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香蜂草对氧化应激诱导的神经毒性的抗氧化和神经保护活性。

Antioxidant and neuroprotective activities of Hyptis suaveolens (L.) Poit. against oxidative stress-induced neurotoxicity.

作者信息

Ghaffari Hadi, Ghassam Behrouz Jalali, Chandra Nayaka S, Ramachandra Kini K, Prakash H S

机构信息

Department of Studies in Biotechnology, University of Mysore, Mysore, 570006, Karnataka, India.

出版信息

Cell Mol Neurobiol. 2014 Apr;34(3):323-31. doi: 10.1007/s10571-013-0016-7. Epub 2014 Jan 14.

Abstract

The present study was carried out to investigate the antioxidant and neuroprotective effects of Hyptis suaveolens methanol extract (HSME) using various in vitro systems. The total phenol and flavonoids contents of the HSME were quantified by colorimetric methods. The HSME extract exhibited potent antioxidant activity as determined by 2,20-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt, 2,2-diphenyl-1-picrylhydrazyl, and ferric reducing antioxidant power assays. The neuroprotective activity of HSME was determined on mouse N2A neuroblastoma cells using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, lactate dehydrogenase, intracellular ROS assays, and upregulation of brain neuronal markers at genetic level. The N2A cells were pretreated with different concentrations (0.5, 1, 1.5, and 2 mg/ml) of the extract and then exposed to H2O2 to induce oxidative stress and neurotoxicity. The survival of the cells treated with different concentrations of HSME and H2O2 increased as compared to cells exposed only to H2O2 (47.3 %) (p < 0.05). The HSME also dose-dependently reduced LDH leakage and intracellular ROS production (p < 0.05). Pretreatment with HSME promotes the upregulation of tyrosine hydroxylase (2.41-fold, p < 0.05), and brain-derived neurotrophic factor genes (2.15-fold, p < 0.05) against H2O2-induced cytotoxicity in N2A cells. Moreover, the HSME showed antioxidant activity and decreased neurotoxicity. These observations suggest that HSME have marked antioxidant and neuroprotective activities.

摘要

本研究旨在利用各种体外系统研究香蜂草甲醇提取物(HSME)的抗氧化和神经保护作用。采用比色法对HSME中的总酚和黄酮含量进行定量。通过2,2'-联氮-双-(3-乙基苯并噻唑啉-6-磺酸)二铵盐、2,2-二苯基-1-苦基肼和铁还原抗氧化能力测定,发现HSME提取物具有强大的抗氧化活性。使用3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐、乳酸脱氢酶、细胞内活性氧测定以及在基因水平上脑神经元标志物的上调,在小鼠N2A神经母细胞瘤细胞上测定了HSME的神经保护活性。用不同浓度(0.5、1、1.5和2mg/ml)的提取物预处理N2A细胞,然后暴露于H2O2以诱导氧化应激和神经毒性。与仅暴露于H2O2的细胞相比,用不同浓度的HSME和H2O2处理的细胞存活率增加(47.3%)(p<0.05)。HSME还剂量依赖性地降低了乳酸脱氢酶泄漏和细胞内活性氧的产生(p<0.05)。HSME预处理促进了酪氨酸羟化酶(2.41倍,p<0.05)和脑源性神经营养因子基因(2.15倍,p<0.05)的上调,以对抗H2O2诱导的N2A细胞毒性。此外,HSME表现出抗氧化活性并降低了神经毒性。这些观察结果表明,HSME具有显著的抗氧化和神经保护活性。

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