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.

Rosiglitazone Suppresses Calcium Oxalate Crystal Binding and Oxalate-Induced Oxidative Stress in Renal Epithelial Cells by Promoting PPAR-γ Activation and Subsequent Regulation of TGF-β1 and HGF Expression

“…PPAR- γ agonists include endogenous ligands such as 15d-PGJ2 and synthetic ligands, such as thiazolidinediones (TZDs) [21, 22]. However, the mechanism of the antilithogenic effects induced by PPAR- γ agonists remains unclear.…”

“…However, the mechanism of the antilithogenic effects induced by PPAR- γ agonists remains unclear. TZDs are highly potent PPAR- γ agonists and include rosiglitazone (RSG), pioglitazone (PGZ), and troglitazone (TGZ) [20–22]. RSG is a typical representative PPAR- γ agonist and has recently been reported to exert antioxidant effects via a PPAR- γ -dependent mechanism [12, 22].…”

“…TZDs are highly potent PPAR- γ agonists and include rosiglitazone (RSG), pioglitazone (PGZ), and troglitazone (TGZ) [20–22]. RSG is a typical representative PPAR- γ agonist and has recently been reported to exert antioxidant effects via a PPAR- γ -dependent mechanism [12, 22]. In this study, we used in vitro and in vivo experiments to investigate the alterations in PPAR- γ and its downstream effects in a hyperoxaluric environment and to determine whether RSG exerts renal protective effects by regulating TGF- β 1 and HGF through a PPAR- γ -dependent signaling pathway.…”

Study of Intracranial Hematoma Removal and High Intracranial Pressure Reduction Using a Novel Three-Needle Brain Puncture Technique

“…Primary brain damage, such as intracranial hypertension or cerebral herniation, can be caused by mechanical compression of hematoma, whereas secondary brain damage can be caused by toxic substances, inflammatory mediators, and free radicals released by hematoma. 6 , 7 In recent decades, minimally invasive procedures have been used to treat patients with medium- and large-volume intracranial hematoma. 5 Brain stereotactic minimally invasive surgery is one of the popular surgical options for minimally invasive intracerebral hematoma removal.…”

Microglia Phenotype and Intracerebral Hemorrhage: A Balance of Yin and Yang

“…TZDs, including pioglitazone and rosiglitazone, have a function in activating M2 microglia as PPAR-γ agonist (Song et al, 2018 ). In the rodent model, intraperitoneal injection of rosiglitazone increases the expression of CD36 on microglia, promotes hematoma clearance, and inhibits inflammatory factors expression (Chang C.-F. et al, 2017 ; Mu et al, 2017 ).…”