Lentinan inhibits tumor necrosis factor α-ferritinophagy and antagonizes hepatic tissue ferroptosis in sodium arsenite-exposed mice
10.3969/j.issn.1671-7856.2025.01.004
- VernacularTitle:香菇多糖抑制TNFα-铁自噬拮抗亚砷酸钠染毒小鼠肝组织铁死亡
- Author:
Yuan YANG
1
;
Jiacheng BAO
;
Yekang DENG
;
Yang CHEN
;
Qin HE
Author Information
1. 广西环境暴露组学与全生命周期健康重点实验室,桂林医学院公共卫生学院,广西 桂林 541199;侗医药研究湖南省重点实验室,湖南医药学院民族医药研究中心,湖南 怀化 418000
- Publication Type:Journal Article
- Keywords:
sodium arsenite;
hepatotoxicity;
ferroptosis;
lentinan;
ferritinophagy
- From:
Chinese Journal of Comparative Medicine
2025;35(1):41-48
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the effect and mechanism of lentinan(LNT)on hepatic tissue ferroptosis in mice exposed to sodium arsenite(SA).Methods C57BL/6N male mice were exposed to SA low-dose,SA high-dose,and LNT intervention combined with SA high-dose,then,hematoxylin and eosin(HE)staining was applied to assess pathological liver tissue damage;Enzyme-linked immunosorbent and Western blot were used to detect the content or expression of tumor necrosis factor α(TNFα),interleukin-6(IL-6),ferritinophagy or ferroptosis biomarkers.Results Compared with the control group,SA exposure induced the elevated levels of TNFα,IL-6,ferritinophagy biomarker ferritin heavy chain 1(FTH1)and microtubule-associated protein 1 light chain 3B(MAP1LC3B)in mice liver tissue,while levels the ferroptosis biomarker GPX4 decreased(P＜0.05).Compared with SA high-dose groups,LNT intervention showed the reduced pathological liver damage and the downregulated levels of TNFα,IL-6,FTH1,and MAP1LC3B,while the level of GPX4 upregulated(P＜0.05).Western blot experiment showed that LNT intervention antagonized the upregulated levels of FTH1,and autophagy biomarker LC3B/A,and antagonized the increased co-expressions of FTH1 with LC3B or Ub protein in SA high-dose group(P＜0.05).Conclusions LNT antagonizes SA-exposed hepatic pathological injury and ferroptosis in mice,possibly associated with inhibition of TNFα-ferritinophagy signaling.
