Protective effects of Xinnao Shutong capsule on acute cerebral ischemic injury of multiple infarcts in rats.
- Author:
Jin ZHANG
1
;
Yun-ling ZHANG
;
Jin-li LOU
;
Hong ZHENG
;
Xue-mei LIU
;
Ran HAO
;
Qi-fu HUANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Brain Infarction; complications; Brain Ischemia; etiology; metabolism; prevention & control; Capsules; Drugs, Chinese Herbal; isolation & purification; pharmacology; Hippocampus; drug effects; metabolism; pathology; L-Lactate Dehydrogenase; metabolism; Male; Malondialdehyde; metabolism; Neuroprotective Agents; isolation & purification; pharmacology; Plants, Medicinal; chemistry; Random Allocation; Rats; Rats, Wistar; Saponins; isolation & purification; pharmacology; Sodium-Potassium-Exchanging ATPase; metabolism; Superoxide Dismutase; metabolism; Tribulus; chemistry
- From: China Journal of Chinese Materia Medica 2006;31(23):1979-1982
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo study the effect of Xinnao Shutong capsule (XNST) on energy metabolism dysfunction, free radical injury and inflammatic factors in the course of acute cerebral ischemic damage, and try to reveal the mechanism of the protection against ischemia.
METHOD60 male Wistar rats weighing 280 - 320 g were randomly divided into five groups: normal, sham operation, model, XNST treatment( XNST-T) , and Western medicine treatment (WM-T) group. Acute multi-infarct model in rats was induced by injecting the embolus of blood powder through the right external carotid artery (ECA) into the internal carotid artery (ICA). At 72 hours after ischemia, morphologic change and the express of tumor necrosis factor-alpha (TNF-alpha) and interleukin -1beta ( IL-1beta) in hippocampus CAl section and cortex were observed, biochemical criterions including the activity of Na+ -K+ -ATPase, lactate dehydrogenase (LDH), superoxide dismutase (SOD), and the content of malondialdehyde (MDA) in hippocampus were examined.
RESULTThe morphologic change of hippocampus and cortex in both XNST-T and WM-T groups was milder than that in model group. The activity of Na+ -K+ -ATPase, LDH and SOD in hippocampus were all significantly decreased in model group (P <0. 01), and elevated in XNST group (P <0. 01) as well as in WM-T group (P <0. 01). The content of MDA in hippocampus was significantly increased in model group (P <0. 05), and was reduced in XNST group (P <0. 05) as well as in WM-T group (P <0. 01).
CONCLUSIONThe results reveal that XNST has the protective effect against cerebral ischemic injury. And its possible mechanism is that XNST can prevent the upper pathological process.
