Lactoferrin mitigates ethanol-induced gastric ulcer via modulation of ROS/ICAM-1/Nrf2 signaling pathway in Wistar rats

乳铁蛋白通过调节 ROS/ICAM-1/Nrf2 信号通路减轻 Wistar 大鼠乙醇诱发的胃溃疡

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作者:Gihan F Asaad, Rasha E Mostafa

Conclusion

Our current study is the first to study the antiulcer effect of LF via its potential modulatory effects on the ROS/ICAM-1/Nrf2 signaling pathway. Moreover, we concluded that pretreatment with LF100 & 300 mitigated the ethanol-induced gastric ulcer via modulation of both oxidative stress and inflammatory responses.

Methods

Rats were randomly allocated into 4 groups: control, ethanol, ethanol+LF100, and ethanol+LF300. LF100 & 300 were given 15 days before ulcer induction. At the end of the experiment, the gastric mucosa was examined macroscopically and microscopically.

Results

The ethanol group showed damage and degeneration of the stomach mucosa in addition to elevation of oxidative and inflammatory biomarkers. LF showed explicit healing of the gastric mucosal damage. LF reduced gastric malondialdehyde (MDA), tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β), myeloperoxidase (MPO), and intracellular adhesion molecule-1 (ICAM-1). On the other hand, LF elevated the depleted reduced glutathione (GSH) and Nuclear factor-erythroid factor 2 (Nrf2).

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