在严重的急性胰腺炎中,m6A激活的BACH1通过表观遗传抑制HSPB1加剧铁亡
Fawei Zhou1,2, Dezhong Li2, Chang Liu3
1Department of Emergency, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Drug development research
|September 17, 2024
概括
严重的急性胰腺炎 (SAP) 涉及胰腺炎症. 过度表达BACH1通过抑制HSPB1而加剧SAP,促进铁和炎症. 减少BACH1提供了一个潜在的治疗策略.
科学领域:
- 生物化学 生物化学
- 分子生物学分子生物学
- 病理学 病理学 病理学
背景情况:
- 严重急性胰腺炎 (SAP) 是胰腺的严重炎症状况.
- 转录因子BACH1在SAP病原体中的作用尚不清楚.
- 氧化应激,细胞亡和细胞循环调节与BACH1活性有关.
研究的目的:
- 调查BACH1在严重急性胰腺炎的发病过程中的作用.
- 在SAP中阐明BACH1和热冲击蛋白B1 (HSPB1) 之间的调控关系.
- 在SAP模型中评估针对BACH1的治疗潜力.
主要方法:
- 在SAP患者,细胞和动物模型中分析BACH1和HSPB1表达.
- 在体外研究中,使用HPDE6-C7细胞进行了用皮素和LPS刺激.
- 在细胞和动物模型中进行BACH1耗尽和HSPB1联合抑制实验.
- 评估细胞存活率,氧化应激,铁亡和炎症标志物.
主要成果:
- 在SAP模型中,BACH1水平升高,而HSPB1表达减少.
- BACH1被确定为HSPB1的转录抑制剂.
- 在实验室中,BACH1 枯竭改善了细胞存活率,并减少了氧化应激,铁亡和炎症.
- 失去BACH1减弱了胰腺损伤,炎症和体内铁亡,通过HSPB1抑制逆转效应.
结论:
- 过度表达BACH1通过转录抑制HSPB1.1,加剧了SAP的进展.
- 这种抑制促进铁和炎症,导致胰腺损伤.
- 准BACH1-HSPB1轴为严重急性胰腺炎提供了潜在的治疗策略.
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Pancreatitis is inflammation of the pancreas, an organ located behind the stomach. It can be either acute or chronic.
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Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
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