Rosiglitazone pretreatment influences thrombin-induced anti-oxidative action via activating NQO1and γ-GCS in rat microglial cells.

Objective To explore the molecular mechanism involved in rosiglitazone against secondary brain damage caused by cerebral hemorrhage, we pretreated thrombin-induced microglial cells by rosiglitazone and then investigated its effect on antioxidant-related genes NQO1and γ-GCS expression change. Methods Primary microglial cells were obtained from the brain tissue of newborn Sprague-Dawley (SD) rats and were randomly divided into three groups: the normal (control), thrombin stimulation (TH), thrombin-treated plus rosiglitazone (TH+RGZ). The expression of NQO1and γ-GCS was measured by immunocytochemistry, real-time PCR, and western blot analysis. Results The immunocytochemistry showed that the number of NQO1and γ-GCS stained cells in TH and TH+RGZ group increased compared to the control group. In addition, the expression of NQO1 and γ-GCS in TH+RGZ group remarkably increased in mRNA and protein level compared to TH only group (p < 0.01). Conclusion Rosiglitazone can increase thrombin-induced microglia anti-oxidative ability by increasing NQO1and γ-GCS expression, which can effectively reduce secondary injury after cerebral hemorrhage.