Dimethyl fumarate (DMF) and Heparin Sulfate Mitigate Cerebral Ischemia-Reperfusion Injury in Male Rats

Ischemic cerebrovascular illness leads in oxygen deprivation to brain tissue, which can generate reactive oxygen species (ROS) and immune cell mediators are released after reperfusion, which can happen naturally through thrombus breakdown or through therapeutic recanalization. After a week of acclimatization, the rats were split into five groups as follows: Sham group: The animals got general anesthesia without having their unilateral carotid artery occluded. The animals in the ischemic-reperfused control group got general anesthesia, a 5-minute occlusion of the carotid artery, and an hour-long reperfusion without the administration of medication. Vehicle group: The animals underwent the same surgery as the control group, but they also received intraperitoneal (i.p.) dose of DSMO 5 min. following the ischemia. Group treated with heparin sulfate: 5 min. after the ischemia, the animals underwent the same surgical approach as the control group, but they additionally received 400IU/kg (i.p.). Group treated with dimethyl fumarate: 5 min. after the ischemia, the animals received the same surgical approach as the control group, plus they were given 50 mg/kg of dimethyl fumarate intraperitoneally (i.p.). ROS levels and brain tissue damage were significantly decreased (P <0.05) in the treated groups. Histologically, the treated animals had less brain tissue damage than the control and vehicle groups (P < 0.05). Compared to the heparin sulfate group, the DMF group displayed a higher reduction in ROD and brain damage. Conclusion, DMF has a neuroproctive impact on cerebral I/R injury by downregulating oxidative stress and lowering the percentage of infarction area, while heparin also has this effect.