| Objective:Cerebral ischemia-reperfusion injury (cerebral ischemia reperfusion injury, CIR) is the phenomenon that cerebral ischemia leading to the brain cell damage and the ischemic injury is further aggravate After restoration of blood perfusion. Cerebral ischemia-reperfusion injury is the important issue of cerebrovascular disease.ischemic cerebral tissues is Lacking blood and hypoxic after cerebral ischemia,and lead to a rapid cascade,that activates the MMP-9, the activated MMP-9 combine with the protein molecules of cerebral vascular basement membrane,so undermine the integrity of the blood-brain barrier, and by the cause of this,the brain is dropsical and scathing.the edema and damage of brain is one of the important reasons about cerebral ischemia-reperfusion injury.in the same time of cerebral ischemic injury, the body tissues activated endogenous protective mechanism,which may protect and repair damaged nerves by abducting the neurotrophic factors. IGF-1 as an important neurotrophic factor could prevent the ischemic/hypoxic injury with the way of confrontating apoptosis of nerve cell, inhibiting the toxicity of excitatory amino acid and stabilize calcium ion concentration in neurons.XingDanTongLuo(DXTLD) decoction as a basic experienced pres-cription has been formed by Professor LiuYun according to several years clinical experiences.The previons section has shown that it could sig-nificantly improve symptom of Ischemic Stroke. However, the exact mechanism also remains unknown. In this paper, we explore the expression of MMP-9 and IGF-1 in rat brain with injury of Cerebral Ischemia and Reperfusion in order to provide evidence for clinical work.Methods:48 healthy and adult SD rats which ignore gender were assigned randomly to 6 groups,8 rats per group:blank group, ischemia/ reperfusion (I/R) group, DXTLD low dosage group, DXTLD midst dosage group,DXTLD high dosage group and Nimodipine(NIMO) group.The blank group was done nothing; Saline was given to I/R group at 1.Oml/100g weight once a day during 7 days; NIMO group at lml/100g,once a day during;DXTLD groups were given to DXTLD at dose of 0.75ml/100g,1.15ml/100g,1.5ml/100g once a day during.;.. After 7-days,the rats of all the groups except blank group were made into cerebral ischemia reperfusion injury models by thread embolism method. All the rats were killed and their brains were taken out after 2h ischemia and 24h reperfusion injury. The MMP-9 expression and IGF-1 expression in brain tissue were measured with immuneohistochemical method.Results:1. Using fast conventional HE staining brain tissue on the rats for histological observation of ultrathin sections:the normal cell structure of the sham operation group; the structural integrity of cortex and hip-pocampus has been damaged in ischemia-reperfusion group,the nerve cells in space broadening, unclear or absent nerve cells, cytoplasm is red, nuclears have been damaged, and even havs the exhibit of condensation and disappeared. In the drug treatment groups, neuronal degeneration cortex and hippocampus are also seen, nucleolus destruction, and also been seen the phenomenon of nuclear condensation or disappear, but the number was significantly less than that in ischemia reperfusion group, DXTLD large dosage group and Nimmo Horizon Group are improved the most.2. To observe the expression level of MMP-9 and IGF-1 by the ultrathin sections of brain tissue and the method of immuno histochemistry technology:expression of MMP-9 in cerebral ischemia-reperfusion group is the most, and in DXTLD's each dose groups and nimodipine group has been reductive.DXTLD large dosage group had been ruducted the most. The expression of IGF-1 in ischemia/reperfusion (I/R) group is less and the expression in all treatment groups were enhanced, in which DXTLD high dose group has the most expression.Conclusion:protective mechanism of DXTLD against cerebral ischemia by inhibiting the expression of MMP-9 and enhancing the expression of IGF-1 to reduce the damage for blood-brain barrier, inhibiting apoptosis of damaged neurons, promoting repair of ischemic injured tissues, thus play a protective role in cerebral ischemia-reperfusion injury of rats.
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