Taurine exerts protective effect against vincristine-induced peripheral and enteric neuropathy in rats: Behavioral, biochemical and histological evidences
摘要
Vincristine chemotherapy is greatly limited by its induction of peripheral neurotoxicity and gastrointestinal dysfunction. Here, we evaluated if taurine (TAU), a β-amino acid, could mitigate peripheral nerve and gastrointestinal alterations in a rat model of neuropathy induced by vincristine. Vincristine sulphate (VS; 0.1 mg/kg) or saline was injected intraperitoneally to rats for a total of 10 days. Other VS-treated groups were also concurrently treated with TAU (25, 50 and 100 mg/kg). The rats were evaluated for thermal sensitivity and motor coordination, while the sciatic nerve and myenteric plexus were examined microscopically. Biochemical assessments were made on the serum, sciatic nerve and colon homogenates and the rate of gastric phenol emptying was also measured. VS caused increased sensitivity of rats to pain, reduced motor coordination, sciatic nerve and myenteric nerve injuries, increased oxidative stress and reduced rate of gastric and colonic emptying. Concurrent administration of TAU to VS-treated rats, however, improved rats’ hanging latency, tolerance to heat and the rate of gastric emptying. Rats treated with TAU showed reduction in tissue levels of H2O2, malondialdehyde and advanced oxidation protein products, improvement in reduced glutathione concentration, glutathione S-transferase, glutathione peroxidase and superoxide dismutase activities, as well as restoration of sciatic nerve calcium. Furthermore, TAU mitigated the VS-induced morphological alterations in the myenteric plexus and sciatic nerve. Therefore, TAU may be a potential natural agent for treatment of VS-induced neuropathy and gastrointestinal disturbances, probably by restoring calcium balance and modulation of oxidative stress markers. Vincristine, myenteric plexus, sciatic nerve, calcium, oxidative stress.