| The Expression and Role of ERK1/2 in Cerebral Cortex of Rats after Brain Ischemic PreconditioningPrefaceGiving animals short time and slim cerebral ischemia can prevent neurons from injury caused by subsequent fatal ischemia. This phenomenon is called brain ischemic preconditioning(BIP). Studing the model of BIP can master the mechanism of BIT and develope a new route to treat cerebral ischemic disease.Some studys showed that extracellular signal regulated protein kinases(ERK) route maybe involved in the mechanism of BIP recently.We observed the variance of infarct volume on rats by using model of left middle cerebral artery occlusion (MCAO) and the activation of ERK1/2 in the cerebral cortex in order to exploring the expression and role of ERK1/2 after BIP.Materials and Method1. GroupsAll rats were divided into two groups randomly:sham group and BIP group. Each group was divided into four subgroups including 6 rats. Three subgroups ERK1/2 activation and expression in the cerebral cortex were examined by Western blotting analysis at 15rain, 2h, 24 h after BIP. The other one was given a left middle cerebral artery occlusion 24h after BIP or sham BIP and the infarct volume was measured2. model of left middle cerebral artery occlusion (MCAO) on ratsThe transient left middle cerebral artery occlusion was made on the basis of Zea-Longa method.3. SDS-PAGE and Western-Blot Equal volumes of PM and IM proteinswere seperated on 10% SDS-polyacrylamide gels and transferred to PVDF, and then determined the expression of P-ERK1/2 and general ERK1/2 in these seperated membrain fractions with Western blot4. Neurological function deficient messurement5. Infarct volume was calculated by TTC stainingResults1 Elevated p-ERK1/2 expression were observed 15min after or 2h after preconditioning, respectively and had significant difference to sham group. (P＜0.01). There were no different p-ERK1/2 expression in two groups 24h after BIP or sham. (p＞0.05)2. There were no different general ERK1/2 expression in two groups 15min after, 2h after or 24h after BIP or sham.(p＞0.05)3. BIP reduced infarct volume significantly than the sham BIP after MCAO(P＜0.01)4. BIP reduced Neurological function deficientDiscussionSome studys showed that extracellular signal regulated protein kinases(ERK) route maybe involved in the mechanism of BIP according by deep research into it recently. Elevated p-ERK1/2 expression after preconditioning can protect neuron by activating neural- protective gene transfer.Patients who suffered from TIA had a similar situation with animals given focal ischemic preconditioning. The vassel construction of rats is alike human so that they are suitable for the study on human vascular disease. So We observed the variance of infarct volume on rats by using model of left middle cerebral artery occlusion (MCAO) and the activation of ERK1/2 in the cerebral cortex in order to exploring the expression and role of ERK1/2 after BIEOur data suggested Elevated p-ERK1/2 expression were observed 15min after or 2h after preconditioning, respectively and had significant difference to sham group. There were no different p-ERK1/2 expression in two groups 24h after BIP or sham. BIP reduced infarct volume and neurological function deficient after MCAO which was important in clinic.We suggest that special gene had been activated through ERK route in 24 hours after BIP and profective effect had been expressed.The mechanism of BIT induced by ERK is unclear. It maybe has relationship with Bcl-2 and NO. Using special inhibitor and stimulator of MAPK can make help to understand the complex route system and develop a new route to treat cerebral ischemic disease.ConclusionsBIP maybe protect cerebral cortex and reduce infarct volume as well as Neurological function deficient through strengthening the activation of ERK1/2.
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