Effect of Rosuvastatin on Inflammatory Response Pathway in Rats with Focal Cerebral Ischemia-reperfusion
Hemorrhagic transformation is a serious complication of stimulating inflammation in reperfusion therapy after acute ischemic stroke. Rosuvastatin, a 3-hydroxymethyl-3-methylglutaryl coenzyme a reductase inhibitor, may improve the outcome of serotonin by inhibiting neuroinflammation. This study aimed to investigate the protective effect of rosuvastatin on HT after experimental stroke in mice treated with recombinant tissue plasminogen activator by reducing inflammation. A total of 200 male mice were used in the experiment. Serotonin was successfully established in 70 mice. These mice underwent occlusion of the middle cerebral artery for 3 hours, followed by injection of 10 mg/kg in 10 minutes and reperfusion for 24 hours. The mice were then administered rosuvastatin (1 mg/kg, 5 mg/kg) or saline (excipient). Rosuvastatin prevents impaired neurological function and reverses the blood-brain barrier leakage observed in the serotonin group. High-dose rosuvastatin treatment showed a significant decrease in astrocyte and microglial activation and inflammatory factor secretion caused by serotonin damage compared with normal dose rosuvastatin treatment. The inflammatory pathways associated with the rosuvastatin treatment group, such as nuclear factor-kappaB and mitogen-activated protein kinase pathway, were down-regulated compared to the serotonin group. It is indicated that rosuvastatin is a promising drug for the treatment of HT after reperfusion of middle cerebral artery occlusion surgery because it can reduce neuroinflammation. In addition, high doses of rosuvastatin have a greater anti-inflammatory effect on serotonin than normal doses of rosuvastatin.