article · Scientific Reports
Cancer burdens continue to rise globally, prompting ongoing searches for effective therapeutic compounds. Investigating mouse models bearing Ehrlich ascites carcinoma reveals that combining the natural compound amygdalin with the standard anticancer drug sorafenib enhances antitumour activity while reducing tumour-induced liver damage. Swiss albino mice receiving both oral amygdalin and intraperitoneal sorafenib experienced marked reductions in tumour volume and viable cancer cell counts, alongside an increase in dead tumour cells. In addition, the combination treatment restored normal liver function markers and improved hepatic tissue structure. Biochemical analyses demonstrated reduced oxidative stress markers alongside enhanced antioxidant levels. Genetic evaluations confirmed the upregulation of the protective Nrf2 gene and the suppression of genes linked to cell migration and blood vessel growth, specifically MMP9 and VEGF. Together, these animal findings demonstrate that amygdalin augments sorafenib therapy and helps shield hepatic tissues from tumour-related injury.
Many cancer treatments face limitations due to severe toxicity and tissue damage, particularly affecting the liver. Demonstrating that a supplementary compound like amygdalin can simultaneously boost the anticancer performance of standard drugs like sorafenib and protect vital organs offers insight into potential combination strategies for managing tumours and mitigating treatment-related complications.
This research points toward potential adjuvant therapeutics for oncology, particularly formulations combining amygdalin with established antitumour agents to protect the liver during therapy. The primary beneficiaries could include pharmaceutical developers exploring combination therapies for cancer care. However, because this work remains at the preclinical stage in animal models, significant clinical testing and validation will be required before any commercial application or clinical translation can occur.
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The burden of cancer diseases is increasing every year, therefore, the demands to figure out novel drugs that can retain antitumor properties have been raised. This study aimed to investigate the anti-tumor properties of amygdalin (Amy) against Ehrlich ascites carcinoma (EAC) bearing mice and its protective properties against liver damage. Amy and the standard anticancer drug Sorafenib (Sor) were given alone or in combination to Swiss albino female mice that had been injected with EAC cells. Biochemical parameters of liver function (AST, ALT, GGT, total protein, albumin), tumor volume, oxidative stress [malondialdehyde, (MDA)] and antioxidative [superoxide dismutase (SOD), and reduced glutathione (GSH)] markers were measured. The hepatic expression of the antioxidant-related gene [nuclear factor erythroid-2-related factor 2 (Nrf2)], the migration-related gene [matrix metalloprotease 9 (MMP9)], and the angiogenesis-related gene [vascular endothelial growth factor (VEGF)] were evaluated by qPCR. The results revealed that EAC-bearing mice treated with Amy and/or Sor showed a decrease in the tumor burden and hepatic damage as evidenced by (1) decreased tumor volume, number of viable tumor cells; (2) increased number of dead tumor cells; (3) restored the liver function parameters; (4) reduced hepatic MDA levels; (5) enhanced hepatic GSH and SOD levels; (6) upregulated expression of Nrf2; (7) downregulated expression of MMP9 and VEGF, and (8) improved hepatic structure. Among all treatments, mice co-treated with Amy (orally) and Sor (intraperitoneally) showed the best effect. With these results, we concluded that the Amy improved the antitumor effect of Sor and had a protective role on liver damage induced by EAC in mice.
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DOI: 10.1038/s41598-022-10517-0
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