Rosiglitazone pretreatment influences thrombin-induced phagocytosis by rat microglia via activating PPAR and CD36
Rosiglitazone pretreatment influences thrombin-induced phagocytosis by rat microglia via activating PPAR and CD36
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罗格列酮预处理通过激活 PPAR 和 CD36 影响凝血酶诱导的大鼠小胶质细胞吞噬作用
DOI：
10.1016/j.neulet.2017.04.038
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发表时间：
2017
期刊：
影响因子：
--
通讯作者：
Guofeng Wu
中科院分区：
文献类型：
--
作者：
Qiong Mu;Likun Wang;Hang Hang;Chunfeng Liu;Guofeng Wu
目的：探讨罗格列酮对脑出血后继发性脑损伤的保护作用，探讨罗格列酮预处理对凝血酶诱导的小胶质细胞吞噬作用的影响，并阐述该过程的分子机制。方法：从新生Sprague-Dawley大鼠脑组织中获取原代小胶质细胞，随机分为4组：正常组、凝血酶刺激组、凝血酶处理组。加罗格列酮和凝血酶罗格列酮加增殖物激活受体-γ(PPAR)拮抗剂组。使用激光扫描共聚焦显微镜测量小胶质细胞吞噬作用。通过定量逆转录PCR和Western blot分析检测各组PPAR和分化簇36（CD36）的表达。结果：与其他组相比，凝血酶加罗格列酮组的吞噬活性显着增加（P < 0.05），而PPAR拮抗剂组与凝血酶加罗格列酮组相比，小胶质细胞的吞噬活性显着降低。和正常组。此外，凝血酶加罗格列酮治疗组中PPAR和CD36的表达显着高于正常组和凝血酶组。然而，与凝血酶加罗格列酮组相比，凝血酶罗格列酮-PPAR组的PPAR和CD36表达水平较低。结论：罗格列酮可以增加凝血酶诱导的小胶质细胞的吞噬作用，其机制可能涉及通过PPAR途径增加PPAR和CD36，这可能为脑出血的治疗提供新的选择。
Objective: To explore the protective role of rosiglitazone against secondary brain injury after cerebral.hemorrhage, we investigated the effect of rosiglitazone pretreatment on thrombin-induced microglial.phagocytosis and described the molecular mechanisms involved in this process..Methods: Primary microglial cells were obtained from the brain tissue of newborn Sprague–Dawley rats.and were randomly divided into four groups: the normal, thrombin stimulation, thrombin-treated plus.rosiglitazone, and thrombin-rosiglitazone plus proliferator-activated receptor-gamma (PPAR) antagonist.groups. Microglial phagocytosis was measured using a laser scanning confocal microscope. The.expression of PPAR and cluster of differentiation 36 (CD36) in each group was detected via quantitative.reverse transcription-PCR and western blot analysis..Results: The thrombin-treated plus rosiglitazone group showed a significant increase in phagocytic.activity compared to the other groups (P < 0.05), while the PPAR antagonist group significantly.reduced microglial phagocytosis compared to the thrombin-treated plus rosiglitazone and the normal.group. Moreover, the expression of PPAR and CD36 was considerably higher in the thrombin-treated.plus rosiglitazone group than in the normal and the thrombin group. Nevertheless, the thrombinrosiglitazone-.PPAR group expressed a lower level of PPAR and CD36 compared to the thrombin-treated.plus rosiglitazone group..Conclusion: Rosiglitazone can increase thrombin-induced microglial phagocytosis, by a mechanism possibly.involved in the increase of PPAR and CD36 through the PPAR pathway, which may provide a new.option for cerebral hemorrhage treatment.