OBJECTIVE: To 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. METHOD: 60 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. RESULT: The 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). CONCLUSION: The 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.
OBJECTIVE: To 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. METHOD: 60 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. RESULT: The 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). CONCLUSION: The 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.