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激素脱乙酶HDAC8的高表达抑制了死角性肠球炎中阿尔金因-林代谢的发生

Ting Guo¹, Shaohua Hu², Weijue Xu¹

¹Department of General Surgery, Shanghai Children's Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai 200040, China.

|June 1, 2023

概括

希斯脱乙酶8 (HDAC8) 在死性肠球炎 (NEC) 中表观遗传调节氨酸代谢. 抑制HDAC8通过调节组织素乙化和微生物代谢物水平来改善NEC.

科学领域:

胃肠病学胃肠病学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
代谢学代谢学代谢学

背景情况:

死性肠球炎 (NEC) 是新生儿严重的胃肠道疾病.
表观遗传修饰,包括基因组乙化,都与NEC病变产生有关.

研究的目的:

为了研究基因素脱乙酶8 (HDAC8) 在NEC期间调节阿尔金因代谢中的作用.
探索HDAC8抑制对NEC发育和相关代谢变化的影响.

主要方法:

在人类和小鼠NEC样本中分析HDAC8表达.
在NEC的小鼠模型中选择性抑制HDAC8.
在基因促进子区域中评估基因素3氨酸9乙化 (乙-H3K9).
测量氨基酸和短链脂肪酸度.
微生物群组成分析 (Firmicutes/Bacteroidetes的比率).

主要成果:

在NEC中,HDAC8被上调,其抑制改善了这种情况.
在PRODH/PRODH2促进体中,HDAC8介导的乙-H3K9调节,影响氨酸代谢.
黄油酸降低与HDAC8和氨酸升高相关,与改变的肠道微生物群有关.

结论:

在NEC中,HDAC8通过表观遗传调节,在协调氨酸代谢方面发挥着至关重要的作用.
针对HDAC8为NEC提供了一个潜在的治疗策略.
微生物代谢物和HDAC8相互作用在NEC病变发生过程中至关重要.

关键词:

生物科学生物科学遗传学是一个遗传学.分子遗传学分子遗传学分子生物学分子生物学

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