Interaction of mTOR and iNOS pathways in protection against Ischemia/Reperfusion injury

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AuthorMaedeh Arabianen
AuthorNahid Aboutaleben
AuthorMarjan Ajamien
AuthorRouhollah Habibeyen
Issued Date2019-04-30en
AbstractChronic morphine (CM) treatment increases the phosphorylation of the mammalian target of rapamycin (mTOR), which confers neuroprotection against ischemia/reperfusion (I/R) injury. Besides its important regulatory role in the proliferation, metabolism, and survival of cells, the mTOR is critically involved in intracellular signaling events during I/R injury. In the present study, we investigated the interaction between the expressions of the mTOR and inducible nitric oxide synthase (iNOS) and their possible protective effects on hippocampal neurons against I/R injury in morphine-dependent mice. Additive doses of morphine were administered for 5 days to BALB/c mice so as to induce CM preconditioning before I/R injury. Global brain ischemia was induced via the occlusion of bilateral common carotid arteries for 30 min. CM attenuated iNOS expression, NO production, and malondialdehyde activity in the hippocampal tissue. Pretreatment with rapamycin, the inhibitor of mTOR, abolished all the above mentioned effects of CM. These findings suggested that CM acted through the mTOR signaling pathways to regulate iNOS expression and oxidative state in the hippocampal tissue after I/R injury.en
DOIhttps://doi.org/10.22037/ijpr.2019.1100680en
KeywordIschemia/reperfusionen
KeywordMorphineen
KeywordiNOSen
KeywordOxidative stressen
KeywordMalondialdehydeen
KeywordRapamycinen
KeywordmTORen
PublisherBrieflandsen
TitleInteraction of mTOR and iNOS pathways in protection against Ischemia/Reperfusion injuryen
TypeOriginal Articleen

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