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Sri Rahavi Boovarahan,Harini Venkatasubramanian,Nidhi Sharma,Sushma Venkatesh,Priyanka Prem,Gino A. Kurian 대한약학회 2021 Archives of Pharmacal Research Vol.44 No.6
Recent studies have shown that pre and postconditioningthe heart with sodium thiosulfate (STS) attenuateischemia–reperfusion (IR) injury. However, the underlyingmechanism involved in the cardioprotective signaling pathwayis not fully explored. This study examined the existinglink of STS mediated protection (as pre and post-conditioningagents) with PI3K, mTOR, and mPTP signaling pathwaysusing its respective inhibitors. STS was administeredto the isolated perfused rat heart through Kreb’s Heinselitbuff er before ischemia (precondition: SIPC) and reperfusion(postcondition: SPOC) in the presence and absence ofthe PI3K, mTOR, and mPTP signaling pathway inhibitors(wortmannin, rapamycin, and glibenclamide respectively). SIPC failed to improve the IR injury-induced altered cardiachemodynamics, increased infarct size, and the releaseof cardiac injury markers in the presence of these inhibitors. On the other hand, the SPOC protocol eff ectively renderedthe cardioprotection even in the PI3K/mTOR/K ATP inhibitorspresence. Interestingly, the SIPC’s identifi ed mode ofaction viz reduction in oxidative stress and the preservationof mitochondrial function were lost in the inhibitors’presence. Based on the above results, we conclude that theunderlying mechanism of SIPC mediated cardioprotectionworks via the PI3K/mTOR/K ATP signaling pathway axisactivation.
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