Ferulic acid attenuated diethylnitrosamine-provoked hepato-renal damage and malfunction by suppressing oxidative stress, abating inflammation and upregulating nuclear factor erythroid related factor-2 signaling

Sawie, Hussein G.; Ahmed, Osama M.; Shabana, Marwa E.; Elqattan, Ghada M.; EL-Kassaby, Mahitab I.; Abou- Seif, Howida S.

Ferulic acid attenuated diethylnitrosamine-provoked hepato-renal damage and malfunction by suppressing oxidative stress, abating inflammation and upregulating nuclear factor erythroid related factor-2 signaling

Authors

Abstract

Background
Diethylnitrosamine (DEN) is a potent environmental toxin that can reach humans through the food chain. It induces proliferative, degenerative and cancerous lesions in the liver and kidneys.
Objective
The principal goal of the existing research was to assess the preventive impacts of ferulic acid (FA) versus DEN- provoked hepato-renal damage and malfunction.
Materials and methods
Adult male rats were divided into four groups: group 1 (normal control) animals orally received saline every day for 14 weeks; group 2 (DEN) animals intraperitoneally received DEN (150 mg/kg twice a week) for 2 weeks; group 3 (DEN + FA) animals were injected intraperitoneally twice a week with DEN for 2 weeks besides to oral administration of FA (100 mg/kg/day) for 14 weeks; group 4 (FA) animals were given a similar dose of FA for a similar period.
Results
The results revealed that FA treatment reversed the DEN-mediated elevation in serum values of the liver enzymes activities as well as urea and creatinine levels; it also augmented the hepato-renal antioxidant system that overcame DEN-induced oxidative stress deteriorations. Moreover, FA markedly reduced the DEN-induced elevated hepato-renal levels of immuno-inflammatory markers (IL-1β and TNF-α) as well as downregulated the inflammatory mediators (Bcl-2, NF-κB, and nuclear factor erythroid related factor-2 (Nrf-2)), reflecting its protective potential.
Conclusion
The existing results elucidate that ferulic acid could prevent and ameliorate DEN-induced hepato-renal toxicological changes and can restore livers and kidneys’ functions; this effect could be mechanized through activation of anti-inflammatory and antioxidant systems, as well as regulation of NF-κB, Bcl2, and nuclear factor erythroid related factor-2 expression.

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