Natarajan Kiruthiga, Chandrasekaran Rajkuberan, Sundararaj Rajamanikandan, Joseph John, Asaithambi Kalaiselvi
Department of Biotechnology, Karpagam Academy of Higher Education, Coimbatore, India.
Centre for Drug Discovery, Department of Biochemistry, Karpagam Academy of Higher Education, Coimbatore, 641 021, India.
Neurochem Res. 2024 Dec 11;50(1):54. doi: 10.1007/s11064-024-04312-8.
The cognitive dysfunction in the brain cause severe pathological consequences such as Alzheimer's disease (AD), Parkinson's disease. The current treatments are cost expensive and also cause negative side effects. Therefore it is inevitable to develop natural phyto-compounds as a drug like molecules to treat neurodegenerative diseases. In this context, we have assayed the neuroprotective effects of betanin, an indole derivative, in the neuroblastoma cell line SHSY-5Y cells. The neuroprotective effect was investigated in the β-amyloid (Aβ) - induced SHSY-5Y cells; betanin (25 µg) protected the SHSY-5Y cells from the toxic effects and maintained the cell viability. Moreover, the acridine orange and ethidum Bromide staining decipher that treatment of betanin in the Aβ-induced SHSY-5Y cells maintain the cell viablity sustainably. The Reactive Oxygen Species (ROS) assay infers that betanin quenches the generation of free radicals progressively in the Aβ-induced SHSY-5Y cells. In addition, the autophagy determination by flow cytometry revealed that betanin induces autophagy to remove the neurodegenerated cells. Further, we examined the docking and simulation patterns with the angiotensin-converting enzyme (ACE), TNF-α converting enzyme (TACE), glycogen synthase kinase 3 (GK3), and acetylcholinesterase enzymes (AChE) and amyloid precursor protein (APP). The insilico docking analysis denotes that betanin had a significant docking score with the target molecules. Thus, from the invitro and insilico studies, betanin strongly inhibit the toxic effects of Aβand protect the cells from degeneration.
大脑中的认知功能障碍会导致严重的病理后果，如阿尔茨海默病（AD）、帕金森病。目前的治疗方法成本高昂，且会产生负面副作用。因此，开发天然植物化合物作为类似药物的分子来治疗神经退行性疾病是不可避免的。在此背景下，我们检测了吲哚衍生物甜菜红素在神经母细胞瘤细胞系SHSY-5Y细胞中的神经保护作用。在β-淀粉样蛋白（Aβ）诱导的SHSY-5Y细胞中研究了其神经保护作用；甜菜红素（25μg）保护SHSY-5Y细胞免受毒性作用并维持细胞活力。此外，吖啶橙和溴化乙锭染色表明，在Aβ诱导的SHSY-5Y细胞中用甜菜红素处理可可持续维持细胞活力。活性氧（ROS）检测推断，甜菜红素可在Aβ诱导的SHSY-5Y细胞中逐渐淬灭自由基的产生。此外，通过流式细胞术进行的自噬测定表明，甜菜红素可诱导自噬以清除神经退行性细胞。此外，我们研究了与血管紧张素转换酶（ACE）、肿瘤坏死因子-α转换酶（TACE）、糖原合酶激酶3（GK3）、乙酰胆碱酯酶（AChE）和淀粉样前体蛋白（APP）的对接和模拟模式。计算机对接分析表明，甜菜红素与靶分子具有显著的对接分数。因此，从体外和计算机研究来看，甜菜红素强烈抑制Aβ的毒性作用并保护细胞免于退化。
