Raphanus sativus Linne Protects Human Nucleus Pulposus Cells against H 2 O 2 -Induced Damage by Inhibiting TREM2.
Hyunseong KimChanghwan YeoJin Young HongWan-Jin JeonHyun KimJunseon LeeYoon Jae LeeSeung-Ho BaekIn Hyuk HaPublished in: Biology (2024)
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 Raphanus sativus Linne (RSL), common radish, against oxidative stress by H 2 O 2 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 (H 2 O 2 ) 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 ACAN and Col2a1 while significantly reducing those of ADAMTS-4 , ADAMTS-5 , MMP3 , and MMP13 , key genes involved in NP degeneration. While H 2 O 2 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.
Keyphrases
- induced apoptosis
- oxidative stress
- cell cycle arrest
- endoplasmic reticulum stress
- cell death
- endothelial cells
- signaling pathway
- hydrogen peroxide
- diabetic rats
- pi k akt
- magnetic resonance imaging
- poor prognosis
- dna damage
- nitric oxide
- binding protein
- mass spectrometry
- heat shock
- cell migration
- smoking cessation
- long non coding rna