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Rosiglitazone Enhances the Phagocytic Ability of Thrombin-Activated Microglia through P38mapk Signaling

Author(s): Qiong Mu, Likun Wang, Siying Ren, Hang Hang, Guofeng Wu1, Jinbiao Luo


Hematoma formed after intracerebral hemorrhage (ICH) could results in secondary brain damage. In vitro thrombin treatment allows investigation of the pathology and mechanisms behind brain injury, and provides extracellular environment that simulates the conditions that result from ICH. Rosiglitazone treatment protects against brain damage through promoting the phagocytosis of red blood cells by microglia. The present study aimed to explore the underlying molecular mechanisms using the thrombin-induced model of ICH.


A total of 54 neonatal rats was used in the present study. Primary microglia were obtained from the brain tissues of neonatal SD rats, and then divided into 4 groups: normal control group (NC group), thrombin treatment group(TH group), RSG pretreatment + thrombin treatment group(RSG group), and RSG pretreatment + thrombin treatment together with p38MAPK signaling inhibitor group (SB group). Then, laser scanning confocal microscopywas used to evaluate microglial phagocytosis by observing phagocytizedred fluorescent microspheres. The mRNA and protein expression levels of CD36 were measured by RT-PCR and western blot.


Microglial phagocytosis was increased in the RSG group compared with the other groups, and phagocytosis in the SB group was decreased compared to the RSG group. The RSG group displayed increased expression of CD36 compared to the other groups, both at protein and mRNA levels (P<0.01). The SB group expressed decreased levels of CD36 compared to the RSG group (P<0.01).


Rosiglitazone enhanced thrombin-induced phagocytosis in microglia;and the mechanism might involve increased expression of CD36 on the microglial surface through p38MAPK signaling. Keywords CD36, Intracerebral hemorrhage, Microglial cells, p38MAPK, Rosiglitazone, Thrombin

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