The expression of TRPM2 cation channels on rat brain tissue that has ischemia reperfusion model done

Stroke is a heterogeneous group of diseases caused by decreased perfusion of the brain due to occlusion of the blood vessels supplying the brain or a haemorrhage originating in them. In ischemic stroke, apoptosis in the brain cells induced by the increased oxidative stress causes dysfunctions. The main objective of this study is to analyze the effects of ischemia reperfusion (I-R) on Transient Receptor Potential Melastatin 2 (TRPM2) channel expression activated by oxidative stress. 28 Wistar albino 8-10 weeks old male rats were used in the study. Experimental animals were divided into 5 groups with 6 animals each. Control group was not administered with anything during the tests. In Sham groups (sham2 – sham6), after bilateral carotid communis arteries were extracted, the dermis was sealed and the rats were decapitated on the 2nd and 6th hours of the experiment. In I-R groups, after the bilateral carotid communis arteries were extracted, they were clipped using aneurysm clips for 45 minutes and then unclipped and left for reperfusion for 2 hours in I-R2 group and for 6 hours in I-R6 group. At the end of the experiment, rats were decapitated under anesthesia and brain tissues were dissected. Brain tissues were stored in -80oC for MDA and TRPM2 mRNA levels until the end of the study. The tissues were buried in paraffin blocks with routine follow-up procedure for histologic study. TUNNEL method was applied to the sections removed from the blocks for determination of apoptotic cells and avidin-biotin-peroxidase method was applied for TRPM2 immunoreactivity. It was observed that MDA, Apoptosis and TRPM2 levels increased in I-R groups, with a significant increase in the I-R6 group, when compared to the control group. It was concluded that empirical ischemia reperfusion increased MDA, apoptosis and TRPM2 levels in brain tissues and TRPM2 could play a significant role in the pathophysiology of the effects of ischemia reperfusion on the brain tissue. Keywords: Ischemia reperfusion, rats, brain, TRPM2, Apoptosis