Osteoarthritis (OA) is an age-related degenerative disease and currently cannot be cured. Transcription factor EB (TFEB) is one of the major transcriptional factors that regulates autophagy and lysosomal biogenesis. TFEB has been shown to be an effective therapeutic target for many diseases including OA. The current study explores the therapeutic effects of 20-Deoxyingenol (20-DOI) on OA as well as its working mechanism on TFEB regulation. The in vitro study showed that 20-DOI may suppress apoptosis and senescence induced by oxidative stress in chondrocytes; it may also promote the nuclear localization of TFEB in chondrocytes. Knock-down of TFEB compromised the effects of 20-DOI on apoptosis and senescence. The in vivo study demonstrated that 20-DOI may postpone the progression of OA in mouse destabilization of the medial meniscus (DMM) model; it may also suppress apoptosis and senescence and promote the nuclear localization of TFEB in chondrocytes in vivo. This work suggests that 20-Deoxyingenol may alleviate osteoarthritis by activating TFEB in chondrocytes, while 20-DOI may become a potential drug for OA therapy.

骨关节炎（OA）是一种与年龄相关的退行性疾病，目前无法治愈。转录因子EB（TFEB）是调节自噬和溶酶体生物发生的主要转录因子之一。TFEB 已被证明是包括 OA 在内的许多疾病的有效治疗靶点。目前的研究探讨了 20-脱氧烯醇 (20-DOI) 对 OA 的治疗作用及其对 TFEB 调节的作用机制。体外研究表明，20-DOI可以抑制氧化应激诱导的软骨细胞凋亡和衰老；它还可能促进 TFEB 在软骨细胞中的核定位。TFEB 的敲低损害了 20-DOI 对细胞凋亡和衰老的影响。体内_研究表明，20-DOI 可延缓 OA 在小鼠内侧半月板 (DMM) 模型不稳定中的进展；它还可以抑制细胞凋亡和衰老，促进TFEB在体内软骨细胞的核定位。这项工作表明，20-脱氧烯醇可能通过激活软骨细胞中的 TFEB 来缓解骨关节炎，而 20-DOI 可能成为 OA 治疗的潜在药物。