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Kirenol Exhibits the Protective Role against N-Methyl-N-Nitrosourea-Induced Gastric Cancer in Rats via Modulating the Oxidative Stress and Inflammatory Markers.

BACKGROUND
Gastric cancer (GC) may arise in any region of the stomach. Poorly diagnosed GC results in almost one million mortalities annually worldwide. Kirenol is a bioactive compound present in the Sieges beckia sps.


OBJECTIVE
In this current, we investigate the anticancer capacity of kirenol against the MNG-stimulated GC in rats via modulating the antioxidants status and inhibition of NF-κB cascade.


METHODOLOGY
GC was provoked in the rats via supplementing 100 mg/kg of MNU through the intragastric route for 16 weeks concomitantly with 30 mg/kg of kirenol treatment. The body weight, tumor volume, and incidence of all animals were tabulated every week. The status of gastrin, ALP, LDH, and γ-GT was studied through the ELISA tests. The lipid peroxidation, enzymatic, and nonenzymatic antioxidants were determined via standard procedures. Expression of thioredoxin, glutaredoxin, NF-κB, TNF-α, IL-6, PGE2 was studied through RT-PCR. The gastric mucosa was analyzed microscopically.


RESULTS
Kirenol treatment appreciably improved the body weight and diminished the tumor volume and incidences in the MNG-challenged rats. The lipid peroxidation was diminished and the enzymatic and non-enzymatic antioxidants were improved by the kirenol treatment. Kirenol suppressed the status of serum markers of GC and gastrin, ALP, LDH, and γ-GT. The mRNA expression of thioredoxin, glutaredoxin, NF-κB, TNF-α, IL-6, PGE2 was downregulated via the kirenol in the MNG-challenged rats. Histopathological analysis result also confirmed the therapeutic role of kirenol.


CONCLUSION
These findings proved that the kirenol appreciably prevented the MNG-triggered GC in rats and it may become a potential drug for the GC treatment in the future.