生香蕉皮中维生素B6的分析、植物化学筛选及其神经保护作用

Priyabrata Pradhan, Vineet Kumar Rai, Saroj Kumar Rout, Biswakanth Kar, Durgamadhab Kar, Shakti Ketan Prusty, Goutam Ghosh, Goutam Rath
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引用次数: 0

摘要

背景:癫痫严重加重了精神疾病负担,全球估计有5000万例。中药生物活性成分对颞叶癫痫的神经保护是一种很有前途的治疗策略。香蕉皮富含抗氧化剂和抗炎化合物。由于维生素B6和黄酮的存在,它具有防止神经元凋亡的效力。目的:本研究考察了溶剂比为90:10、80:20和70:30的香蕉皮水酒精提取物(HAE)的神经保护作用,重点研究了其抗凋亡、抗氧化和抗炎活性。方法:用10 ~ 200 μg/mL浓度的HAE处理神经元或神经元细胞系。ELISA法检测细胞凋亡标志物(cleaved caspase-3和Bcl-2),计算caspase-3/Bcl-2比值。通过谷氨酸脱羧酶(GAD)和过氧化氢酶活性测定来评估抗氧化作用,同时量化促炎细胞因子(TNF-α, IL-1β和IL-6)。采用MTT法分析细胞活力,并测定细胞凋亡抑制的IC50值。结果:100 μg/mL浓度的HAE(90:10)显著降低caspase-3/Bcl-2比值(0.45±0.02),IC50为37.5±2.1 μg/mL,显示出较好的抗凋亡活性。HAE(80:20)和HAE(70:30)的IC50值分别为48.2±2.5 μg/mL和62.7±3.0 μg/mL,药效较低。HAE增强GAD(121.4±5.2 U/mg)和过氧化氢酶(89.7±3.4 U/mg)活性(90:10),表明其具有强大的抗氧化作用。包括TNF-α在内的促炎标志物显著降低(100 μg/mL时降低45.6±2.3%),进一步强调了其抗炎潜力。MTT实验显示细胞活力提高,在100 μg/mL浓度下,HAE(90:10)维持93.5±2.6%的活力。HAE的优越性能(90:10)可归因于其生物活性化合物的优化平衡,支持其神经保护特性。结论:HAE(90:10)成为最有希望的神经保护候选者,显示出有效的抗凋亡、抗氧化和抗炎作用。这些发现提示其在治疗神经退行性疾病方面的潜在应用,需要进一步的体内和临床研究。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Analysis of Vit B6 in Raw Banana Peel, Phytochemical Screening, and Neuroprotective Effects.

Background: Epilepsy contributes significantly to the burden of mental illness, with an estimated 50 million cases globally. Neuroprotection with herbal bioactives is a promising therapeutic strategy for the prevention and treatment of temporal lobe epilepsy. Banana peel is rich in antioxidants and anti-inflammatory compounds. It has the potency to protect against neuronal apoptosis primarily due to the presence of Vit B6 and flavones.

Objectives: This: study investigated the neuroprotective effects of Hydro-Alcoholic Extracts (HAE) of banana peel, prepared at solvent ratios of 90:10, 80:20, and 70:30, focusing on their anti- apoptotic, antioxidant, and anti-inflammatory activities.

Methods: Neurons or neuronal cell lines were treated with HAE at 10-200 μg/mL concentrations. Apoptotic markers (cleaved caspase-3 and Bcl-2) were evaluated using ELISA, and the cleaved caspase-3/Bcl-2 ratio was calculated. Antioxidant effects were assessed via Glutamate Decarboxylase (GAD) and catalase activity assays, while pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6) were quantified. Cell viability was analyzed using the MTT assay, and IC50 values were determined for apoptosis inhibition.

Results: HAE (90:10) at 100 μg/mL significantly reduced the cleaved caspase-3/Bcl-2 ratio (0.45±0.02), with an IC50 of 37.5±2.1 μg/mL, demonstrating superior anti-apoptotic activity. HAE (80:20) and HAE (70:30) exhibited IC50 values of 48.2±2.5 μg/mL and 62.7±3.0 μg/mL, respectively, indicating comparatively lower potency. Enhanced GAD (121.4±5.2 U/mg) and catalase (89.7±3.4 U/mg) activities with HAE (90:10) highlight its potent antioxidant effects. Significant reductions in pro-inflammatory markers, including TNF-α (decreased by 45.6±2.3% at 100 μg/mL), further underscore its anti-inflammatory potential. The MTT assay revealed improved cell viability, with HAE (90:10) maintaining 93.5±2.6% viability at 100 μg/mL. The superior performance of HAE (90:10) can be attributed to its optimized balance of bioactive compounds, supporting its neuroprotective properties.

Conclusion: HAE (90:10) emerged as the most promising candidate for neuroprotection, demonstrating potent anti-apoptotic, antioxidant, and anti-inflammatory effects. These findings suggest its potential application in managing neurodegenerative disorders, warranting further in vivo and clinical studies.

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