中文摘要：

研究人参皂苷Rg1对皮质酮介导的星形胶质细胞损伤的保护作用,并对其作用机制进行初步探索。分离培养原代海马和前额叶皮质区星形胶质细胞,给予皮质酮（corticosterone,CORT）模拟应激条件,采用Western blot方法检测Rg1对Cx43磷酸化水平的影响;利用Cell Counting Kit（CCK8）方法检测Rg1对细胞生存率的影响考察及蛋白酶抑制剂是否影响Rg1对细胞生存率的保护作用。结果显示,人参皂苷Rg1显著降低CORT介导的Cx43磷酸化水平升高。与CORT（200μmol·L-1）组相比,人参皂苷Rg1（10μmol·L-1）可显著增加海马和前额叶皮质星形胶质细胞的生存率;人参皂苷Rg1的保护作用在海马星形胶质细胞可被蛋白激酶Src抑制剂PP2、p38抑制剂SB203580及Akt的抑制剂BAY1125976抑制,而在前额叶皮质星形胶质细胞仅可被Src抑制剂PP2和Akt的抑制剂BAY1125976抑制。结果表明,人参皂苷Rg1可显著减轻CORT所致的星形胶质细胞缝隙连接通道蛋白Cx43活性的降低,并通过激活Src、p38与Akt信号通路发挥抗皮质酮损伤的作用,这种作用在海马和前额叶皮质存在脑区差异性。

英文摘要：

The study was designed to explore the effects and the underlying mechanism of ginsenoside Rg1 on corticosterone（CORT）-induced astrocytes injury. The primary hippocampal and prefrontal cortical astrocytes from rats were cultured and purified. CORT was used to stimulate stress condition. Western blot was used to detect the effects of ginsenoside Rg1 on the phosphorylation of Cx43. Cell Counting Kit（CCK8） was used to detect the effects of ginsenoside Rg1 on astrocytes viability. The roles of ginsenoside Rg1 was reversed by protein kinase inhibitors in the change of astrocytes morphology. Our results showed that ginsenoside Rg1 reversed the phosphorylation of Cx43 induced by CORT; ginsenoside Rg1 significantly upregulated the cell viability of astrocytes against CORT; the role of ginsenoside Rg1 was obviously inhibited by Src protein kinase inhibitors PP2 and Akt protein kinase inhibitors BAY1125976 in prefrontal cortical astrocytes; in hippocampal astrocytes, Src protein kinase inhibitor PP2, p38 protein kinase inhibitor SB203580, Akt protein kinase inhibitor BAY1125976 significantly inhibited the cell protective effects of ginsenoside Rg1. In conclusion, ginsenoside Rg1 improved the activity of Cx43 gap junctions in astrocytes exposed to CORT; ginsenoside Rg1 protected astrocytes against that CORT activated the Src, p38 and Akt signaling pathways, and the mechanism was different in prefrontal cortical and hippocampal astrocytes.