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

Abstract

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.

Keywords:

• Microglial cell
• rosiglitazone
• thrombin
• NQO1
• γ-GCS

Acknowledgments

We are grateful for the Western blot technical help provided by The Guizhou Key Laboratory of Molecular Biology. We would like to thank the Department of Radiology of Guizhou Medical University for valuable discussion on the ICH model. We also would like to thank all the postgraduates involved for their hard work during the study. Anjun Song is a researcher in the Affiliated Hospital of Guizhou Medical University, and focuses on cerebral hemorrhage and epilepsy direction.