P2X7受体对于在β-上腺素刺激后的ST36减弱心脏纤维化至关重要
Ting Zhang1, Jing Lv1, Zhong-Yue Liu2
1Acupuncture and Tuina School, Chengdu University of Traditional Chinese Medicine, 1166 Liutai Avenue, Wenjiang District, Chengdu, 611137, Sichuan Province, China.
Purinergic signalling
|April 27, 2024
概括
在Zusanli (ST36) 针点进行电针 (EA) 有效地降低了小鼠的异二烯素诱导的心脏纤维化和炎症. 这种效应是通过P2X7受体 (P2X7R) 的调节来调节的,P2X7R淘汰小鼠缺乏益处证明了这一点.
科学领域:
- 心血管研究研究心血管研究
- 炎症和免疫学 炎症和免疫学
- 整合和补充医学是整合和补充医学.
背景情况:
- P2X7受体 (P2X7R) 与炎症和纤维化有关.
- 苏珊利 (ST36) 电针 (EA) 在调节P2X7R对心脏保护的作用尚不清楚.
研究的目的:
- 通过调节P2X7R.ST36的EA是否可以抑制炎症和纤维化.
- 评估ST36EA在异上腺素诱导心脏损伤的小鼠模型中的治疗潜力.
主要方法:
- 异上被用于诱导野生型和P2X7R淘汰赛小鼠的心脏损伤.
- 在ST36.6应用了电 (EA) 刺激.
- 用组织学,生化和分子技术评估心脏纤维化,炎症,增高和P2X7R表达.
主要成果:
- 在ST36的EA显著降低了异上腺素诱导的心脏纤维化,缩和炎症.
- ST36 EA降低了P2X7R和NLRP3的表达,并降低了血清炎症细胞因子 (IL-1β,IL-6,IL-18).
- 在P2X7R淘汰赛小鼠中,ST36 EA的心脏保护作用被废除了.
结论:
- 在ST36的EA减弱了异上腺素诱导的心脏纤维化和炎症.
- P2X7受体 (P2X7R) 是这些保护作用的关键媒介.
- ST36 EA代表了治疗心脏纤维化和炎症的潜在治疗策略.
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