRIM
| ID: wpr-403037
ABSTRACT
AIM:
To observe the effects of Salvia miltiorrhiza Bunge.f.alba. (Sal) on the mitochondrial ultra-structure, oxidative stress and apoptosis induced by ischemia injury in a rat model of focal cerebral ischemia and reperfusion.METHODS:
The middle cerebral artery occlusion/reperfusion (MCAO/R) rat model was established by a modified Longa occlusion method. Adult male SD rats were randomly divided into control group, simple ischemia reperfusion group, Sal with ischemia reperfusion group and butylphthalide with ischemia reperfusion group. To study the protective effects of Sal and its mechanism, the intervention of Sal was given and the ultra-structure of mitochondria, functions of mitochondria under oxidative stress and the incidence of apoptosis of brain cells were determined.RESULTS:
Many electron dense toxic granulation and vacuolus in mitochondria were observed in the rat brain of focal cerebral ischemia and reperfusion. Under the condition of ischemia and reperfusion, the mitochondria membrane was disaggregative, and the tubular cristae of mitochondrion disappeared. MDA content was obviously increased and the activity of glutathione peroxidase decreased significantly. The apoptosis of brain cells were observed in a great quantity. The changes of ultra-structure of mitochondria and the activity of GSH-Pxase were significantly improved by the treatment of Sal. Furthermore, treatment with Sal delayed the decrease of GSH-Pxase activity, and inhibited the increase in MDA content in brain tissue after ischemia and reperfusion. The incidence of apoptosis of brain cells was also decreased.CONCLUSION:
Sal protects the brain tissue from ischemia injury.
Full text:
Available
Index:
WPRIM (Western Pacific)
Language:
Chinese
Journal:
Chinese Journal of Pathophysiology
Year:
2010
Type:
Article
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