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素通过调节热和ROS参与Nrf2激活来缓解LPS诱导的骨解

Zhijuan Liu¹, Yijie Gao¹, Xiaoliang Feng¹

¹Collaborative Innovation Centre of Regenerative Medicine and Medical BioResource Development and Application Co-constructed by the Province and Ministry, Guangxi Medical University, Nanning, Guangxi, China; Guangxi Key Laboratory of Regenerative Medicine, Orthopaedics Trauma and Hand Surgery, the First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

|June 20, 2024

概括

热原素 (HG) 通过激活Nrf2,减少活性氧化物种 (ROS),并抑制热和骨质结晶生成来缓解炎症性骨解. 这表明HG是炎症性骨损失的潜在治疗方法.

科学领域:

生物化学生物化学
免疫学免疫学免疫学
药理学药理学是指药理学的学科.

背景情况:

反应性氧化物种 (ROS) 驱动热和炎症性骨解.
素 (HG) 具有抗炎和抗氧化性质,但其在炎症性骨解中的作用尚不清楚.

研究的目的:

在体外和体内研究HG在热的机制及其对炎症性骨解的治疗作用.
探索HG对骨质细胞形成和相关信号通路的影响.

主要方法:

在体外:细胞毒性,TRAcP染色,骨再吸收试验,RNA测序,RT-qPCR,西部斑,免疫光学,ELISA.
在体内:脂聚糖 (LPS) 诱导骨解的小鼠模型,微型CT,组织学检查.
Nrf2 抑制剂 (ML385) 用于确认途径的参与.

主要成果:

HG抑制了RANKL诱导的骨质细胞分化,骨再吸收,NFATc1活性和下游因素.
HG调节了炎症反应和巨细胞两极分化,抑制了骨质细胞生成.
HG抑制了NF-κB通路,禁用了NLRP3炎症体,并激活了Nrf2以减少ROS.
HG的NLRP3炎症酶抑制被ML385.5逆转.
在体内,HG通过抑制骨质结晶发生和炎症来保护LPS诱导的骨解.

结论:

HG激活了Nrf2,减少了ROS,抑制了NLRP3炎症酶和热,抑制了骨质细胞形成.
HG在体内减轻炎症性骨解,表明其作为治疗剂的潜力.

关键词:

这就是HECOGENININ.在NLRP3炎症酶体中,NLRP3炎症 Nrf2 没有任何问题.骨质结晶体骨质结晶体是一个骨质溶解是一种骨质分解.这就是ROSOS ROS.

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