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Pinitol suppresses TNF-alpha-induced chondrocyte senescence

机译：拼胶醇抑制TNF-α-诱导的软骨细胞衰老

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摘要

Osteoarthritis (OA) is a highly prevalent joint disorder that is tightly correlated with age. As the body ages, cell replication and function decline until homeostasis can no longer be maintained. This process involves cellular senescence as well as replicative senescence. Telomere length, cell cycle arrest, expression of p16 and p53, and the release of senescence-associated beta-galactosidase (SA-beta-Gal) are all markers of cell senescence. In OA joints, chondrocytes undergo cellular senescence prematurely, thereby ceasing to synthesize and maintain cartilage tissue. Upregulation of proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha), and oxidative stress induced by overproduction of reactive oxygen species (ROS) are key events in the pathogenesis of OA. In the present study, we investigated the effects of pinitol, a naturally occurring compound, on the effects of TNF-alpha on chondrocyte senescence and cell cycle arrest. We found that pinitol has a favorable safety profile in terms of cell viability. Pinitol significantly inhibited cellular senescence and cell cycle arrest in the G0/G1 phase induced by TNF-alpha. We also found that pinitol could inhibit TNF-alpha-induced increased telomerase activity and expression of p16 and p53. Importantly, we found that the effects of pinitol may be mediated through rescue of Nrf2 signaling, which is recognized as a key protective factor in OA. This finding was verified through a Nrf2 silencing experiment using Nrf2 siRNA. Together, our findings reveal the potential of pinitol as a safe therapeutic option for the prevention of OA-associated chondrocyte senescence and oxidative stress.
机译：骨关节炎（OA）是一种高度普遍的关节障碍，与年龄紧密相关。由于身体年龄，细胞复制和功能下降，直到无法再保持稳态。该过程涉及细胞衰老以及复制衰老。端粒长度，细胞周期停滞，p16和p53的表达，以及衰老相关的β-半乳糖苷酶（Sa-beta-gal）的释放是细胞衰老的所有标记。在OA关节中，软骨细胞过早地经过细胞衰老，从而停止合成和维持软骨组织。促炎细胞因子的上调，例如肿瘤坏死因子-α（TNF-α），并通过过量产生反应性氧物质（ROS）诱导的氧化应激是OA发病机制中的关键事件。在本研究中，我们研究了吡啶醇，天然存在的化合物对TNF-α对软骨细胞衰老和细胞循环捕获的影响的影响。我们发现在细胞活力方面，拼块具有有利的安全性。吡咯醇在TNF-α诱导的G0 / G1相中显着抑制细胞衰老和细胞周期停滞。我们还发现拼胶醇可以抑制TNF-α诱导的增加的端粒酶活性和P16和P53的表达。重要的是，我们发现，PINITOL的效果可以通过NRF2信号传导的拯救来介导，其被认为是OA中的关键保护因子。通过使用NRF2 siRNA的NRF2沉默实验验证了该发现。我们的研究结果在一起揭示了Pinitol作为预防OA相关的软骨细胞衰老和氧化应激的安全治疗选择。

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