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Linne通过抑制TREM2保护人髓核细胞免受血红素加氧酶诱导的损伤。

Linne Protects Human Nucleus Pulposus Cells against HO-Induced Damage by Inhibiting TREM2.

作者信息

Kim Hyunseong, Yeo Changhwan, Hong Jin Young, Jeon Wan-Jin, Kim Hyun, Lee Junseon, Lee Yoon Jae, Baek Seung Ho, Ha In-Hyuk

机构信息

Jaseng Spine and Joint Research Institute, Jaseng Medical Foundation, Seoul 06110, Republic of Korea.

College of Korean Medicine, Dongguk University, 32 Dongguk-ro, Ilsandong-gu, Goyang-si 10326, Republic of Korea.

出版信息

Biology (Basel). 2024 Aug 9;13(8):602. doi: 10.3390/biology13080602.

Abstract

Intervertebral disc degeneration (IDD) progresses owing to damage and depletion of nucleus pulposus (NP) cells. Cytoprotection mitigates oxidative stress, nutrient deprivation, and mechanical stress, which lead to cell damage and necrosis. We aimed to examine the protective effect of Linne (RSL), common radish, against oxidative stress by HO in human NP cells and whether the RSL extracts can inhibit triggering receptor expressed on myeloid cells 2 (TREM2), an inducer of apoptosis and degeneration in NP cells. We administered hydrogen peroxide (HO) to cultured human NP cells treated with RSL extracts. We used immunoblotting and quantitative PCR to investigate expression of the apoptosis-associated proteins in cultured cells. RSL significantly enhanced cell survival by suppressing the activation of cleaved caspase-3 and Bax. In contrast, RSL extract increased Bcl2 concentration to downregulate apoptosis. Additionally, RSL treatment notably enhanced the mRNA levels of and while significantly reducing those of , , , and , key genes involved in NP degeneration. While HO elevated TREM2 expression, causing disc degeneration, RSL downregulated TREM2 expression. Thus, our findings imply that RSL supports human NP cells under oxidative stress and regulates the pathways underlying disc degeneration, particularly TREM2, and that RSL extracts may potentially prevent IDD.

摘要

椎间盘退变(IDD)因髓核(NP)细胞的损伤和耗竭而进展。细胞保护可减轻氧化应激、营养剥夺和机械应激,这些应激会导致细胞损伤和坏死。我们旨在研究欧洲防风(RSL),即常见的萝卜,对人NP细胞中HO诱导的氧化应激的保护作用,以及RSL提取物是否能抑制髓样细胞表达的触发受体2(TREM2),TREM2是NP细胞凋亡和退变的诱导因子。我们将过氧化氢(HO)应用于用RSL提取物处理的培养人NP细胞。我们使用免疫印迹和定量PCR来研究培养细胞中凋亡相关蛋白的表达。RSL通过抑制裂解的半胱天冬酶-3和Bax的激活显著提高细胞存活率。相反,RSL提取物增加了Bcl2浓度以下调细胞凋亡。此外,RSL处理显著提高了 和 的mRNA水平,同时显著降低了 、 、 和 的mRNA水平,这些是参与NP退变的关键基因。虽然HO会升高TREM2表达,导致椎间盘退变,但RSL会下调TREM2表达。因此,我们的研究结果表明,RSL在氧化应激下对人NP细胞有支持作用,并调节椎间盘退变的潜在途径,特别是TREM2,并且RSL提取物可能有预防IDD的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9adb/11351166/c33dfd13d9f0/biology-13-00602-g001.jpg

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