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Beijing, China

Wu Q.-Y.,Basic MedicalInstitute | Zhang J.-Y.,Basic MedicalInstitute | Deng Z.-H.,Basic MedicalInstitute | Yan G.-T.,Basic MedicalInstitute
Journal of Sichuan University (Medical Science Edition) | Year: 2012

Objective To explore the effect of leptin on expression of C×43 after rat cerebral ischemia/ reperfusion injury and its related mechanism. Methods Forty-five male kunming mice were randomly divided into 3 groups: sham group, model group and leptin group. Mouse models of transient focal cerebral ischemia were established by occlusion of the right middle cerebral artery for 2 h followed by 24 h reperfusion in model and leptin group. Mice of leptin group were intraperitoneally injected with 1 mg/kg leptin at 0 minute after ischemia. The infarct volume and neurological deficit scores following leptin treatment were determined using TTC staining and the Longa's score, respectively, to evaluate the protective effect of leptin against ischemic cerebral injury. The histopathological changes in the brain were observed with HE staining. The astrocytes of SD rat cerebral cotex were cultured primaryly and purified, and then divided them into four groups: control, model, leptin 100 μg/L, and leptin 500 μg/L. The cerebral astrocytes with hypoxia/reoxygenation injury were induced. The cellular viability of injury was detected by MTT assay. The effect of leptin on C×43 expression was detected by Western blot in brain tissues and astrocytes. Results Compared with the model group, the neurological deficits and cerebral infarct volume of leptin group were reduced (P<0. 05) , the histopathological injury in the brain tissues was alleviated and the expression of C×43 was decreased markedly ( P < 0. 01). The survival rate of astrocytes was increased significantly in leptin 500μg/L group (P<0. 01), whereas the C×43 expression of astrocytes decreased (P<0. 01). But the difference of leptin 100 μg/L was not significant (P>0. 05). Conclusion Leptin can ameliorate cerebral pathological changes in the event of IR injury by suppressing the expression of C×43 both in vivo and vitro experiments. Source

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