| Acute cerebral infarction is a familiar critical and dangerous disease. Resuming the cerebral bloods flow (CBF) quickly and limiting the ischemic injury to reduce the infarct size and cerebral edema, namely brain protection, is the principle in the treatment on acute cerebral infarction. The pathological mechanism of cerebral ischemic injury is not clear yet, and there are many factors concerned with or adjusting the injury. Facts have proved that regulating some factors in some plane cannot hold back the progress of ischemic injury. Possibly, to study the multitarget and multiple levels' effect of Chinese traditional medicine could be a worthy research.XinNao ShuTong Capsule (XNST), whose components are gross saponins from Tribulus Terrestri L. (GSTT), Whose effect in traditional Chinese medical theory is activating blood circulation and resolving stasis, has proved effective in treating ischemic heart disease or ischemic cerebrovascular disease for 20 years' clinical practice. This study was to investigate the effects of XNST on cerebral ischemic injury. On the basis of study at the levels of gross appearance, organ and tissue, farther study on the mechanism of brain protection was carried out in follow aspects of ischemic injury: acid intoxication, energy metabolism dysfunction, free radical injury and inflammatory reaction. Objectives: To study the protective effect and its mechanism of XNST on acute cerebral ischemic injury in rats. To discuss the hypothesis of the injury of brain collaterals by toxins based upon the pathophysiologic course of acute cerebral ischemic injury and the protective effect of Chinese traditional medicine. Methods: 100 male Wistar rats weighing 280-320g were randomly divided into five groups: normal, sham operation, model, Chinese medicine treatment (CMT), and Western medicine treatment (WMT) 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), physiological saline substituted for the embolus in sham operation. Neurological deficit scores were assessed according to Bederson' s method. Morphologic change and the expression of tumor necrosis factor-α (TNF-α) and interleukin -1β (IL-1β)in hippocampus and cortex was observed, and biochemical criterions including the activity of NaH-K+-ATPase, lactate dehydrogenase (LDH), superoxide dismutase (SOD), and the content of malondialdehyde (MDA) in hippocampus were examined, 72 hours after ischemia Results: Compared with that in model group, the death rate of the animalsin CM or WMT group was much lower, and the neurological deficit was improved. The morphologic change of hippocampus and cortex in both CMT and WMT treatment groups was milder than 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 CMT group (P<0.01) as well as in WMT group (P<0.01). The content of MDA in hippocampus was significantly increased in model group (P<0.05), and was reduced in CMT group (P<0.05) as well as in WMT group (P<0.01). TNF-a markedly expressed in the neuroplasm of hippocampus and cortex in model. There' s no difference in the expression of TNF-α in hippocampus between CMT and model group, but the expression in cortex was obviously reduced in CMT group. TNF-a of hippocampus and cortex expressed lower in WMT group than in model group. While IL-1β expressed more in hippocampus than in cortex in model group, and the expression was reduced in CMT but not in WMT group. Conclusions: The results reveal that XNST has the protective effect against cerebral ischemic injury. And its possible mechanism is that XNST can improve energy metabolism dysfunction in brain induced by ischemia to prevent the following injury such as acid intoxication, can prevent lipid peroxidation, and can control inflanmation. |
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