新型制剂(Bncs 配方)对脑肿瘤的保护性评估。

Anuradha Mishra, Afza Ahmad, Irfan Ahmad Ansari, Rohit Kumar Tiwari
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引用次数: 0

摘要

背景:氧化应激是指细胞内活性氧(ROS)水平的非稳态升高,与多种神经相关病症有关。双氯芬酸是一种常用的非甾体抗炎药(NSAID),通过减轻炎症来治疗疼痛。双氯芬酸还可通过改变线粒体内的平衡而诱导细胞凋亡。在本报告中,研究了由百服宁叶、黑升麻和莪术根茎种子构成的 BNC 配方对神经的保护作用:方法:采用傅立叶变换红外光谱和液相色谱-质谱法对合成的制剂进行表征,同时进行感官评价。随后研究了 BNC 制剂对 SH-SY5Y 细胞中双氯芬酸诱导的氧化应激的神经保护功效。用合成制剂对细胞进行预处理,然后评估其对双氯芬酸诱导的细胞毒性和 ROS 增强的改善作用。通过评估核形态的变化、细胞凋亡的缓解以及对 caspase-3 和 -9 激活的调节作用,进一步探讨了合成制剂的神经保护作用:结果:发现双氯芬酸对人神经母细胞瘤 SHSY5Y 细胞具有显著的细胞毒性。耐人寻味的是,双氯芬酸介导的毒性在用 BNC 制剂预处理的 SH-SY5Y 细胞中明显降低。在 BNC 制剂预处理的 SH-SY5Y 细胞中,双氯芬酸处理的 SHSY5Y 细胞中增加的 ROS 水平也有所降低。此外,BNC制剂预处理的SH-SY5Y细胞在双氯芬酸处理后,线粒体膜电位、caspase-3和-9的耗散以及细胞凋亡也有所减少:结论:这些研究结果表明,双氯芬酸确实能诱导SH-SY5Y细胞发生大量ROS介导的细胞凋亡,并能进一步改善双氯芬酸对SH-SY5Y细胞的细胞毒性作用。本手稿进一步收集了有关已公布或已授权的国家和国际专利的信息,这些专利正在准备中,并已申请用于治疗大脑运动和非运动功能障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Protective Assessment of Novel (Bncs Formulation) against Brain Tumor.

Background: 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.

Methods: 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.

Results: 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.

Conclusion: 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.

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