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昆氏植物水提取物和乙醇提取物对丙烯酰胺诱导的神经毒性的保护作用。

Protective effect of aqueous and ethanolic extracts of Kunth on acrylamide-induced neurotoxicity.

作者信息

Tandisehpanah Zahra, Foroutanfar Amir, Aziminia Ali, Ghasemzadeh Rahbardar Mahboobeh, Razavi Bibi Marjan, Hosseinzadeh Hossein

机构信息

School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.

Targeted Drug Delivery Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, Iran.

出版信息

Avicenna J Phytomed. 2022 May-Jun;12(3):281-294. doi: 10.22038/AJP.2021.19173.

DOI:10.22038/AJP.2021.19173
PMID:36186928
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9482716/
Abstract

OBJECTIVE

Acrylamide (ACR) neurotoxicity is induced by different mechanisms such as oxidative stress and apoptosis. Scientific researchs have indicated the antioxidative properties of . The protective effect of aqueous and ethanolic extracts on ACR-induced neurotoxicity was investigated.

MATERIALS AND METHODS

Male Wistar rats were randomly divided into 13 groups: (1) control, (2) ACR (50 mg/kg, i.p.), (3-6) ACR+aqueous extract (12.5, 25, 50, and 100 mg/kg, i.p.), (7-10) ACR+ethanolic extract (12.5, 25, 50, and 100 mg/kg, i.p.), (11) aqueous extract (100 mg/kg), (12) ethanolic extract (100 mg/kg), and (13) ACR+Vitamin E (200 mg/kg, every other day, i.p.). After 11 days, gait score, MDA, and GSH levels in brain cortical tissue were measured. In the test, the viability of PC12 cells (using MTT test), the amount of reactive oxygen species (ROS; using DCFH-DA method), and the protein levels of Bax, Bcl2 and caspase 3 (by western blotting) were measured.

RESULTS

In the study, the IC for the treatment of PC 12 cells with ACR after 24 hr was 6 mM. ACR decreased cell viability, but increased ROS level, Bax/Bcl-2 ratio, and caspase-3 protein level. Pre-treatment by extracts (15-120 µg/ml) ameliorated the toxic effects of ACR on PC12 cells. In the experiment, ACR-induced movement disorders increased MDA but decreased GSH content. The extracts of improved ACR toxic effects.

CONCLUSION

Aqueous and ethanolic extracts of were found to reduce ACR-induced neurotoxicity via inhibiting oxidative stress and apoptosis.

摘要

目的

丙烯酰胺(ACR)的神经毒性是由氧化应激和细胞凋亡等不同机制诱导的。科学研究表明了……的抗氧化特性。研究了……水提取物和乙醇提取物对ACR诱导的神经毒性的保护作用。

材料与方法

将雄性Wistar大鼠随机分为13组:(1)对照组,(2)ACR组(50mg/kg,腹腔注射),(3 - 6)ACR + 水提取物组(12.5、25、50和100mg/kg,腹腔注射),(7 - 10)ACR + 乙醇提取物组(12.5、25、50和100mg/kg,腹腔注射),(11)水提取物组(100mg/kg),(12)乙醇提取物组(100mg/kg),以及(13)ACR + 维生素E组(200mg/kg,隔日腹腔注射)。11天后,测量脑皮质组织中的步态评分、丙二醛(MDA)和谷胱甘肽(GSH)水平。在……实验中,测量PC12细胞的活力(使用MTT试验)、活性氧(ROS;使用二氯荧光素二乙酸酯(DCFH - DA)法)的量以及Bax、Bcl2和半胱天冬酶3的蛋白质水平(通过蛋白质印迹法)。

结果

在……研究中,24小时后用ACR处理PC12细胞的半数抑制浓度(IC)为6mM。ACR降低了细胞活力,但增加了ROS水平、Bax/Bcl - 2比值和半胱天冬酶 - 3蛋白质水平。……提取物(15 - 120μg/ml)预处理减轻了ACR对PC12细胞的毒性作用。在……实验中,ACR诱导的运动障碍增加了MDA,但降低了GSH含量。……提取物改善了ACR的毒性作用。

结论

发现……的水提取物和乙醇提取物通过抑制氧化应激和细胞凋亡来降低ACR诱导的神经毒性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/5f8d3ab5517e/AJP-12-281-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/ec6dd9ae5657/AJP-12-281-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/4c1bc769c755/AJP-12-281-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/b15f834f07cb/AJP-12-281-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/2004eee17041/AJP-12-281-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/c62b9a5d4082/AJP-12-281-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/b974307b16a8/AJP-12-281-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/5f8d3ab5517e/AJP-12-281-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/ec6dd9ae5657/AJP-12-281-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/4c1bc769c755/AJP-12-281-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/b15f834f07cb/AJP-12-281-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/2004eee17041/AJP-12-281-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/c62b9a5d4082/AJP-12-281-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/b974307b16a8/AJP-12-281-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/958a/9482716/5f8d3ab5517e/AJP-12-281-g007.jpg

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