Abstract：
Oxidative stress refers to non-homeostatic elevation within intracellular reactive oxygen species (ROS) levels and is associated with several neuro-related pathological conditions. Diclofenac is a commonly prescribed non-steroidal anti-inflammatory drug (NSAID) for treating aches and pain by reducing inflammation. Diclofenac is also associated with the induction of apoptotic cell death by altering the homeostatic balance within mitochondria. In the present report, the neuroprotective effects of BNC formulation constituted by Bacopa monnieri leaves, Nigella sativa and Curcuma longa rhizome seeds were investigated.
The synthesized formulation was characterized using FT-IR and LC-MS along with organoleptic evaluation. Thereafter neuroprotective efficacy of BNC formulation was subsequently investigated against Diclofenac-induced oxidative stress in SH-SY5Y cells. The cells were pretreated with synthesized formulation and subsequently evaluated for amelioration in Diclofenac-induced cytotoxicity, and ROS augmentation. The neuroprotective effect of synthesized formulation was further explored by evaluating the changes in nuclear morphology, and apoptosis alleviation with concomitant regulatory effects on caspase-3 and -9 activation.
Diclofenac was found to be considerably cytotoxic against human neuroblastoma SHSY5Y cells. Intriguingly, Diclofenac-mediated toxicity was reduced significantly in SH-SY5Y cells pretreated with BNC formulation. Augmented ROS levels within Diclofenac-treated SHSY5Y cells were also reduced in the BNC formulation pretreated SH-SY5Y cells. Furthermore, BNC formulation pretreated SH-SY5Y cells also exhibited reduced dissipation of mitochondrial membrane potential, caspase-3 and -9, along with apoptosis after Diclofenac treatment.
These findings indicated that, indeed, Diclofenac induces considerable ROSmediated apoptosis in SH-SY5Y cells, which further intriguingly ameliorated Diclofenacmediated cytotoxic effects on SH-SY5Y cells. This manuscript further collected information about available National and International patents published or granted in preparation of and thereof applications against motor and non-motor brain dysfunctions.
The synthesized formulation was characterized using FT-IR and LC-MS along with organoleptic evaluation. Thereafter neuroprotective efficacy of BNC formulation was subsequently investigated against Diclofenac-induced oxidative stress in SH-SY5Y cells. The cells were pretreated with synthesized formulation and subsequently evaluated for amelioration in Diclofenac-induced cytotoxicity, and ROS augmentation. The neuroprotective effect of synthesized formulation was further explored by evaluating the changes in nuclear morphology, and apoptosis alleviation with concomitant regulatory effects on caspase-3 and -9 activation.
Diclofenac was found to be considerably cytotoxic against human neuroblastoma SHSY5Y cells. Intriguingly, Diclofenac-mediated toxicity was reduced significantly in SH-SY5Y cells pretreated with BNC formulation. Augmented ROS levels within Diclofenac-treated SHSY5Y cells were also reduced in the BNC formulation pretreated SH-SY5Y cells. Furthermore, BNC formulation pretreated SH-SY5Y cells also exhibited reduced dissipation of mitochondrial membrane potential, caspase-3 and -9, along with apoptosis after Diclofenac treatment.
These findings indicated that, indeed, Diclofenac induces considerable ROSmediated apoptosis in SH-SY5Y cells, which further intriguingly ameliorated Diclofenacmediated cytotoxic effects on SH-SY5Y cells. This manuscript further collected information about available National and International patents published or granted in preparation of and thereof applications against motor and non-motor brain dysfunctions.
摘要：
背景：氧化应激是指细胞内活性氧（ROS）水平内的非稳态升高，并且与几种神经相关的病理状况有关。双氯芬酸是一种常用的非甾体抗炎药（NSAID），用于通过减少炎症来治疗疼痛和疼痛。双氯芬酸还通过改变线粒体内的稳态平衡而与凋亡细胞死亡的诱导相关。在本报告中，由Bacopamonnieri叶构成的BNC制剂的神经保护作用，对黑麦草和姜黄根茎种子进行了研究。
方法:使用FT-IR和LC-MS以及感官评价表征合成的制剂。此后,随后在SH-SY5Y细胞中研究BNC制剂对双氯芬酸诱导的氧化应激的神经保护功效。用合成制剂预处理细胞，随后评估双氯芬酸诱导的细胞毒性的改善，和ROS增强。通过评估核形态的变化，进一步探索合成制剂的神经保护作用。和细胞凋亡的缓解，并伴随着对caspase-3和-9激活的调节作用。
结果：发现双氯芬酸对人神经母细胞瘤SHSY5Y细胞具有相当大的细胞毒性。有趣的是，双氯芬酸介导的毒性在用BNC制剂预处理的SH-SY5Y细胞中显著降低。双氯芬酸处理的SHSY5Y细胞内的增加的ROS水平在BNC制剂预处理的SH-SY5Y细胞中也降低。此外，BNC制剂预处理的SH-SY5Y细胞也表现出减少的线粒体膜电位耗散。caspase-3和-9，以及双氯芬酸处理后的细胞凋亡。
结论：这些发现表明，的确,双氯芬酸在SH-SY5Y细胞中诱导大量ROS介导的凋亡，这进一步有趣地改善了双氯芬酸钠介导的对SH-SY5Y细胞的细胞毒性作用。该手稿进一步收集了有关针对运动和非运动脑功能障碍的准备及其申请中已发布或授予的可用国家和国际专利的信息。
方法:使用FT-IR和LC-MS以及感官评价表征合成的制剂。此后,随后在SH-SY5Y细胞中研究BNC制剂对双氯芬酸诱导的氧化应激的神经保护功效。用合成制剂预处理细胞，随后评估双氯芬酸诱导的细胞毒性的改善，和ROS增强。通过评估核形态的变化，进一步探索合成制剂的神经保护作用。和细胞凋亡的缓解，并伴随着对caspase-3和-9激活的调节作用。
结果：发现双氯芬酸对人神经母细胞瘤SHSY5Y细胞具有相当大的细胞毒性。有趣的是，双氯芬酸介导的毒性在用BNC制剂预处理的SH-SY5Y细胞中显著降低。双氯芬酸处理的SHSY5Y细胞内的增加的ROS水平在BNC制剂预处理的SH-SY5Y细胞中也降低。此外，BNC制剂预处理的SH-SY5Y细胞也表现出减少的线粒体膜电位耗散。caspase-3和-9，以及双氯芬酸处理后的细胞凋亡。
结论：这些发现表明，的确,双氯芬酸在SH-SY5Y细胞中诱导大量ROS介导的凋亡，这进一步有趣地改善了双氯芬酸钠介导的对SH-SY5Y细胞的细胞毒性作用。该手稿进一步收集了有关针对运动和非运动脑功能障碍的准备及其申请中已发布或授予的可用国家和国际专利的信息。
