Abstract
Introduction: This study was designed to evaluate the effect activity of RAIL-gel in comparison with Citicoline on nitroxydergic system during acute cerebrovascular accident. Methods: In this study, 80 white nonlinear rats were randomly assigned to 4 groups (20 rats in each): 1) intact; 2) control - untreated with acute cerebrovascular accident (ACVA), examined on the 4th day; 3) animals with ACVA, receiving RAIL, examined on the 18th day; 4) animals with ACVA, treated with Citicoline, examined on the 4th day. The expression of inducible NOS was determined by Western blotting. The nitrosative stress marker, nitrotyrosine, was determined using the ELISE kit NITROTYROSINE (kit no. HK501-02, series 12825k1212-k). To assess the state of iNOS mRNA expression, we used the method of polymerase chain reaction with reverse transcription in real time (RT-PCR). Results: Our research demonstrated that course administration of the RAIL and Citicoline to animals with ACVA for 4 days leads to the stabilization of the parameters of the brain nitroxydergic system. However, Citicoline does not provide a full effect on the shifts of the NO system in the brain. It does not have the proper effect on such an important link in the pathogenesis of ischemic brain damage as nitrosative stress. RAIL leads to a significant decrease in NOS activity due to its inducible form (decrease in the expression of iNOS and iNOS mRNA) and a decrease in NO metabolits, and inhibition of nitrosative stress (decrease in nitrotyrosine). Conclusion: IL-1b antagonist RAIL (Intranal Gel) significantly exceeds Citicoline in terms of the severity of the effect on the nitroxydergic system indicators.
Highlights
This study was designed to evaluate the effect activity of RAIL-gel in comparison with Citicoline on nitroxydergic system during acute cerebrovascular accident
As a result of the conducted studies, it was found that modeling of acute cerebrovascular accident (ACVA) leads on the 4th day of the experiment to disruption of the nitroxydergic system and initiation of nitrosative stress in the brain of experimental animals, as evidenced by a significant increase in the cytosolic and mitochondrial fractions of the brain homogenate of animals in the NOS activity by 439.5% and 189.2%, nitrites by 157.7% and 96.1%, as well as nitrotyrosine by 162% and 66.1%, respectively (Tables 1 and 2)
We found that Citicoline inhibits the reactions of initiation of neuroapoptosis (He et al 2017)
Summary
This study was designed to evaluate the effect activity of RAIL-gel in comparison with Citicoline on nitroxydergic system during acute cerebrovascular accident. RAIL leads to a significant decrease in NOS activity due to its inducible form (decrease in the expression of iNOS and iNOS mRNA) and a decrease in NO metabolits, and inhibition of nitrosative stress (decrease in nitrotyrosine). ACVA launches a complex staged cascade of molecular biochemical reactions of neuronal damage, including energy deficit, lactate acidosis, transmitter autocoidosis, oxidative stress and neuroinflammation. In this case, a closed “vicious” circle is formed- inflammation leads to the activation of sensitive to redox potential signal transduction pathways (MAPK, NFkB), which increases oxidative stress.
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