相关实验视频

Updated: Jun 29, 2025

Histological Analyses of Acute Alcoholic Liver Injury in Zebrafish

Histological Analyses of Acute Alcoholic Liver Injury in Zebrafish

Published on: May 25, 2017

删除混合血统激酶域像伪激酶加剧慢性酒精诱导的肝损伤通过增加亡

Keon Hwi Im¹, Waqar Khalid Saeed², Eun Bin Kim³

¹Department of Translational Medicine, Graduate School of Biomedical Science and Engineering, Hanyang University, 222 Wangsimni-Ro, Seongdong-Gu, Seoul, Republic of Korea.

Digestive diseases and sciences

|March 29, 2024

概括

混合血统激酶域像伪激酶 (MLKL) 删除恶化了酒精诱导的肝损伤和小鼠脂肪通过增加肝细胞亡,尽管MLKL.

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
免疫学免疫学免疫学

背景情况:

混合基因酶域,如伪基因酶 (MLKL),因其在非酒精性脂肪肝疾病 (NAFLD) 中通过抑制亡而发挥保护作用而得到认可.
在酒精性肝病 (ALD) 的背景下,MLKL的特定功能仍然在很大程度上未被描述.

研究的目的:

调查MLKL在酒精性肝病 (ALD) 病原发生中的作用.
为了确定MLKL缺乏是否会影响ALD的小鼠模型中的肝损伤,炎症和脂肪.

主要方法:

在C57BL/6N野生型 (WT) 和MLKL-Knockout (KO) 小鼠中,长期食乙醇 (EtOH) 进行了长达8周的时间.
评估了死亡率,肝炎,肥胖症和肝细胞亡.
进行了批量mRNA转录组分析,以确定差异表达的基因和途径.

主要成果:

与WT小鼠相比,在8周的EtOH养后,MLKL淘汰赛小鼠的生存率显著下降.
肝硬化和炎症在MLKLKO小鼠中在4周和8周的EtOH暴露后加剧.
转录组分析揭示了EtOH养MLKLKO小鼠的高调脂肪酸合成,脂质生成,线粒体和亡相关途径,肝细胞亡增加.

结论:

除去MLKL不会保护慢性酒精诱导的肝损伤独立于亡.
缺乏MLKL会在ALD中加剧肝硬化和肝损伤,主要是通过增加肝细胞亡.

更多相关视频

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Mechanism of Kemeng Fang's Inhibition of Podocyte Apoptosis in Rats with Membranous Nephropathy through the PI3K/AKT Signaling Pathway

Published on: August 23, 2024

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen

Published on: November 27, 2019

相关概念视频

The Intrinsic Apoptotic Pathway

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

Abnormal Proliferation

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...