向Src同质酸酶2通过减弱ERK/NF-κB通路介导的脏炎症来改善小鼠糖尿病脏病
Che Yu1,2,3, Zhuo Li1, Cuili Nie4
1Department of Nephrology, Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Cell communication and signaling : CCS
|December 19, 2023
概括
抑制SHP2 (Src同质酸酶2) 降低了糖尿病病 (DN) 中的炎. 这项研究强调了SHP2作为DN治疗的潜在治疗标.
科学领域:
- 生物化学 生物化学
- 免疫学 免疫学 免疫学
- 病理生理学 病理生理学
背景情况:
- 糖尿病病 (DN) 涉及显著的炎.
- 在DN病变发生过程中,Src同质酸酶2 (SHP2) 的作用尚不清楚.
- SHP2与糖尿病相关的炎症有关.
研究的目的:
- 研究SHP2在DN中的作用和分子机制.
- 评估DN中SHP2抑制的治疗潜力.
主要方法:
- 在DN患者和db/db小鼠中评估了SHP2活性.
- 在db/db小鼠和HK-2细胞中使用SHP2抑制剂PHPS1.
- 研究了PHPS1对炎症标志物和ERK/NF-κB通路的影响.
- 利用ERK特异性抑制剂来确认途径的参与.
主要成果:
- 在DN患者和db/db小鼠中,SHP2活性升高.
- 在db/db小鼠中,PHPS1治疗减少了炎并减轻了DN.
- PHPS1抑制了高葡萄糖诱导的炎症和HK-2细胞中的ERK/NF-κB激活.
- 在体内和体外,SHP2抑制抑制了ERK/NF-κB通路.
- 在DN患者中,SHP2活性与ERK/NF-κB激活具有正相关性.
结论:
- 在糖尿病病中,SHP2活性被上调.
- 用PHPS1抑制SHP2的药理抑制通过抑制ERK/NF-κB通路来改善DN.
- SHP2代表了DN治疗的潜在治疗标.
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