在急性-慢性肝衰竭损伤中发生类似PANoptosis的死亡
Qianling Ye1,2, Hanjing Wang1,2, Yue Chen1,2
1School of Traditional Chinese Medicine, Capital Medical University, Beijing, 100069, China.
Scientific reports
|January 3, 2024
概括
细胞死亡途径PANoptosis与急性至慢性肝衰竭 (ACLF) 有关. 这项研究证实了ACLF模型中的PANoptosis激活,并确定了关键蛋白质,表明它是肝脏疾病的治疗点.
科学领域:
- 细胞和分子生物学 细胞和分子生物学
- 肝病学 肝病学是一种肝病学.
- 免疫学 免疫学 免疫学
背景情况:
- 急性至慢性肝衰竭 (ACLF) 发病过程涉及多种细胞死亡形式,包括热亡,细胞亡和死亡,统称为PANoptosis.
- 在ACLF中PANoptosis的确切作用仍未得到充分研究,因此需要进一步研究其对肝损伤的贡献.
研究的目的:
- 研究PANoptosis作为受调节的细胞死亡途径在ACLF病变发生过程中的作用.
- 在ACLF模型中识别与PANoptosis相关的关键基因和蛋白质.
- 探索针对PANoptosis进行ACLF治疗干预的潜力.
主要方法:
- 生物信息分析以确定与ACLF中PANoptosis相关的差异表达基因.
- 关于PANoptosis和肝功能衰竭的研究的文献选.
- 建立碳四化物诱导的ACLF老鼠模型,使用D-银胺和脂多糖胺挑战.
- 在ACLF大鼠血清中检测炎症因素和PANoptosis相关蛋白质.
- 在体外实验中使用用TNF-α/INF-γ治疗的L02细胞进行实验.
主要成果:
- 生物信息分析揭示了ACLF中PANoptosis相关途径的上调调节,BAX被确定为一个关键的交叉基因.
- 在ACLF小鼠模型中,炎症因子 (IL-6,IL-18,TNFα,IFNγ) 和关键的PANoptosis蛋白 (NLRP3,CASP1,GSDMD,BAX,CASP8,CASP3,CASP7,MLKL) 显著释放.
- 结合TNF-α和INF-γ治疗在L02细胞中诱导了PANoptosis.
结论:
- PANoptosis积极参与ACLF的病变发生.
- 特定的PANoptosis相关分子和炎症性细胞因子在ACLF中显著改变.
- 向PANoptosis为ACLF治疗提供了一个有前途的治疗策略.
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