谢欣梅, 庞晓斌, 赵艳, 王保全, 陈若芸, 杜冠华. 消栓通络有效成分组对氧糖剥夺损伤原代培养神经元的保护作用J. 药学学报, 2014,49(8): 1130-1135.
引用本文: 谢欣梅, 庞晓斌, 赵艳, 王保全, 陈若芸, 杜冠华. 消栓通络有效成分组对氧糖剥夺损伤原代培养神经元的保护作用J. 药学学报, 2014,49(8): 1130-1135.
XIE Xin-mei, PANG Xiao-bin, ZHAO Yan, WANG Bao-quan, CHEN Ruo-yun, DU Guan-hua. Neuroprotective effects of the effective components group of Xiaoshuantongluo against oxygen-glucose deprivation in primary cultured rat cortical neuronsJ. Acta Pharmaceutica Sinica, 2014,49(8): 1130-1135.
Citation: XIE Xin-mei, PANG Xiao-bin, ZHAO Yan, WANG Bao-quan, CHEN Ruo-yun, DU Guan-hua. Neuroprotective effects of the effective components group of Xiaoshuantongluo against oxygen-glucose deprivation in primary cultured rat cortical neuronsJ. Acta Pharmaceutica Sinica, 2014,49(8): 1130-1135.

消栓通络有效成分组对氧糖剥夺损伤原代培养神经元的保护作用

Neuroprotective effects of the effective components group of Xiaoshuantongluo against oxygen-glucose deprivation in primary cultured rat cortical neurons

  • 摘要: 研究消栓通络有效成分组(XECG) 对原代培养皮质神经元氧糖剥夺(OGD) 损伤的保护作用,并探讨其可能的作用机制。采用3日龄SD大鼠皮质制备原代培养神经元;将细胞随机分为正常对照组、OGD模型组和XECG组(1、3及10 mg·L-1);四甲基偶氮唑盐(MTT) 法测定细胞存活率;酶标法试剂盒测定乳酸脱氢酶(LDH) 漏出量;Hoechst染色检测细胞凋亡;RT-PCR检测JAK2、STAT3 mRNA表达变化;Western blotting检测Bcl-2、Bax、p-JAK2、p-STAT3蛋白表达变化。结果显示,XECG能明显改善OGD对神经元的损伤,提高细胞存活率,减少LDH的释放量,抑制缺氧缺糖引起的细胞凋亡;能提高缺糖缺氧神经元Bcl-2/Bax比值,增加JAK2、STAT3基因和蛋白的表达。以上结果表明,XECG对OGD损伤的原代培养神经元具有明显保护作用,其机制可能与激活JAK2/STAT3通路、影响凋亡相关基因Bcl-2及Bax的表达有关。

     

    Abstract: This study is to investigate the effect of the effective components group of Xiaoshuantongluo (XECG) on neuronal injury induced by oxygen-glucose deprivation (OGD) in primary cortical cultures isolated from SD rat cortex at day 3 and the possible mechanism. Cells were divided into control group, OGD model group and XECG group (1, 3 and 10 mg·L-1). The cell viability was assessed with MTT assay and the LDH release rate was measured by enzyme label kit. The cell apoptosis was analyzed using Hoechst staining. RT-PCR was applied to detect the mRNA levels of JAK2 and STAT3. Western blotting was used to detect the expressions of Bcl-2, Bax, p-JAK2 and p-STAT3 proteins. Results showed that XECG resulted in an obvious resistance to oxygen-glucose deprivation-induced cell apoptosis and decrement of cell viability, decrease the cell LDH release rate. XECG could adjust the expression of Bcl-2 and Bax proteins and increase Bcl-2/Bax ratio, up-regulate the expression of p-JAK2 and p-STAT3. In conclusion, XECG could protect against the neuronal injury cells exposed to OGD, which may be relevant to the promotion of JAK2/STAT3 signaling pathway, and impact the expression of Bax and Bcl-2.

     

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