Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, the Republic of Korea.
Department of Pharmacology, Faculty of Veterinary Medicine, Cairo University, 12211 Giza, Egypt; Department of Medical Pharmacology, Medical Faculty, Ataturk University, Erzurum 25240, Turkey.
Tissue Cell. 2024 Feb;86:102275. doi: 10.1016/j.tice.2023.102275. Epub 2023 Nov 14.
The prevalence of tendinopathy in patients with diabetes is well documented. Despite efforts to improve diabetes management, there is a lack of research on therapeutic agents targeting the core features of tendinopathy, namely, tenocyte apoptosis and extracellular matrix (ECM) damage. In this study, we investigated the potential of ginsenoside compound K (CK), known for its antidiabetic properties, to mitigate tenocyte apoptosis, inflammation, oxidative stress, and the metalloproteinase (MMP) system under hyperglycemic conditions. Our research also aimed to unravel the molecular mechanism underlying the effects of CK. The assessment of apoptosis involved observing intracellular chromatin condensation and measuring caspase 3 activity. To gauge oxidative stress, we examined cellular ROS levels and hydrogen peroxide and malondialdehyde concentrations. Western blotting was employed to determine the expression of various proteins. Our findings indicate that CK treatment effectively countered high glucose-induced apoptosis, inflammation, and oxidative stress in cultured tenocytes. Furthermore, CK normalized the expression of MMP-9, MMP-13, and TIMP-1. Notably, CK treatment boosted the expression of PPARγ and antioxidant enzymes. We conducted small interfering (si) RNA experiments targeting PPARγ, revealing its role in mediating CK's effects on tendinopathy features in hyperglycemic tenocytes. In conclusion, these in vitro results offer valuable insights into the potential therapeutic role of CK in managing tendinopathy among individuals with diabetes. By addressing crucial aspects of tendinopathy, CK presents itself as a promising avenue for future research and treatment development in this domain.
患有糖尿病的患者中肌腱病的发病率很高，这是有充分文献记录的。尽管人们努力改善糖尿病的管理，但针对肌腱病核心特征（即肌腱细胞凋亡和细胞外基质（ECM）损伤）的治疗药物研究仍然缺乏。在这项研究中，我们研究了人参皂苷化合物 K（CK）的潜力，它以其抗糖尿病特性而闻名，可减轻高糖条件下肌腱细胞的凋亡、炎症、氧化应激和金属蛋白酶（MMP）系统。我们的研究还旨在揭示 CK 作用的分子机制。通过观察细胞内染色质浓缩和测量半胱天冬酶 3 活性来评估凋亡。为了评估氧化应激，我们检查了细胞 ROS 水平、过氧化氢和丙二醛浓度。采用 Western blot 测定各种蛋白的表达。我们的研究结果表明，CK 治疗可有效抵抗高糖诱导的培养肌腱细胞中的凋亡、炎症和氧化应激。此外，CK 使 MMP-9、MMP-13 和 TIMP-1 的表达正常化。值得注意的是，CK 治疗可增强 PPARγ 和抗氧化酶的表达。我们针对 PPARγ 进行了小干扰（si）RNA 实验，揭示了它在介导 CK 对高糖肌腱细胞中肌腱病特征的作用中的作用。总之，这些体外结果为 CK 在管理糖尿病个体肌腱病方面的潜在治疗作用提供了有价值的见解。通过解决肌腱病的关键方面，CK 为该领域的未来研究和治疗开发提供了一个有前途的途径。
