Assessing the ability of Polysaccharides extracted from Date Palm Fruit to salvage Wistar rats from cisplatin-linked hepatic damage

Background Cisplatin is a platinum-based chemotherapeutic drug utilized in the treatment of many solid-tissue cancers; it is associated with several organ toxicities. For ages, Phoenix Dactylifera, known as the " large jujube " or " dà zǎo," in Chinese traditional medicine, has been employed for several medicinal applications. The present study assesses the role of Date Fruit Polysaccharides (DFP) in cisplatin-induced liver injury Method Rats were intraperitoneally treated with a single therapeutic dose of cisplatin (5 mg/kg body weight) and then orally treated daily with or without 50/100 mg/kg body weight of DFP for 7 successive days.The salvaging effects of DFP were assessed on Cisplatin-induced hepatic damage, by investigating the hepatic function markers, oxidative stress, and pro-inflammatory biomarkers, with histopathological assessment of the liver morphology by hematoxylin/eosin stain. To elucidate the contents, functional groups, and antioxidative potentials of DFP, chromatographic, spectroscopic, and in vitro antioxidative assays were analysed. Results Exposure to a single dose of cisplatin led to a considerable escalation in the tested hepatic function biomarkers (ALP and ALT), with an associated upsurge in levels/activities of malondialdehyde, cytokines, myeloperoxidase and a significant drop in the level of GSH (P < 0.05) in the liver as compared to the control. Moreover, there is also an obvious decline in antioxidant enzymes (catalase, SOD and GPx) activities. Contrarily, post-treatment with DFP significantly (P < 0.05) inhibited the heightened hepatic function markers, lipid peroxidation, inflammation, and oxidative stress dose-dependently. Analysis of chemical constituents, functional groups, and in vitro activities demonstrated important monosaccharides and antioxidative properties of DFP. Conclusion This study shows the ability of DFP to serve as a probable salvaging agent in hepatic damage associated with cisplatin treatment.