Allicin Attenuated Advanced Oxidation Protein Product-Induced Oxidative Stress and Mitochondrial Apoptosis in Human Nucleus Pulposus Cells.

Allicin Attenuated Advanced Oxidation Protein Product-Induced Oxidative Stress and Mitochondrial Apoptosis in Human Nucleus Pulposus Cells.
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大蒜素减弱高级氧化蛋白产物诱导的人髓核细胞的氧化应激和线粒体凋亡

DOI:
10.1155/2020/6685043
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发表时间:
2020
影响因子:
--
通讯作者:
Zhang Y
Zhang Y
中科院分区:
生物学2区
文献类型:
--
作者:
Xiang Q;Cheng Z;Wang J;Feng X;Hua W;Luo R;Wang B;Liao Z;Ma L;Li G;Lu S;Wang K;Song Y;Li S;Wu X;Yang C;Zhang Y

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椎间盘退行性变(IDD)是最常见的慢性退行性肌肉骨骼疾病之一。氧化应激诱导的髓核(NP)细胞凋亡在IDD的发展过程中起着关键作用。高级氧化蛋白产物(AOPP)是氧化应激的新生物标志物,由于其具有破坏氧化还原平衡的潜力,已被报道在各种疾病中发挥作用。本研究旨在探讨AOPP在氧化应激诱导的人NP细胞凋亡中的作用,以及大蒜素在这一过程中的缓解作用。AOPP以时间和浓度依赖的方式抑制NP细胞的存活和增殖,并显著诱导细胞凋亡。AOPP刺激后NP细胞内出现高水平的活性氧(ROS)和脂质过氧化产物丙二醛(MDA),导致线粒体膜电位(MTP)去极化。相应地,在人类退行性间盘(IVD)中发现了更高水平的AOPP。研究还发现,大蒜素可以通过抑制p38-MAPK通路来保护NP细胞免受AOPP介导的氧化应激和线粒体功能障碍的影响。这些结果揭示了AOPP在氧化应激诱导NP细胞凋亡中的重要作用,这可能参与了IDD的原发病机制。研究还表明,大蒜素可能是一种有前景的治疗方法,以对抗AOPP介导的氧化应激在IDD进展中的作用。
Intervertebral disc degeneration (IDD) is one of the most common chronic degenerative musculoskeletal disorders. Oxidative stress-induced apoptosis of the nucleus pulposus (NP) cells plays a key role during IDD progression. Advanced oxidation protein products (AOPP), novel biomarkers of oxidative stress, have been reported to function in various diseases due to their potential for disrupting the redox balance. The current study is aimed at investigating the function of AOPP in the oxidative stress-induced apoptosis of human NP cells and the alleviative effects of allicin during this process which was known for its antioxidant properties. AOPP were demonstrated to hamper the viability and proliferation of NP cells in a time- and concentration-dependent manner and cause cell apoptosis markedly. High levels of reactive oxygen species (ROS) and lipid peroxidation product malondialdehyde (MDA) were detected in NP cells after AOPP stimulation, which resulted in depolarized mitochondrial transmembrane potential (MTP). Correspondingly, higher levels of AOPP were discovered in the human degenerative intervertebral discs (IVD). It was also found that allicin could protect NP cells against AOPP-mediated oxidative stress and mitochondrial dysfunction via suppressing the p38-MAPK pathway. These results disclosed a significant role of AOPP in the oxidative stress-induced apoptosis of NP cells, which could be involved in the primary pathogenesis of IDD. It was also revealed that allicin could be a promising therapeutic approach against AOPP-mediated oxidative stress during IDD progression.
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