Protective effect of hydroxysafflor yellow A against rat cortex mitochondrial injuries induced by cerebral ischemia.
- Author:
Jing-wei TIAN
1
;
Feng-hua FU
;
Wang-lin JIANG
;
Chao-yun WANG
;
Fang SUN
;
Tai-ping ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Brain Ischemia; metabolism; pathology; Calcium; metabolism; Chalcone; analogs & derivatives; pharmacology; Male; Malondialdehyde; metabolism; Membrane Fluidity; drug effects; Mitochondria; metabolism; pathology; Mitochondrial Swelling; drug effects; NAD; metabolism; Neuroprotective Agents; pharmacology; Quinones; pharmacology; Rats; Rats, Sprague-Dawley; Superoxide Dismutase; metabolism
- From: Acta Pharmaceutica Sinica 2004;39(10):774-777
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo study the effects of hydroxysafflor yellow A (HSYA) on the mitochondrial function of cortex mitochondrial during cerebral ischemia in rats.
METHODSRat focal cerebral ischemia model in rats was established by ligation of middle cerebral central artery. Cortex mitochondria were isolated and prepared for the measurement of membrane fluidity, swelling, respiratory function, activities of mitochondrial respiratory enzymes and superoxide dismutase (SOD), contents of phospholipid, malondial dehyde (MDA) and Ca2+ to evaluate the function of mitochondria.
RESULTSFocal cerebral ischemia resulted in severe neuronal mitochondrial injuries, which could be alleviated by i.v. HSYA (10, 20 mg x kg(-1)), and nimodipine (Nim, 1.0 mg x kg(-1)). The swelling of mitochondria was ameliorated, the decomposability of membrane phospholipid was decreased, the membrane fluidity of mitochondria was increased, HSYA also significantly inhibited the decrease in the activities of respiratory enzymes and SOD of mitochondria, and the increase in MDA and Ca2+ levels caused by cerebral ischemia in rats.
CONCLUSIONHSYA showed a protective action against the cortex mitochondrial injuries in rats induced by cerebral ischemia. The mechanisms may be derived from reducing lipid peroxides, inhibiting Ca2+ overload, scavenging free radicals and improving the energy metabolism.
