Effect Of Astrocytic Gap Junction On The Expression Of Caspase-3 In Rats After Cerebral Ischemia-reperfusion

Background and Purpose: Stroke lesion increasesprogressively after ischemia. Neurons in the core lesion dieimmediately after ischemia; however, some neurons in the penumbraare still viable for several hours. The cells in the penumbra maysuccumb to apoptosis, which may cause the expansion of the strokelesion. To rescue the penumbra is critical in considering strategies forischemic stroke treatment. Under the ischemic condition, the role ofastrocytes is still controversial. Astrocytes may play a vital role inneuroprotection by providing energy substrates to neurons andregulating the concentration of K+ and neurotransmitters through gapjunctions. Connexin 43 (Cx43) is one of the major gap junctionproteins in astrocytes. We have shown that, gap junction blockadeeffectively reduce infarct volume by in a rodent model of stroke. Weexplored the underlying mechanism by which gap junctionalintercellular communication influences apoptosis and neuroprotectionin ischemia.Method: The MCAO/R model was induced using intraluminalsuture technique first described by Longa with a little modification.Praxiology changes and neurologic impairment were assessed byLonga's five-grade scoring standard. The model was evaluated by thescore and histopathology changes. To identify the influence of thefunction of astrocytic gap junction on focal ischemia stroke, octanol,the specific blocker for gap junctions was used in an interventionstudy. 36 animals were divided randomly into 6 groups.Sham-operated group, control group, octanol-treatment group andDMSO vehicle control group. Control group were divided furtherinto two subgroups, the ischemia 6h/reperfusion6h one andischemia6h./reperfusion12h. one. The animals of sham-operatedgroup and control group were injected normal saline intraperitoneally30min before operation .The animals of octanol-treatment group wereinjected octanol solution and animals of DMSO group, DMSO vehicleonly. After the animals were decapitated, the brains were removedcarefully and cut into 2mm slice. The infarction volumes wereevaluated after TTC staning. Expression of Cx43 and Caspase-3 wasassessed by Immunohistochemistry. Result: After operation, animals of all groups except the sham-operated one displayed obvious manifestation of neurologicimpairment. The modified method was easy to grasp and the ratio ofsuccess was high. The model was superior for its stability. It wasconcluded that there was high similarity between the animalmodel and the focal ischemic stroke in human being. Thus, the animalmodel could be used to study the mechanisms of focal cerebralischemia/reperfusion injury. After MCAO, the octanol group showed...