Necroptosis and NLPR3 inflammasome activation mediated by ROS/JNK pathway participate in AlCl3-induced kidney damage

被引：9

作者：

Du, Jiayu ^{[1
]}

Zhang, Xuliang ^{[1
]}

Zhang, Jian ^{[1
]}

Huo, Siming ^{[1
]}

Li, Bo ^{[1
]}

Wang, Qi ^{[1
]}

Song, Miao ^{[1
]}

Shao, Bing ^{[1
]}

Li, Yanfei ^{[1
,2
]}

机构：

[1] Northeast Agr Univ, Coll Vet Med, Dept Heilongjiang Common Anim Dis Prevent & Treatm, Key Lab Prov Educ, Harbin 150030, Peoples R China

[2] Northeast Agr Univ, Coll Vet Med, 600 Changjiang Rd, Harbin 150030, Peoples R China

来源：

FOOD AND CHEMICAL TOXICOLOGY | 2023年 / 178卷

基金：

中国国家自然科学基金;

关键词：

Aluminum; ROS; JNK pathway; Necroptosis; NLRP3; inflammasome; Kidney damage; NLRP3; INFLAMMASOME; HISTOPATHOLOGICAL CHANGES; OXIDATIVE STRESS; ALUMINUM; APOPTOSIS; IDENTIFICATION; MECHANISMS; MITOPHAGY;

D O I：

10.1016/j.fct.2023.113915

中图分类号：

TS2 [食品工业];

学科分类号：

0832 ;

摘要：

Aluminum (Al) is a common environmental pollutant that can induce kidney damage. However, the mechanism is not clear. In the present study, to explored the exact mechanism of AlCl3-induced nephrotoxicity, C57BL/6 N male mice and HK-2 cells were used as experimental subjects. Our results showed that Al induced reactive ox-ygen species (ROS) overproduction, c-Jun N-terminal kinase (JNK) signaling activation, RIPK3-dependent nec-roptosis, NLRP3 inflammasome activation, and kidney damage. In addition, inhibiting JNK signaling could downregulate the protein expressions of necroptosis and NLRP3 inflammasome, thereby alleviating kidney damage. Meanwhile, clearing ROS effectively inhibited JNK signaling activation, which in turn inhibited nec-roptosis and NLRP3 inflammasome activation, ultimately alleviating kidney damage. In conclusion, these find-ings suggest that necroptosis and NLPR3 inflammasome activation mediated by ROS/JNK pathway participate in AlCl3-induced kidney damage.

引用

页数：12

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