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This research aimed to examine the antioxidant polysaccharide activity (PsPc-3) derived from Pleurotus columbinus (P. columbinus) on oxidative renal injury (ORI) induced by cisplatin (CP). The principal components of crude polysaccharide were assessed. We studied the preventive impact of polysaccharide on cisplatin-induced renal damage in this study. For 21 days, we employed the CP-induced ORI rat model and divided the rats into four groups: control, CP alone, polysaccharide post CP (100 mg/kg) orally, and CP + polysaccharide (pre and post). The chemical characterization of the polysaccharide fraction PsPc-3 stated that protein was not present. PsPc-3 contained 7.2% uronic acid as assessed as 0% sulfate. PsPc-3 hydrolysate structured of Galacturonic:Glucose:Xylose and their molar proportions were 1:4:5, respectively. The average molecular weight (Mw) and molecular mass (Mn) per molecule of PsPc-3 were 5.49 × 104 g/mol and Mn of 4.95 × 104 g/mol respectively. DPPH radical scavenging activity was demonstrated by the polysaccharide of 65.21–95.51% at 10 mg/ml with IC50 less than 10 mg/ml. CP increased serum urea to 92.0 mg/dl and creatinine up to 1.0 mg/dl, with a concurrent decrease in the levels of total protein to 4.0 mg/dl. Besides, Also, CP-induced ORI raised levels of malondialdehyde (MDA), alkaline phosphatase (ALP), and renal hormones (renin and aldosterone), with a decline in antioxidants compared to control rats. In addition, in the presence of CP, interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) levels increased. PsPc-3 decreased these changes dramatically. PsPc-3 improves pathological renal damage caused by CP and decreases tubular apoptosis measured by DNA ladder formation and cleaved caspase- 3. These findings showed that PsPc-3 isolated from P. columbinus protects and inhibits tubular apoptosis in cisplatin-induced ORI. Furthermore, PsPc-3 has no influence on the anticancer efficacy of CP in rats. Thus, PsPc-3 derived from P. columbinus might provide a novel therapy method for cisplatin-induced nephrotoxicity. [ABSTRACT FROM AUTHOR]

Chemotherapeutic medications, including 5 – fluorouracil (5FU), are the same old technique to most cancers and are associated with numerous peripheral toxicities. We investigated exopolysaccharide (EPSST) produced from the isolated streptomycete of the Mediterranean Sea for the capability to lower the severity of mucositis in vivo. The streptomycete was isolated from Mediterranean Sea sediment from the beaches of Port Said Governorates, Egypt and identified morphologically, physiologically, and biochemically and confirmed by molecularly 16S rDNA analysis. The EPSST was extracted from the supernatant of streptomycete by using 4 volumes chilled ethanol and then the functional groups, MW, and chemical evaluation have been detected via Fourier-transform infrared (FTIR), and high-performance liquid chromatography (HPLC). In addition, antioxidant activity was measured through the usage of 2, 2-diphenyl-1-picrylhydrazyl (DPPH). Thirty-two male rats (180–200 g) were randomly divided into a control group (normal saline), intraperitoneal injection of 5-fluorouracil (5-FU, 150 mg/kg), normal rats were treated with EPSST and 5-FU + EPSST group. These groups were continued up to the day of sacrifice (28 days post treatments). The isolated strain became recognized based totally on 16S rDNA sequence as Streptomyce sp. with accession number SAMN08349905. The chemical evaluations of EPSST were galacturonic, glucose, galactose, mannose, and arabinose with a relative ratio of 2.1: 1: 5.37: 1.62: 1.29 individually, with an average molecular weight (Mw) 9.687 × 103 g/mol. Also, the EPSST contained uronic acid (16%) and sulfate (12.149%) and no protein was detected. EPSST inhibited the DPPH radical activity. The findings of this study propose that EPSST inhibits 5-FU-induced mucositis through adjustment of oxidative stress, apoptosis, inflammatory factors, activation of antioxidant enzymes. The clinical administration of EPSST may recover the chemotherapy-induced intestinal dysfunction, consequently increasing the clinical efficiency of chemotherapy. In addition, the administration of EPSST reduced 5-FU-induced histopathological incongruities such as neutrophil infiltration, loss of cellular integrity, and villus and crypt distortion. The clinical administration of EPSST may recover the chemotherapy-induced intestinal dysfunction, consequently increasing the clinical efficiency of chemotherapy. [ABSTRACT FROM AUTHOR]