Asiaticoside protects against lung injury induced by intestinal ischemia/reperfusion via the upregulation of FoxM1.

Autor: Zheng M; Department of Gastroenterology Surgery, Central Hospital of Dalian University of Technology (Dalian Municipal Central Hospital), Dalian 116033, China; Department of Graduate School, Dalian Medical University, Dalian 116044, China., Wang Y; Department of Gastroenterology Surgery, Central Hospital of Dalian University of Technology (Dalian Municipal Central Hospital), Dalian 116033, China; Department of Graduate School, Dalian Medical University, Dalian 116044, China., Wang P; Department of Gastroenterology Surgery, Central Hospital of Dalian University of Technology (Dalian Municipal Central Hospital), Dalian 116033, China; Department of Graduate School, Dalian Medical University, Dalian 116044, China., Tan X; Department of Pancreas and Thyroid Ward, China Medical University, Shenyang 110136, China., Chen H; Department of General Surgery, The First Affiliated Hospital of Dalian Medical University, Dalian 116000, China., Zhang X; Department of Gastroenterology Surgery, Central Hospital of Dalian University of Technology (Dalian Municipal Central Hospital), Dalian 116033, China., Zu G; Department of Gastroenterology Surgery, Central Hospital of Dalian University of Technology (Dalian Municipal Central Hospital), Dalian 116033, China. Electronic address: zuguodl@dlut.edu.cn.
Jazyk: angličtina
Zdroj: International immunopharmacology [Int Immunopharmacol] 2024 Dec 25; Vol. 143 (Pt 2), pp. 113405. Date of Electronic Publication: 2024 Oct 20.
DOI: 10.1016/j.intimp.2024.113405
Abstrakt: Systemic inflammatory response syndrome and respiratory distress syndrome can be induced by lung injury caused by intestinal ischemia/reperfusion (II/R). There is no effective medical treatment for II/R-induced lung injury. Studies have shown that asiaticoside (AS) protects against lung injury and ischemia/reperfusion injury in several organs. We established a rat II/R damage model and collected lung tissue. Six groups (n = 10) were created: (1) the sham group; (2) the II/R group; (3) the II/R + AS (40) group; (4) the II/R + AS (80) group; (5) the II/R + TST group; and (6) the II/R + AS + TST group. To assess the degree of lung damage induced by II/R, we also evaluated HE staining, the wet/dry ratio, oxidative stress, inflammation and apoptosis in the lung tissues. Our results indicated that the severity of lung injury score, wet/dry ratio, oxidative stress, inflammatory factor expression and amount of apoptosis were greater in the II/R-induced lung injury group than in the sham group. Furthermore, when AS was administered, lung injury, oxidative stress, inflammation and amount of apoptosis in the lung tissues were obviously lower than those in the II/R group. Additionally, compared with that in the sham group, the expression of FoxM1 in the lung tissue in the II/R group was significantly greater, and FoxM1 expression in the lung tissue was significantly greater following AS administration. Compared with the AS alone, the administration of thiostrepton (a FoxM1 inhibitor) and AS exacerbated the lung damage induced by II/R. According to our research, AS prevents the lung damage induced by II/R by reducing oxidative stress, inflammation and apoptosis by activating FoxM1 expression.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier B.V. All rights reserved.)
Databáze: MEDLINE
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