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<p>The hypothesis that protein kinase C (PKC) participates in the signaling stage of the cardioprotective response to the administration of probiotics was tested in experiments on male Wistar rats using a model of systemic inflammatory response syndrome (SIRS), which includes obesity and chemically induced colitis. To provide probiotic cardioprotective effects, <i>Lactobacillus acidophilus</i> (LA-5) and <i>Bifidobacterium animalis</i> subsp. <i>lactis</i> (BB-12) were administered orally. PKC inhibitor chelerythrine at a dose of 0.5 mg/kg was administered intraperitoneally 20 min before the start of isolated Langendorff heart perfusion. Global ischemia (30 min) and reperfusion (90 min) were simulated, after which the size of the necrosis zone was histochemically determined. In the SIRS group, we observed a significant increase in leukocyte count and the size of the necrosis zone (by 39%; <i>p</i> &lt; 0.05) in comparison with the control. In groups with probiotic correction and PKC + probiotic, the size of the necrosis zone was significantly lower than in the SIRS group. Administration of chelerythrine did not abolish the cardioprotective effect of probiotics. In the SIRS model, probiotic-induced cardioprotection is mediated by mechanisms that prevent ischemic/reperfusion damage that differ from the PKC pathway.</p>

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Protein Kinase C Blockers Do Not Reverse the Cardioprotective Effect of Probiotic Strains in Rats with a Systemic Inflammatory Response

  • 期刊论文

  • 发表日期：

    2026年7月30日

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  • Yu. Yu. Borshchev,
  • S. M. Minasyan,
  • I. Yu. Burovenko,
  • A. D. Gordeev,
  • V. Yu. Borshchev,
  • O. V. Borshcheva,
  • M. M. Galagudza

摘要

The hypothesis that protein kinase C (PKC) participates in the signaling stage of the cardioprotective response to the administration of probiotics was tested in experiments on male Wistar rats using a model of systemic inflammatory response syndrome (SIRS), which includes obesity and chemically induced colitis. To provide probiotic cardioprotective effects, Lactobacillus acidophilus (LA-5) and Bifidobacterium animalis subsp. lactis (BB-12) were administered orally. PKC inhibitor chelerythrine at a dose of 0.5 mg/kg was administered intraperitoneally 20 min before the start of isolated Langendorff heart perfusion. Global ischemia (30 min) and reperfusion (90 min) were simulated, after which the size of the necrosis zone was histochemically determined. In the SIRS group, we observed a significant increase in leukocyte count and the size of the necrosis zone (by 39%; p < 0.05) in comparison with the control. In groups with probiotic correction and PKC + probiotic, the size of the necrosis zone was significantly lower than in the SIRS group. Administration of chelerythrine did not abolish the cardioprotective effect of probiotics. In the SIRS model, probiotic-induced cardioprotection is mediated by mechanisms that prevent ischemic/reperfusion damage that differ from the PKC pathway.