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Background: Herbal plant extracts are a more common alternative to conventional medicine to treat sleep disorders and intermittent hypoxia. Notably, obstructive sleep apnea causes injuries similar to those observed in models of ischemia-reperfusion including the decrease of nitric oxide (NO) availability. Kidney transplantation in end-stage renal disease reverses the sleep apnea. The underlying mechanism linking hypoxia, sleep apnea, and renal protection remains to be defined at the cellular level. Objective: The aim of this study was to demonstrate the safety and efficacy of herbal plant infusions with a potential for donating NO, to attenuation of damage induced during a hypoxia/reperfusion sequence, on kidney epithelial cells LLC-PK1. Materials and Methods: Cell death (Lactate Dehydrogenase release assay) and a viability test (MTS assay) after 24 h of incubation with different concentrations of plant infusion were assessed using the LLC-PK1 cell line. Then, measurement of the breakdown product of NO (the NaNO2) and LDH assay were carried out after 24 h of hypoxia, followed by 4 h or 24 h of reperfusion. Results: The effect of different dilutions of herbal plant infusion on the LLC-PK1 cell viability, after 24 h of incubation, was maximal at a 30% dilution compared to control. After 24 h of hypoxia, there was an increase of NaNO2 and thus of NO, and a concentration-dependent decrease of cell death. Similar results were observed after hypoxia followed by 4 h of reperfusion. These effects were always maximal at 50% dilution of plants infusion. Conclusion: Safe infusion of plant extracts causes a dose-dependent increase of NO and has a protective effect against the cellular stress caused by hypoxia and reoxygenation. Since it has been demonstrated that there is a NO-dependent mechanism allowing the reduction of injuries induced by ischemia/reoxygenation process, such a mechanism could be responsible for our observations.

canadian journal of biotechnology

Infusion of herbal plant extracts for insomnia and anxiety causes a dose-dependent increase of NO and has a protective effect on the renal cellular stress caused by hypoxia and reoxygenation