Rosiglitazone Promotes Microglial Distribution via Activation of PPARγ and CD36 in the ICH Rat Model

Intracerebral hemorrhage (ICH) is a serious public health problem with high mortality and morbidity. The current study aims to investigate the effects of rosiglitazone on the microglial distribution and the expression of PPARγ and CD36 in the ICH rat model.

Sprague-Dawley male rats (n=116) were randomly divided into four groups: control, ICH, rosiglitazone, and PPARγ antagonist (GW9662). Hematoxylin-eosin staining was used to observe the brain edema in the ICH rat model. The effect of rosiglitazone on the expression of OX-42, a microglial marker, was evaluated by immunohistochemistry. Immunohistochemistry, quantitative real-time PCR, and western blot were utilized to assess the role of rosiglitazone in the expression of PPARγ and CD36.

ICH rats exhibited a remarkable brain edema at 72 h. OX-42 expression was significantly increased in brain tissues of ICH rats. Rosiglitazone remarkably promoted the OX-42 expression in ICH rats, whereas GW9662 suppressed OX-42 expression. In addition, immunohistochemistry analysis showed that rosiglitazone markedly enhanced the expression of PPARγ and CD36 in brain tissues around the hematoma in ICH rats, while GW9662 inhibited their expression in ICH rats. Moreover, rosiglitazone significantly promoted the mRNA and protein expression of PPARγ and CD36 in the brain tissues of ICH rats, while GW9662 showed the opposite trend.

Rosiglitazone may improve microglial distribution via promoting the expression of PPARγ and CD36 around the hematoma in the ICH rat model, which may provide effective therapeutic targets for the treatment of ICH.