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卡斯蒂辛通过PI3K/AKT/HIF-1α信号传递改善了老鼠的骨关节炎软骨损伤

Deren Liu¹, Wei Mei², Junfeng Kang³

¹Department of Orthopedics, The Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210029, People's Republic of China; Jiangsu Province Hospital of Chinese Medicine, Nanjing, Jiangsu, 210029, People's Republic of China; Key Laboratory for Metabolic Diseases in Chinese Medicine, First College of Clinical Medicine, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, 210029, People's Republic of China.

Chemico-biological interactions

|February 3, 2024

概括

卡斯蒂辛 (CAS) 是一种黄类药物,在治疗膝关节关节炎 (KOA) 中表现有前途. 它保护软骨,减少炎症,并抑制PI3K/AKT/HIF-1α通路,为KOA提供了潜在的治疗策略.

科学领域:

生物医学研究的研究.
药理学药理学是指药理学的学科.
骨关节炎的研究研究.

背景情况:

膝关节关节炎 (KOA) 是一种衰弱的疾病,其特点是软骨退化.
卡斯蒂辛 (CAS) 是一种来自Vitex物种的黄,具有抗炎和抗瘤的特性.

研究的目的:

为了研究卡斯蒂辛 (CAS) 对膝关节骨关节炎 (KOA) 鼠标模型中的软骨损伤的治疗和机械效应.
探索CAS对状细胞活力,亡和炎症反应的影响.

主要方法:

使用前交叉带切割 (ACLT) 建立KOA大鼠模型和用IL-1β治疗的肌肉细胞进行体外OA模型.
通过微型CT和组织学评估软骨形态.
评估了冠状细胞活力 (CCK-8,EDU),细胞亡 (流细胞计,Hoechst/PI),炎症调解剂 (西方抹杀,qRT-PCR,ELISA) 和软骨矩阵组件.
研究PI3K/AKT/HIF-1α信号通路,使用免疫组织化学和西式涂抹.

主要成果:

在ACLT模型中,CAS治疗改善了骨结构的改变,减少了软骨损伤,并抑制了骨菌的形成.
在体外,CAS减弱了IL-1β诱导的软骨基质降解,细胞亡和炎症反应.
在体内和体外OA模型中,CAS抑制了PI3K/AKT/HIF-1α信号通路.

结论:

卡斯蒂辛 (CAS) 通过改善软骨损伤,证明了对膝关节骨关节炎 (KOA) 的治疗潜力.
CAS通过抑制PI3K/AKT/HIF-1α信号通路来发挥其保护作用.
CAS代表了一种有前途的治疗策略来管理KOA.

关键词:

造成软骨损伤的情况.在卡斯蒂辛 (Casticin) 这里.膝关节骨关节炎是一种关节炎.在PI3K/AKT/HIF-1α中.

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