赛尔图因4通过调节HIF-1α/HO-1介导的铁灭症来缓解严重的急性胰腺炎
Yanna Liu1,2,3, Huning Cui1,2,3,4, Chaopeng Mei1,2,3,4
1Department of Emergency, The First Affiliated Hospital of Zhengzhou University, No 1 Eastern Jianshe Road, Zhengzhou, 450052, Henan, China.
Cell death & disease
|October 21, 2023
概括
赛尔图因4 (SIRT4) 通过抑制铁亡来预防严重的急性胰腺炎 (SAP). 较低的SIRT4水平会使胰腺炎恶化,而增加SIRT4表达则提供保护.
科学领域:
- 胃肠病学 胃肠病学
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
背景情况:
- 严重急性胰腺炎 (SAP) 是一种危及生命的疾病,死亡率高.
- Sirtuin4 (SIRT4) 涉及炎症和氧化应激,但其在SAP中的作用尚不清楚.
研究的目的:
- 调查SIRT4在严重急性胰腺炎 (SAP) 病变发生中的作用.
- 阐明SIRT4影响SAP进展的分子机制.
主要方法:
- 在公共数据库中选人类AP中的SIRT4表达.
- 使用L-氨酸诱导SIRT4淘汰和过度表达的小鼠模型中的SAP.
- 评估胰腺,肺和脏组织损伤.
- 测量抗氧化因子 (GSH,SOD) 和脂质过氧化标志物.
- 分析低氧诱导因子-1α (HIF-1α) 和与铁亡相关的蛋白质的表达.
主要成果:
- 人类AP中SIRT4表达的下调.
- 在SIRT4淘汰的小鼠中,SAP,肺和损伤加剧.
- 在SAP模型中,SIRT4过度表达显著减少了损伤.
- SIRT4调节的抗氧化剂水平和氧化应激标志物.
- SIRT4调节HIF-1α和HIF-1α/HO-1通路,影响铁亡.
结论:
- 在严重的急性胰腺炎中,SIRT4起着保护作用.
- 通过HIF-1α/HO-1通路抑制铁亡,SIRT4可以缓解SAP.
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