The present study was done to evaluate the protective and therapeutic role of mango pulp (M), eprosartan drug (E), and their co-administration (EM) against hepatotoxicity induced by thioacetamide (T). Seven groups of rats were prepared as follows: the control (C) group (normal rats), T group (the rats were injected with T), T-M group (the rats were injected with T, and then treated with M), T-E group (the rats were injected with T, and then treated with E), T-EM group (the rats were injected with T, and then treated with E and M), M-TM-M group (the rats were administered with M before, during, and after T injection), and M group (the healthy rats were administered with M only). Firstly, the characterizations of M were determined. Also, the markers of hepatic oxidative stress [malondialdehyde (MDA) and glutathione (GSH) levels and the activities of superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione reductase (GSR)], inflammation and fibrosis [(tumor necrosis factor-α (TNF-α) and platelet-derived growth factor-BB (PDGF-BB) levels and gene expression of transforming growth factor-beta1(TGF-β1)], and liver functions and microscopic examination were evaluated. The present results revealed that M contains 419 ± 1.04 μg total phenolics as gallic acid equivalent and 6.8 ± 0.05 μg total flavonoids as quercetin equivalent. The analysis of phenolics and flavonoids showed the presence of chlorogenic, caffeic, 2,5-dihydroxy benzoic, 3,5-dicaffeoylquinic, 4,5-dicaffeoylquinic, tannic, cinnamic acidS, and catechin, phloridzin, and quercetin with different concentrations. Also, M contains various minerals with different concentrations involving potassium, calcium, magnesium, sodium, iron, copper, zinc, and manganese. The current results showed that the total antioxidant capacity of 1 g of M was 117.2 ± 1.16 as μg ascorbic acid equivalent. Our biochemical studies showed that all treatments significantly reduced T-induced hepatotoxicity and liver injuries, as the oxidative stress and inflammatory and fibrotic markers were diminished where MDA level and the activities of GST, GSSG, and GR were decreased when compared with T group. In contrast, GSH level and the activities of SOD and GPx and GSH/GSSG ratio were increased. In addition, TNF-α and PDGF-BB levels were reduced, and the gene expression of TGF-β1 was down-regulated. Consequently, the liver functions were significantly improved. In conclusion, each E, M, and EM has a therapeutic effect against T-induced hepatotoxicity via the reduction of the OS, inflammation, and fibrosis. Unfortunately, treatment with M and E simultaneously revealed the less effectiveness than the treatment with M or E demonstrates the presence of anti-synergistic effect between them. Additionally, M-TM-M treatment showed a better effect than T-M treatment against T-induced hepatotoxicity revealing the prophylactic role of M. The administration of healthy rats with M for 12 weeks has no side effect. Graphical abstract
Background: Digestive cancer is among the major causes of mortality and morbidity worldwide. Rutin, a bioactive secondary metabolite belonging to flavonoids and distributed in many fruits and vegetables has shown anti-proliferative, anti-cancer, and neuroprotective activities. In this study, the antiproliferative, antioxidant and apoptotic activities of rutin on hepatic and pancreatic cancer cell lines were investigated. Materials and Methods: The effect on cellular viability was monitored by SRB assay. Increasing activity of caspases (3/7) was used as an indicator of apoptosis. Additionally, the anti-inflammatory and antioxidant activities of rutin were evaluated after measuring amount of prostaglandin E2 (PGE2) produced and through DPPH free radical scavenging assays, respectively. Moreover, the inhibitory effect on both CYP3A4 and GST enzymes has also been evaluated. Results: According to the data presented here, rutin has anti-proliferative effect and raises the number of caspases 3/7 in investigated cell lines. Conclusion: HepG-2 cells showed the highest cellular growth inhibition, followed by BxPC-3, Huh-7, MiaPaCa-2, Suit-2, and the normal cell line HPDE. Rutin also inhibited the cyctochrome P450 enzyme (CYP450 3A4) and glutatihione-S-transferase activity, with dose-dependent inhibition. Furthermore, suppression of PGE2 synthesis in BxPC-3 cells supported rutin's anti-inflammatory action (high COX-2 expression).
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