Protective effect of shenqi fuzheng injection on cerebral ischemia/reperfusion injured aged rats.
- Author:
Ying-min CAI
1
;
Hai-tao HU
;
Xiao-ya MA
Author Information
- Publication Type:Journal Article
- MeSH: Age Factors; Animals; Brain; enzymology; metabolism; Brain Ischemia; chemically induced; metabolism; prevention & control; Calcium; metabolism; Cerebral Infarction; metabolism; prevention & control; Creatine Kinase; metabolism; Disease Models, Animal; Drugs, Chinese Herbal; administration & dosage; therapeutic use; Injections; L-Lactate Dehydrogenase; metabolism; Lipid Peroxidation; drug effects; Male; Malondialdehyde; metabolism; Medicine, Chinese Traditional; Neurons; drug effects; Protective Agents; administration & dosage; pharmacology; therapeutic use; Rats; Rats, Sprague-Dawley; Reperfusion Injury; chemically induced; metabolism; prevention & control; Superoxide Dismutase; metabolism; Water; metabolism
- From: Chinese Journal of Integrated Traditional and Western Medicine 2006;26 Suppl():10-14
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the protective effects of Shenqi Fuzheng Injection (SFI) on cerebral ischemia/reperfusion injured aged rats.
METHODSAged SD male rats, weighing 200-300 g, were randomly divided into 4 groups: the model group, the sham-operative group, the nimodipine positive control group (abbreviated as nimodipine group) and the SFI group. Focal cerebral ischemia/reperfusion injured rat model was established by modified Longa method. SFI was administered by intravenous dripping 1 week before ischemia. Nervous function disorder, brain infarction area, serum lactate dehydrogenase (LDH) and creatine kinase (CK) levels, brain contents of Ca2+ , water, MDA and SOD levels were observed 3 hrs after ischemia and 3 hrs after reperfusion.
RESULTSperimental results showed that SFI could obviously improve the deficit of nerve function, decrease water content of brain, reduce the infarction area of brain, and inhibit Ca2 + aggregation. LDH and CK levels in serum and MDA in brain were obviously lower than those in the model group and SOD activity in cerebral tissue was obviously higher than that in the model group.
CONCLUSIONSFI had protective effect on cerebral ischemia/reperfusion injured aged rats, whose mechanism might be related to the inhibition of lipid peroxidation and Ca2+ aggregation.
