输注治疗失眠和焦虑的草药植物提取物可引起NO的剂量依赖性增加,并对缺氧和再氧化引起的肾细胞应激具有保护作用

J. Maixent, M. Fares, C. François
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摘要

背景:草药植物提取物是治疗睡眠障碍和间歇性缺氧更常见的替代传统药物。值得注意的是,阻塞性睡眠呼吸暂停引起的损伤与在缺血再灌注模型中观察到的损伤相似,包括一氧化氮(NO)可用性的降低。终末期肾病肾移植可逆转睡眠呼吸暂停。连接缺氧、睡眠呼吸暂停和肾保护的潜在机制仍有待在细胞水平上确定。目的:本研究的目的是证明草药植物输注在缺氧/再灌注序列中对肾上皮细胞LLC-PK1损伤的衰减具有潜在的提供NO的安全性和有效性。材料与方法:采用lc - pk1细胞系,测定不同浓度植物灌注24 h后细胞死亡(乳酸脱氢酶释放法)和活力(MTS法)。缺氧24 h,再灌注4 h或24 h,测定NO分解产物(NaNO2)和LDH测定。结果:不同稀释度的植物冲剂对lc - pk1细胞活力的影响,在孵育24 h后,与对照相比,稀释30%时影响最大。缺氧24 h后,NaNO2升高,NO升高,细胞死亡率呈浓度依赖性降低。低氧再灌注4 h后观察到相似的结果。这些效应总是在50%稀释植物输注时达到最大。结论:安全输注植物提取物可使一氧化氮呈剂量依赖性增加,并对缺氧和再氧化引起的细胞应激具有保护作用。由于已经证明存在一氧化氮依赖的机制,可以减少缺血/再氧化过程引起的损伤,因此这种机制可能是我们观察到的原因。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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
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.
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