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在酒精性肝炎小鼠中通过BEX2基因沉默调节JNK/MAPK通路:对氧化应激的影响

Shuai Zhou¹, Hai Zhong², Yong Wang¹

¹Department of General Surgery, Anhui No. 2 Provincial People's Hospital, Anhui Medical University, Hefei, China.

Alcohol, clinical & experimental research

|October 21, 2023

概括

大脑表达的X链基因2 (BEX2) 在酒精性肝炎 (AH) 中被上调. 沉默BEX2可以减少肝损伤和炎症,这表明BEX2是AH的潜在治疗标.

科学领域:

肝病学肝病学是一种肝病学.
分子生物学分子生物学
基因表达分析基因表达分析

背景情况:

酒精性肝炎 (AH) 是一种严重的肝病,治疗选择有限.
大脑表达的X链基因2 (BEX2) 在AH中的作用还未得到充分研究.
调查BEX2在AH病变发生过程中的参与至关重要.

研究的目的:

探索BEX2对酒精性肝炎进展的影响.
阐明BEX2在AH中c-Jun NH2终端激酶/线原激活蛋白激酶 (JNK/MAPK) 途径中的作用.

主要方法:

利用基因表达综合数据集GSE28619用于AH的差异基因表达分析.
在AH的小鼠模型中采用免疫组织化学,TUNEL测定,西部斑块和流动细胞计.
评估了BEX2表达,氧化应激标志物,亡以及JNK/MAPK通路激活.

主要成果:

在酒精性肝炎中,BEX2表达显著升高.
BEX2基因沉默改善了抗氧化能力 (增加了GPx,SOD;减少了MDA).
BEX2沉默降低了JNK/MAPK通路激活,包括p-JNK,p-c-JUN和p-p38MAPK,并降低了亡.

结论:

BEX2的上调与酒精性肝炎的发病有关.
准BEX2可能为酒精性肝炎提供一种新的治疗策略.
BEX2通过JNK/MAPK信号通路影响AH的进展.

关键词:

在JNK/MAPK路径中.酒精性肝炎是一种酒精性肝炎.大脑表达的X链基因2 (BEX2)基因沉默是对基因进行沉默的方法.肝脏组织肝脏组织微阵列数据集是微阵列数据集.氧化应激是一种氧化应激.

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