Procyanidin B2 alleviates oxidative stress-induced nucleus pulposus cells apoptosis through upregulating Nrf2 via PI3K-Akt pathway.
Yan-Pei ZouQi-Chen ZhangQian-Yi ZhangLi-Bo JiangXi-Lei LiPublished in: Journal of orthopaedic research : official publication of the Orthopaedic Research Society (2022)
Oxidative stress can lead to nucleus pulposus cell (NPC) apoptosis, which is considered to be one of the main contributors to intervertebral disc degeneration (IVDD). Procyanidin B2 is a natural antioxidant that protects against oxidative stress. However, whether procyanidin B2 protects NPCs from oxidative stress remains unknown. In this study, we demonstrated that procyanidin B2 could reduce tert-butyl hydroperoxide-induced reactive oxygen species in rat NPCs and attenuate rat NPC apoptosis. Further experiments revealed that procyanidin B2 upregulated the expression of both Nrf2 and p-Akt. We then used siNrf2 and LY294002 to silence Nrf2 expression and block the PI3K/Akt pathway, respectively, and found that the protective roles of procyanidin B2 in NPCs were inhibited. Therefore, we demonstrated that procyanidin B2 alleviated rat NPC apoptosis induced by oxidative stress by upregulating Nrf2 via activation of the PI3K/Akt signaling pathway. This study provides a potential therapeutic approach for procyanidin B2 in IVDD, which might help in the development of new drugs for IVDD treatment. This article is protected by copyright. All rights reserved.
Keyphrases
- oxidative stress
- induced apoptosis
- diabetic rats
- ischemia reperfusion injury
- signaling pathway
- dna damage
- cell cycle arrest
- poor prognosis
- reactive oxygen species
- endoplasmic reticulum stress
- single cell
- pi k akt
- binding protein
- cell proliferation
- stem cells
- mesenchymal stem cells
- drug induced
- high glucose
- bone marrow
- combination therapy
- mouse model
- heat shock protein