Protective Effect of Polyethylene Glycol (PEG) 3350 on a Cisplatin-Induced Rat Model of Neuropathy

Abstract

Background and Objective: Peripheral neuropathy is the most important side effect, leading to a decrease in the dose of cisplatin or its complete cessation in the early period. For this purpose, the study aimed to investigate the therapeutic potential of PEG in cisplatin-induced neuropathy and to measure the levels of MDA, GSH, IL-6 and TNF-alpha, which are key markers of lipid peroxidation and antioxidant capacity. Materials and Methods: Cisplatin was given to 16 rats twice a week for 4 weeks at a rate of 2.5 mg/kg/day. Cisplatin-treated rats were split into two groups. For 4 weeks, the rats in Group 1 (n = 8) received 1 mL/kg/day of 0.9% NaCl intraperitoneally, while the rats in Group 2 received 30 mg/kg/day of PEG. The control group consisted of the eight surviving rat specimens. The motor abilities of all the animals were assessed after the research. Blood samples were collected for the measurement of plasma lipid peroxidation malondialdehyde (MDA), Tumour Necrosis Factor (TNF-alpha), glutathione (GSH) and IL-6 levels. Results: Electromyography findings revealed that compound muscle action potential (CMAP) amplitude was significantly higher in the cisplatin-PEG group than in the cisplatin-saline group. Also, cisplatin-PEG treated group showed significantly lower TNF-alpha, MDA and IL-6 levels and hig her GSH levels than the cisplatin-saline group (p<0.01, p<0.001). In addition, while the CMAP latency was decreased in the PEG-treated group, the CMAP amplitude was increased and a significant improvement was observed in the Inclined test scores. Besides, histological examinations showed an increase in axon diameter and NGF expression with PEG treatment. Conclusion: This study demonstrated that PEG exerts protective activity against cisplatin-induced neurotoxicity by increasing endogenous antioxidants and reducing lipid peroxidation and inflammation.