Title : σ1-Receptor Agonism Protects against Renal Ischemia-Reperfusion Injury.

Pub. Date : 2017 Jan

PMID : 27056295






5 Functional Relationships(s)
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1 In rats, pretreatment with either dehydroepiandrosterone or fluvoxamine, a high-affinity sigma1-receptor agonist, improved survival, renal function and structure, and the inflammatory response after sublethal renal ischemia-reperfusion injury. Fluvoxamine sigma non-opioid intracellular receptor 1 Rattus norvegicus
2 In human proximal tubular epithelial cells, stimulation by fluvoxamine or oxidative stress caused the sigma1-receptor to translocate from the endoplasmic reticulum to the cytosol and nucleus. Fluvoxamine sigma non-opioid intracellular receptor 1 Rattus norvegicus
3 Fluvoxamine stimulation in these cells also activated nitric oxide production that was blocked by sigma1-receptor knockdown or Akt inhibition. Fluvoxamine sigma non-opioid intracellular receptor 1 Rattus norvegicus
4 Similarly, in the postischemic rat kidney, sigma1-receptor activation by fluvoxamine triggered the Akt-nitric oxide synthase signaling pathway, resulting in time- and isoform-specific endothelial and neuronal nitric oxide synthase activation and nitric oxide production. Fluvoxamine sigma non-opioid intracellular receptor 1 Rattus norvegicus
5 Concurrently, intravital two-photon imaging revealed prompt peritubular vasodilation after fluvoxamine treatment, which was blocked by the sigma1-receptor antagonist or various nitric oxide synthase blockers. Fluvoxamine sigma non-opioid intracellular receptor 1 Rattus norvegicus