Corilagin induces apoptosis and inhibits HMBG1/PI3K/AKT signaling pathways in a rat model of gastric carcinogenesis induced by methylnitronitrosoguanidine

Gastric cancer, invasive cancer of the gastrointestinal tract, found in developing countries. Chemotherapy to patients with advanced gastric cancer, exhibits greater drug resistance to standard chemotherapy drugs. Therefore, important to establish anti-cancer drugs that are successful for cancer therapy. Corilagin is a natural ellagitannin (ET) with profound pharmacological properties has been used for the study to assess its anticancer effects against N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) stimulated gastric cancer rats. Biochemical studies showed Thiobarbituric acid reactive substances (TBARS) and enzymatic and non-enzymatic antioxidants increased in corilagin treated animals compared with controls. Histopathologic evaluation revealed corilagin treated rats showed cell morphology similar that control showing its ameliorating effects. In corillagen treament mRNA protein expression levels of HIF-1 alpha, AKT, PI3K, CT4, CD147 and HMGB1 were drastically lowered transcription factors triggering gastric cancer. In Western blot analysis showed released higher apoptotic marker of caspase-3, -9, Bax while Bcl-2 levels were significantly reduced confirming that corilagin triggers apoptosis in gastric cancer.

Automated summary

Corilagin exhibits significant anticancer effects in gastric cancer treatment by increasing antioxidants levels, improving cell morphology, and reducing the expression of transcription factors, ultimately inducing apoptosis in gastric cancer cells.