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石榴籽油通过天然抗氧化活性抑制美沙酮诱导的细胞死亡。

Punica granatum Seed Essential Oil Suppressed Methadone-Induced Cell Death by Natural Antioxidant Activity.

机构信息

Substance Abuse Prevention Research Center, Health Institute, Kermanshah University of Medical Sciences, Kermanshah, Iran.

Department of Medicinal Plant, Kermansha ACECR Institute of Higher Education, KErmanshah, Iran.

出版信息

Asian Pac J Cancer Prev. 2023 Mar 1;24(3):801-810. doi: 10.31557/APJCP.2023.24.3.801.

DOI:10.31557/APJCP.2023.24.3.801
PMID:36974531
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10334093/
Abstract

OBJECTIVES

Methadone is an opioid used in treating chronic and acute pains as well as opioid dependence. It induces death in neural cells. This study investigates Punica granatum oil's effects as a natural antioxidant on methadone-induced cell death.

MATERIALS AND METHODS

The cell death index indicating the apoptosis occurrence is calculated using the TUNEL test. Rhodamine123 evaluated mitochondrial membrane permeability. Griess reaction was used to detect nitric oxide production. Furthermore, IL-1β, IL-6, INFγ, and TNFα inflammatory cytokines were measured using the Rat inflammatory cytokine assay kit, Rat Kit V-Plex, and the caspase-3 activity was calculated through the Caspase-3 Colorimetric Assay Kit.

RESULTS

Different treatment processes of Punica granatum oil reduced cell cytotoxicity and cell death index and increased viability and proliferation in methadone-treated PC12 cells. NO production decreased in different treatment processes compared to methadone-induced PC12 cells and decreased IL-1β, IL-6, INFγ, and TNFα inflammatory cytokines. In these treatment processes, mitochondrial membrane potential increased, and caspase-3 activity decreased compared to methadone-induced PC12 cells.

CONCLUSION

Punica granatum essential oil declined methadone-induced cell death in PC12 cells in a dose-dependent manner through suppressing NO production, IL-1β, IL-6, INF-γ, and TNF-α inflammatory cytokines production, mitochondrial membrane disruption, and caspase-3 activities.

摘要

目的

美沙酮是一种阿片类药物,用于治疗慢性和急性疼痛以及阿片类药物依赖。它会导致神经细胞死亡。本研究旨在探讨石榴籽油作为一种天然抗氧化剂对美沙酮诱导的细胞死亡的影响。

材料和方法

使用 TUNEL 试验计算表明细胞凋亡发生的细胞死亡指数。罗丹明 123 评估线粒体膜通透性。使用硝酸还原酶法检测一氧化氮(NO)的产生。此外,使用大鼠炎症细胞因子测定试剂盒、大鼠 V-Plex 试剂盒测定白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)、干扰素-γ(INFγ)和肿瘤坏死因子-α(TNFα)等炎症细胞因子的水平,通过 Caspase-3 比色法测定试剂盒计算 caspase-3 活性。

结果

不同浓度的石榴籽油处理降低了美沙酮处理的 PC12 细胞的细胞毒性和细胞死亡指数,增加了细胞活力和增殖。与美沙酮诱导的 PC12 细胞相比,不同处理过程中的 NO 产生减少,IL-1β、IL-6、INFγ和 TNFα 炎症细胞因子减少。在这些处理过程中,与美沙酮诱导的 PC12 细胞相比,线粒体膜电位增加,caspase-3 活性降低。

结论

石榴籽油通过抑制 NO 产生、IL-1β、IL-6、INF-γ 和 TNF-α 炎症细胞因子产生、线粒体膜破坏和 caspase-3 活性,以剂量依赖的方式降低了美沙酮诱导的 PC12 细胞死亡。

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