【摘要】 目的:探讨可卡因-苯丙胺调节转录(CART)肽抑制星形胶质细胞氧糖剥夺(OGD)性损伤及调节水通道蛋白4(AQP-4)表达的分子机制。方法:体外培养新生ICR小鼠大脑皮层星形胶质细胞,通过胶质纤维酸性蛋白(GFAP)免疫荧光染色鉴定细胞。所得细胞随机分为4组:对照组、模型组、CART组和CART+PD98059 (ERK信号通路特异性阻断剂)组,MTT法检测星形胶质细胞活力,Western blot检测ERK及AQP-4的表达。结果:OGD处理后,CART肽能显著提高OGD后星形胶质细胞的活力(P<0.01);CART肽能够提升星形胶质细胞内ERK的磷酸化水平(P<0.05);PD98059能够阻断CART肽诱导的ERK磷酸化(P<0.01),并减弱CART肽抑制AQP-4表达的作用(P<0.05)。结论:CART肽提高OGD处理后星形胶质细胞的活力,并通过激活ERK通路抑制OGD处理后细胞AQP-4的表达。更多还原

【Abstract】 AIM: To study the protective effect of cocaine-and amphetamine-regulated transcript(CART) peptide on astrocytes of mice with oxygen-glucose deprivation(OGD) injury and the related mechanism involving regulation of aquaporin 4(AQP-4) expression. METHODS: Mouse cortical astrocytes from neonatal ICR mice were cultured, and were identified with immunofluorescence staining of glial fibrilillary acidic protein(GFAP). The astrocytes were divided into 4 groups: control group, model group, CART group and CART+PD98059 group. The viability of the cells were measured by MTT assay. The protein levels of ERK and AQP-4 were analyzed by Western blot. RESULTS: CART peptide induced a significant increase in the cell viability after OGD(P<0.01). CART peptide enhanced the phosphorylation level of ERK after OGD, which was inhibited by PD98059 pretreatment(P<0.05). PD98059 also inhibited down-regulation of AQP-4 expression induced by CART peptide after OGD(P<0.05).CONCLUSION: CART peptide enhances the viability, and inhibits AQP-4 expression in the astrocytes of mice after OGD through activating ERK signaling pathway.更多还原