痴呆症的患病率正在增加,大多数原因与神经元细胞死亡有关。不幸的是,没有有效的策略可用于预防这种情况。基于协同概念的使用以及桑果和桑叶对痴呆症的积极调节作用,我们假设桑果和桑叶(MFML)的组合提取物应减轻神经元细胞死亡。通过暴露于200μM剂量的过氧化氢在SH-SY5Y细胞中诱导神经元细胞损伤。在诱导细胞毒性之前,给予SH-SY5Y细胞62.5和125μg/mL剂量的MFML。然后,通过MTT测定细胞活力,并通过超氧化物歧化酶(SOD)的改变研究了可能的潜在机制,过氧化氢酶(CAT),谷胱甘肽过氧化物酶(GSH-Px),丙二醛(MDA),核因子-κB(NF-κB),和肿瘤坏死因子-α(TNF-α),与凋亡因子一起,包括(B细胞淋巴瘤2)BCL2,Casapase-3和Caspase-9。结果显示,MFML显著增强细胞活力。它也显著降低MDA水平,NF-κB,TNF-α,Casapase-3,Caspase-9,但增加SOD,GSH-Px和BCL2。这些数据证明了MFML的神经保护作用。可能的潜在机制可能部分地通过BCL2,Casapase-3和Caspase-9改善不适当的凋亡机制以及由炎症和氧化应激减少引起的神经变性的减少而发生。总之,MFML是针对神经元细胞损伤的潜在神经保护剂候选物。然而,毒性,动物研究,和临床试验是必要的,以确认这些好处。
The prevalence of dementia is increasing, and most of the causes are related to neuronal cell death. Unfortunately, no effective strategy is available for protecting against this condition. Based on the use of the synergistic concept together with the positive modulation effect of both mulberry fruit and mulberry leaf on dementia, we hypothesized that the combined extract of mulberry fruit and mulberry leaf (MFML) should mitigate neuronal cell death. Neuronal cell damage was induced in SH-SY5Y cells by exposure to hydrogen peroxide at a dose of 200 μM. SH-SY5Y cells were given MFML at doses of 62.5 and 125 μg/mL before induced cytotoxicity. Then, the cell viability was determined via MTT assay, and the possible underlying mechanisms were investigated via the alterations of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), nuclear factor-κB (NF-κB), and tumor necrosis factor-alpha (TNF-α), together with apoptotic factors including (B-cell lymphoma 2) BCL2, Casapase-3 and Caspase-9. The results showed that MFML significantly enhanced cell viability. It also significantly decreased MDA level, NF-κB, TNF-α, Casapase-3, Caspase-9, but increased SOD, GSH-Px and BCL2. These data demonstrated the neuroprotective effect of MFML. The possible underlying mechanisms might occur partly via the improvement of the inappropriate apoptotic mechanisms via BCL2, Casapase-3 and Caspase-9 together with the decrease in neurodegeneration induced by the reduction of inflammation and oxidative stress. In conclusion, MFML is a potential neuroprotectant candidate against neuronal cell injury. However, toxicity, animal studies, and clinical trials are essential to confirm these benefits.