Can idebenone protect gastric tissue against oxidative stress, inflammation, and necrosis?

This study aims to investigate the antiulcer effects of Idebenone (IDE) in Wistar rats with indomethacininduced gastric ulcer and compare its effectiveness with famotidine (FAM). 36 rats were randomly divided into six groups: healthy; healthy+IDE200; ulcer (U); U+FAM; U+IDE100; U+IDE200. Six hours after the administration of 25 mg/kg of indomethacin, the antiulcer effects of FAM (40 mg/kg) and two different doses of IDE (100 and 200 mg/kg) in the gastric tissue of rats were examined through macroscopic, biochemical, molecular, and histopathological analyses. Comparative assessments were conducted between the healthy control group and the group treated with indomethacin alone. IDE effectively suppressed the indomethacin-induced increase in malondialdehyde (MDA) and mitigated the reduction in glutathione (GSH) levels. Furthermore, IDE treatment led to a significant decrease in mRNA expressions of interleukin 1 beta (IL-1(3), tumor necrosis factor-alpha (TNF-alpha), and nuclear factor kappa beta (NF-kappa B)-p65 in ulcerative rats. Histopathological examinations revealed that both IDE doses improved the ulcer damage caused by indomethacin in the rats' stomach tissues. This study demonstrates that IDE administration exhibits a protective effect against indomethacin-induced gastric ulcers by reducing oxidative stress and inflammatory processes. IDE's potential to prevent ulcer formation in the gastric tissue of rats suggests that it could be a valuable therapeutic agent in clinical practice.

Journal

BRAZILIAN JOURNAL OF PHARMACEUTICAL SCIENCES

Year

2025

Volume

61

ISSN

1984-8250

eISSN

2175-9790

DOI

10.1590/s2175-97902025e24246

WoS UID

WOS:001673026500001