Liu Ling, Wang Shu-Ying, Wang Jian-Gang
Zhongguo Zhong Yao Za Zhi. 2014 Oct;39(20):4045-9.
To study the role of PI3K/Akt pathway in the neuroprotective effect of paeoniflorin on PC12 cells.
The paeoniflorin group (5, 10, 20 μmol · L(-1)) was pretreated for 30 min, and then added with Aβ25-35 (20 μmol · L(-1)) for interaction for 24 h. Inhibitor LY294002 (10 μmol · L(-1)) was pretreated for 30 min before the action of paeoniflorin (10 μmol · L(-1)). The MTT colorimetric method was used to detect the cell viability. The apoptosis rate was tested by the FITC-Annexin V/PI staining. The protein expression of p-AKT, Bax, Bcl-2 and cleaved caspase-3 protein were detected by Western blot analysis.
Paeoniflorin could significantly inhibit the Aβ25-35-induced PC12 cell toxicity and apoptosis. Its protection effect may be achieved by up- regulating AKT phosphorylation level, increasing Bcl-2 protein expression, reducing Bax protein expression, inhibiting the activation of caspase-3. Inhibitor LY294002 could weaken the above protective effects of paeoniflorin.
Paeoniflorin could activate PI3K/Akt signaling pathway to protect the PC12 cell injury induced by Aβ25-35.
研究PI3K/Akt信号通路在芍药苷对PC12细胞神经保护作用中的作用。
芍药苷组（5、10、20 μmol·L⁻¹）预处理30分钟，然后加入Aβ25 - 35（20 μmol·L⁻¹）作用24小时。在芍药苷（10 μmol·L⁻¹）作用前，抑制剂LY294002（10 μmol·L⁻¹）预处理30分钟。采用MTT比色法检测细胞活力。通过FITC-Annexin V/PI染色检测凋亡率。采用蛋白质免疫印迹法检测p-AKT、Bax、Bcl-2和裂解的caspase-3蛋白的表达。
芍药苷能显著抑制Aβ25 - 35诱导的PC12细胞毒性和凋亡。其保护作用可能通过上调AKT磷酸化水平、增加Bcl-2蛋白表达、降低Bax蛋白表达、抑制caspase-3的激活来实现。抑制剂LY294002可削弱芍药苷的上述保护作用。
芍药苷可激活PI3K/Akt信号通路，保护Aβ25 - 35诱导的PC12细胞损伤。
