|کد مقاله||کد نشریه||سال انتشار||مقاله انگلیسی||ترجمه فارسی||نسخه تمام متن|
|5738214||1615048||2017||6 صفحه PDF||سفارش دهید||دانلود رایگان|
- Rosiglitazone enhances thrombin-induced phagocytosis by rat microglia.
- The PPARÎ³ antagonist inhibits the phagocytic activity of microglia.
- Rosiglitazone enhances the phagocytic function of microglia via the PPARÎ³ pathway.
ObjectiveTo 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.MethodsPrimary 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 (PPARÎ³) antagonist groups. Microglial phagocytosis was measured using a laser scanning confocal microscope. The expression of PPARÎ³ and cluster of differentiation 36 (CD36) in each group was detected via quantitative reverse transcription-PCR and western blot analysis.ResultsThe thrombin-treated plus rosiglitazone group showed a significant increase in phagocytic activity compared to the other groups (PÂ <Â 0.05), while the PPARÎ³ antagonist group significantly reduced microglial phagocytosis compared to the thrombin-treated plus rosiglitazone and the normal group. Moreover, the expression of PPARÎ³ and CD36 was considerably higher in the thrombin-treated plus rosiglitazone group than in the normal and the thrombin group. Nevertheless, the thrombin-rosiglitazone-PPARÎ³ group expressed a lower level of PPARÎ³ and CD36 compared to the thrombin-treated plus rosiglitazone group.ConclusionRosiglitazone can increase thrombin-induced microglial phagocytosis, by a mechanism possibly involved in the increase of PPARÎ³ and CD36 through the PPARÎ³ pathway, which may provide a new option for cerebral hemorrhage treatment.
Journal: Neuroscience Letters - Volume 651, 9 June 2017, Pages 159-164