Changes in the expression of oxidative stress genes in toxic hepatitis of different etiologies and their correction

The study aims to study of changes in transcriptional activity of oxidative stress genes in acute toxic hepatitis. Materials and methods. The study material was white mongrel male rats weighing 180-200 grams. The studied toxicants were: carbon tetrachloride, ethanol, acetaminophen. As hepatoprotectors were introduced: oxymethyluracil, ademethionine and ethylmethylhydroxypyridine succinate. RNA was isolated, which was subjected to reverse transcription. RT-PCR was performed using a real-time PCR system in the presence of SYBR Green. GAPDH was used as a normalized control. The expression of the studied genes was evaluated by PCR analysis using pre-selected primers. Statistical significance was checked using IBM SPSS Statistics software. Results. In comparison of experimental groups, statistically significant differences were found in the level of expression of the CASP7 gene. Transcriptional activity of the CHEK gene (k=11.25; p=0.024). The GCLC gene (k=21.70; p=0.001) reached its minimum value of -3.6 [-3.72; -3.32] in the Mexidol group. The multiplicity of expression of the GSTM1 gene (k=15.54; p=0.004) had the highest value -0.14 [-1.11; 1] in the group that did not receive TCM. The NQO1 gene achieved its statistical significance in a 72-hour experiment (p=0.005). Statistical analysis of the RIPK gene showed significant differences. The expression level of the GSTP1 gene (k=10.39; p=0.034) reached its maximum value in the untreated group of 0.03 [-0.74; 0.48]. Expression of the NFE2L2 gene with acetaminophen administration showed the following results (k=13.64; p=0.009). Glutathione activity (k=10.29; p=0.036) reached its minimum value in the group receiving Mexidol -1.6 [-1.7; -1.29]. The multiplicity of superoxide dismutase expression showed statistical significance (p=0.003). Conclusions. Markers of the clinical course, prognosis and outcomes of toxic hepatitis were found. These data make it possible to determine the severity of the disease at the stage of early molecular response, when active clinical symptoms have not yet developed, which makes it possible to prescribe targeted therapy and adjust treatment tactics.

gene expression, toxic hepatitis, oxidative stress, correction

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