Role of TIPE2 in endogenous protective mechanism against acute lung injury in septic mice: relationship with ferroptosis
10.3760/cma.j.cn131073-20241012-00814
- VernacularTitle:TIPE2在脓毒症小鼠ALI内源性保护机制中的作用：与铁死亡的关系
- Author:
Yuxuan WANG
1
;
Qian WANG
1
;
Jingxue QIN
1
;
Xue CHEN
1
;
Zihan LEI
1
;
Xiaojing WU
1
Author Information
1. 湖北省人民医院（武汉大学第一临床学院）麻醉科，武汉 430060
- Publication Type:Journal Article
- Keywords:
Sepsis;
Acute lung injury;
Ferroptosis;
TIPE2
- From:
Chinese Journal of Anesthesiology
2025;45(8):998-1001
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To evaluate the role of tumor necrosis factor-α-induced protein 8-like molecule-2 (TIPE2) in the endogenous protective mechanism against acute lung injury in septic mice and the relationship with ferroptosis.Methods:Twenty SPF healthy wild-type male C57BL/6N mice and 20 TIPE2 gene knockout C57BL/6N mice, aged 6-8 weeks, weighing 20-25 g, were assigned to wild-type sham operation group (WT-Sham group), wild-type sepsis group (WT-SEP group), TIPE2 knockout sham operation group (KO-Sham group), and TIPE2 knockout sepsis group (KO-SEP group) using a random number table method, with 10 mice in each group. Acute lung injury was induced by cecal ligation and perforation in anesthetized mice. The animals were sacrificed after anesthesia at 24 h after operation and lung tissues were obtained for examination of the morphological results of lung tissues (with a light microscope) and for determination of wet to dry lung weight (W/D) ratio, contents of ferrous ions (Fe 2+ ), glutathione (GSH) and malondialdehyde (MDA) and expression of solute carrier family 7 member 11 (SLC7A11), glutathione peroxidase 4 (GPX4) and Acyl-CoA synthetase long-chain family member 4 (ACSL4) (by Western blot). Results:Compared with WT-Sham group, the lung injury score, W/D ratio and contents of Fe 2+ and MDA were significantly increased, the content of GSH was decreased, the expression of GPX4 and SLC7A11 was down-regulated, and the expression of ACSL4 was up-regulated in WT-SEP group ( P<0.05). Compared with WT-SEP group, the lung injury score, W/D ratio and contents of Fe 2+ and MDA were significantly increased, the content of GSH was decreased, the expression of GPX4 and SLC7A11 was down-regulated, and the expression of ACSL4 was up-regulated in KO-SEP group ( P<0.05). Conclusions:TIPE2 is involved in the endogenous protective mechanism against acute lung injury, which may be related to the inhibition of ferroptosis in lung tissues of septic mice.
