β趋化因子通过小胶质细胞活化引起小鼠感光细胞凋亡的实验研究
发布时间：2018-12-07 15:04
【摘要】：目的观察β趋化因子对小鼠小胶质细胞的活化及诱导感光细胞凋亡的作用。设计实验性研究。研究对象β趋化因子、小鼠BV-2小胶质细胞系及661w感光细胞系。方法将β趋化因子(RANTES、MIP-1α及MIP-1β)加入到BV-2细胞中,观察BV-2细胞活化反应。然后将被激活的BV-2细胞培养液上清加入661w细胞中,观察661w的凋亡情况。或将β趋化因子直接加入到661w细胞中,观察其凋亡情况。事先加入β趋化因子抑制剂met-RANTES后,重复上述操作。主要指标钙内流、ROS及NO的产生、TUNEL阳性感光细胞百分比。结果β趋化因子加入BV-2细胞后,细胞内钙流曲线明显上升、细胞外ROS及NO产生较对照组均明显增高(P0.01);将激活后的BV-2细胞上清加入到661w细胞中,后者凋亡率增加30%。β趋化因子直接加入661w细胞中,上述指标无明显变化。在加入β趋化因子之前先加入其抑制剂met-RANTES,BV-2细胞的ROS产生较未加抑制剂组明显降低(P0.01)、NO产生较未加抑制剂组降低(P=0.0187),661w细胞凋亡明显减少。结论β趋化因子可活化小鼠小胶质细胞导致感光细胞凋亡。β趋化因子抑制剂可抑制遗传性视网膜变性小鼠小胶质细胞活化,保护感光细胞。
[Abstract]:Objective to observe the effect of 尾 chemokine on the activation of mouse microglia and the induction of photoreceptor cell apoptosis. Design experimental studies. Object 尾 chemokine, mouse BV-2 microglia cell line and 661w photoreceptor cell line were studied. Methods 尾 chemokines (RANTES,MIP-1 伪 and MIP-1 尾) were added to BV-2 cells to observe the activation of BV-2 cells. Then the supernatant of activated BV-2 cells was added to 661w cells to observe the apoptosis at 661w. Or 尾 chemokine was added directly to 661w cells to observe its apoptosis. After adding 尾 chemokine inhibitor met-RANTES in advance, repeat the above operation. Main outcome measures calcium influx, production of ROS and NO, percentage of TUNEL positive photosensitive cells. Results after the addition of 尾 chemokine to BV-2 cells, the intracellular calcium flow curve increased significantly, and the production of extracellular ROS and NO increased significantly compared with the control group (P0.01). When the activated supernatant of BV-2 cells was added to 661w cells, the apoptotic rate of the latter increased by 30%, and 尾 chemokine was added directly into 661w cells. The ROS production of met-RANTES,BV-2 cells with 尾 chemokine was significantly lower than that of non-inhibitor group (P0.01), NO production was lower than that of non-inhibitor group (P0. 0187), and apoptosis was significantly decreased at 661w. Conclusion 尾 chemokine can activate mouse microglia and induce photoreceptor cell apoptosis. 尾 chemokine inhibitor can inhibit the activation of microglia and protect photoreceptor cells in mice with hereditary retinal degeneration.
【作者单位】： 首都医科大学附属北京同仁医院北京同仁眼科中心北京市眼科研究所;眼科学与视觉科学北京市重点实验室;中国科学院北京基因研究所;
【基金】：国家自然科学基金(81100675) 北京市自然科学基金(7102034)
【分类号】：R774.13
，
本文编号：2367374
[Abstract]:Objective to observe the effect of 尾 chemokine on the activation of mouse microglia and the induction of photoreceptor cell apoptosis. Design experimental studies. Object 尾 chemokine, mouse BV-2 microglia cell line and 661w photoreceptor cell line were studied. Methods 尾 chemokines (RANTES,MIP-1 伪 and MIP-1 尾) were added to BV-2 cells to observe the activation of BV-2 cells. Then the supernatant of activated BV-2 cells was added to 661w cells to observe the apoptosis at 661w. Or 尾 chemokine was added directly to 661w cells to observe its apoptosis. After adding 尾 chemokine inhibitor met-RANTES in advance, repeat the above operation. Main outcome measures calcium influx, production of ROS and NO, percentage of TUNEL positive photosensitive cells. Results after the addition of 尾 chemokine to BV-2 cells, the intracellular calcium flow curve increased significantly, and the production of extracellular ROS and NO increased significantly compared with the control group (P0.01). When the activated supernatant of BV-2 cells was added to 661w cells, the apoptotic rate of the latter increased by 30%, and 尾 chemokine was added directly into 661w cells. The ROS production of met-RANTES,BV-2 cells with 尾 chemokine was significantly lower than that of non-inhibitor group (P0.01), NO production was lower than that of non-inhibitor group (P0. 0187), and apoptosis was significantly decreased at 661w. Conclusion 尾 chemokine can activate mouse microglia and induce photoreceptor cell apoptosis. 尾 chemokine inhibitor can inhibit the activation of microglia and protect photoreceptor cells in mice with hereditary retinal degeneration.
【作者单位】： 首都医科大学附属北京同仁医院北京同仁眼科中心北京市眼科研究所;眼科学与视觉科学北京市重点实验室;中国科学院北京基因研究所;
【基金】：国家自然科学基金(81100675) 北京市自然科学基金(7102034)
【分类号】：R774.13
，
本文编号：2367374
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