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灵芝发酵作物提取物对人神经母细胞瘤 SH-SY5Y 细胞中过氧化氢或β-淀粉样肽诱导损伤的保护作用。

Protective effect of Ganoderma lucidum-fermented crop extracts against hydrogen peroxide- or β-amyloid-induced damage in human neuronal SH-SY5Y cells.

机构信息

Department of Food Science, National Taiwan Ocean University, 2 Pei-Ning Road, Keelung, 202, Taiwan ROC.

Center for Marine Bioscience and Biotechnology, National Taiwan Ocean University, Keelung, Taiwan.

出版信息

BMC Complement Med Ther. 2024 Apr 5;24(1):148. doi: 10.1186/s12906-024-04409-1.

DOI:10.1186/s12906-024-04409-1
PMID:38580956
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10996153/
Abstract

BACKGROUND

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the accumulation of stacked β-amyloid peptides in the brain and associated with the generation of oxidative stress. So far, there is no cure for AD or a way to stop its progression. Although the neuroprotective effects of Ganoderma lucidum aqueous extract and G. lucidum-derived triterpenoids and polysaccharides have been reported, the influence of G. lucidum-fermented crops on AD still lacks clarity.

METHODS

This study aimed to investigate the protective effect of G. lucidum-fermented crop extracts against hydrogen peroxide- or β-amyloid peptide (Aβ)-induced damage in human neuroblastoma SH-SY5Y cells.

RESULTS

Various extracts of G. lucidum-fermented crops, including extract A: 10% ethanol extraction using microwave, extract B: 70˚C water extraction, and extract C: 100˚C water extraction followed by ethanol precipitation, were prepared and analyzed. Extract B had the highest triterpenoid content. Extract C had the highest total glucan content, while extract A had the highest gamma-aminobutyric acid (GABA) content. The median inhibitory concentration (IC, mg/g) for DPPH and ABTS scavenging activity of the fermented crop extracts was significantly lower than that of the unfermented extract. Pretreatment with these extracts significantly increased the cell viability of SH-SY5Y cells damaged by HO or Aβ, possibly by reducing cellular reactive oxygen species (ROS) and malondialdehyde (MDA) levels and increasing superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) activities. Moreover, extract B markedly alleviated the activity of acetylcholinesterase (AChE), which is crucial in the pathogenesis of AD.

CONCLUSION

These results clearly confirmed the effects of G. lucidum-fermented crop extracts on preventing against HO- or Aβ-induced neuronal cell death and inhibiting AChE activity, revealing their potential in management of AD.

摘要

背景

阿尔茨海默病(AD)是一种神经退行性疾病,其特征是大脑中β-淀粉样肽的堆积,并与氧化应激的产生有关。到目前为止,还没有治愈 AD 或阻止其进展的方法。虽然已经报道了灵芝水提取物和灵芝衍生的三萜类化合物和多糖的神经保护作用,但灵芝发酵作物对 AD 的影响仍不清楚。

方法

本研究旨在探讨灵芝发酵作物提取物对过氧化氢或β-淀粉样肽(Aβ)诱导的人神经母细胞瘤 SH-SY5Y 细胞损伤的保护作用。

结果

制备并分析了灵芝发酵作物的各种提取物,包括提取物 A:使用微波的 10%乙醇提取,提取物 B:70°C 水提取,提取物 C:100°C 水提取后用乙醇沉淀。提取物 B 具有最高的三萜含量。提取物 C 具有最高的总葡聚糖含量,而提取物 A 具有最高的γ-氨基丁酸(GABA)含量。发酵作物提取物对 DPPH 和 ABTS 清除活性的半数抑制浓度(IC,mg/g)明显低于未发酵提取物。这些提取物预处理可显著提高 HO 或 Aβ 损伤的 SH-SY5Y 细胞的细胞活力,这可能是通过降低细胞内活性氧(ROS)和丙二醛(MDA)水平,以及提高超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPx)和过氧化氢酶(CAT)活性来实现的。此外,提取物 B 显著减轻了乙酰胆碱酯酶(AChE)的活性,这在 AD 的发病机制中至关重要。

结论

这些结果清楚地证实了灵芝发酵作物提取物在预防 HO 或 Aβ 诱导的神经元细胞死亡和抑制 AChE 活性方面的作用,揭示了其在 AD 管理中的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81be/10996153/1ba19aa909f5/12906_2024_4409_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81be/10996153/f1fe23ab0ab2/12906_2024_4409_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81be/10996153/ed7c0b732255/12906_2024_4409_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81be/10996153/757fbc6138b8/12906_2024_4409_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81be/10996153/27e2f4b81fa7/12906_2024_4409_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81be/10996153/4f3a4f9b2716/12906_2024_4409_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81be/10996153/1ba19aa909f5/12906_2024_4409_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81be/10996153/f1fe23ab0ab2/12906_2024_4409_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81be/10996153/ed7c0b732255/12906_2024_4409_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81be/10996153/757fbc6138b8/12906_2024_4409_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81be/10996153/27e2f4b81fa7/12906_2024_4409_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81be/10996153/4f3a4f9b2716/12906_2024_4409_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/81be/10996153/1ba19aa909f5/12906_2024_4409_Fig6_HTML.jpg

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