齐墩果酸拮抗赭曲霉毒素A诱导的HEK293T细胞自噬性死亡

廖忻; 陈文莹; 李逸舟; 李晨; 刘鑫淼; 谌小立

doi:10.13386/j.issn1002-0306.2019.03.045

齐墩果酸拮抗赭曲霉毒素A诱导的HEK293T细胞自噬性死亡

廖忻¹,
陈文莹^1,2,
李逸舟³,
李晨¹,
刘鑫淼³,
谌小立^1,2, ,

1. 遵义医科大学公共卫生学院, 贵州遵义 563000;
2. 贵州省预防医学实验教学示范中心, 贵州遵义 563000;
3. 遵义医科大学基础医学院, 贵州遵义 563000

基金项目:

市校联合项目(遵市科合社字(2017)18号)

贵州省科学技术基金重点项目(黔科合LH字[2014]7546号)

遵义医学院博士学位授权支撑学科建设经费(2015-0996037)。

遵义医学院优秀青年人才项目(17zy-006)

国家自然科学基金(31460426)

大学生创新训练项目(遵医20163738)

详细信息

作者简介:
廖忻(1989-),女,硕士研究生,研究方向:卫生毒理学,E-mail:lx_persevere@163.com。

通讯作者:
谌小立(1983-),男,博士,副教授,研究方向:食品营养与安全,E-mail:xiaolishen1983@163.com。

中图分类号: TS201
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出版历程
- 收稿日期: 2018-06-25
- 网络出版日期: 2020-11-12
- 刊出日期: 2019-01-31

Oleanolic Acid Antagonized Autophagic Death of HEK293T Cells Induced by Ochratoxin A

1. School of Public Health, Zunyi Medical University, Zunyi 563000, China;
2. Experimental teaching Demonstration center for Preventive medicine of Guizhou province, Zunyi 563000, China;
3. School of Basic Medical Sciences, Zunyi Medical University, Zunyi 563000, China

摘要

摘要: 目的:探索齐墩果酸(oleanolic acid,OA)对赭曲霉毒素A(ochratoxin A,OTA)的肾细胞毒性的拮抗机制。方法:将实验分为6组(对照组、OTA组、OA组、OA预处理组、OA和OTA同时处理组和OA后处理组)处理人胚肾上皮细胞(HEK293T),通过测定细胞存活率确定OA的拮抗剂量为1 μmol/L,并进一步通过OA和OTA对活性氧簇(ROS)含量和自噬相关蛋白表达影响的研究,探明OA拮抗OTA诱导的HEK293T细胞毒性的机制。结果:低浓度的OA(1 μmol/L)能够显著提高细胞存活率(p<0.05)。虽然1 μmol/L OA不会明显诱导ROS产生和激活自噬(p>0.05),但是能够通过调节p-mTOR、p-p70S6K、p-Beclin1和LC3的表达来不同程度缓解OTA诱导的HEK293T细胞的自噬性死亡,OA后处理方式效果最为明显(p<0.05)。结论:摄入含OA的食品能够对OTA诱导的肾细胞毒性有一定的拮抗作用。
- 齐墩果酸 /
- 赭曲霉毒素A /
- 人胚肾上皮细胞 /
- 自噬
Abstract: Objective:To explore the antagonism mechanism of oleanolic acid (OA) on the renal cytotoxicity of ochratoxin A (OTA). Methods:The experiment was divided into 6 groups (control group, OTA group, OA group, OA pretreatment group, OA and OTA simultaneous treatment group and OA post-treatment group) to treat human embryonic kidney epithelial cells (HEK293T). The amount of OA antagonist was determined to 1 μmol/L by measuring cell viability, and the effects of OA and OTA on the content of reactive oxygen species (ROS) and the expression of autophagy-related proteins were further investigated to elucidate the mechanism of OA antagonizing OTA-induced HEK293T cytotoxicity. Results:The low concentrations of OA (1 μmol/L) could significantly increase cell viability (p<0.05). Although 1 μmol/L OA did not significantly induce ROS production and activate autophagy (p>0.05), it could alleviate the autophagic death of OTA-induced HEK293T cells to different extents by regulating the expression of p-mTOR, p-p70S6K, p-Beclin1, and LC3.Post-processing of OA is the most effective method (p<0.05). Conclusion:To some extent, people can have some antagonistic effects on OTA-induced renal cytotoxicity by ingesting OA-containing foods.
- oleanolic acid /
- ochratoxin A /
- HEK293T cells /
- autophagy