Özet:

Purpose: As the TRP melastatin 2 (TRPM2) channel can be activated by oxidative stress, it has recently been defined as a potential therapeutic target in the fight against oxidative stress-related diseases such as diabetes, inflammation, myocardial infarction. The main objective of this study is to explore the expression and histopathological effects of the TRPM2 kation channel in a rats' cerebral ischemic-reperfusion model. In the study, a total of 30 adult male Wistar-Albino rats were used. The animals were divided into 5 groups. In the Sham groups, in the 2nd and 6th hours of the experiment, the bilateral main carotid arteries were removed and the rats were decaptivated. In the I/R/reperfusion (I/R) groups (I/R-2 and I/R-6) bilateral main carothyde arteries were removed after 45 minutes clamped with aneurysm clips and 2 and 6 hours of reperfusion were provided, respectively. At the end of the test, the tissues were fixed in the formalin solution, the measurement of the MDA and TRPM2 mRNA levels and then the routine histological follow-up series were applied and paraffin was buried in blocks. The TUNEL method was used for the detection of apoptotic cells and the avidin-biotin-peroxidase complex was used for the assessment of the immune reactivity of TRPM2. Results: MDA, apoptosis and TRPM2 levels were significantly increased in I/R groups, compared to I/R-6 groups. The experimental I/R also increased the levels of MDA, apoptosis and TRPM2 in the brain tissue. The result: TRPM2 may play an important role in the pathophysology of brain I/R damage.

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