Signaling pathway MEK1/2–ERK1/2 is involved in the cardioprotective effect of probiotic strains in the systemic inflammatory response in rats

Aim. To experimentally test the hypothesis of the participation of MEK1/2 and ERK1/2 kinases in the mechanism of the probiotic cardioprotection in the implementation of the signaling stage of the cardioprotective response to the administration of probiotic strains in the systemic inflammatory response in rats.
Materials and methods. The experiments were performed on male Wistar rats using a model of systemic inflammatory response syndrome, which includes obesity and chemically induced colitis. To provide probiotic cardioprotective effects, the animals were administered probiotic strains LA-5 and BB-12 orally. An inhibitor of MEK1/2 kinase and its associated ERK1/2 kinase PD98059 at a dose of 0.3 mg/kg were administered intravenously 20 minutes before the start of Langendorff perfusion of an isolated heart., The size of the necrosis zone (SNZ) was histochemically determined after 30 minutes of global ischemia and 90 minutes of reperfusion were simulated. Markers of the systemic inflammatory response (SIR) were detected in the blood.
Results. In the group of rats on the model of SIR in comparison with the control, a significant increase in the number of leukocytes and an increase in the level of proinflammatory cytokines in the blood, as well as a significant increase in SNZ (by 39% in relation to CTR, p < 0.05). In the group with probiotic correction, a significantly lower SNZ was noted in relation to SIR, whereas in rats with the introduction of probiotics and the substance PD98059, SNZ was significantly higher, i.e. the cancellation of the cardioprotective effect of probiotic therapy occurred.
Conclusion. Based on the conclusion that the cardioprotective effect has been abolished by PD98059 administration, it can be assumed that the probiotic effect is provided by the MEK1/2 and ERK1/2 kinase pathways.

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