Protective effect of amifostine and hydrogen sulfide pathway / ATP - dependent potassium channel in experimental hemorrhagic cystitis
| Autor: | Batista, Cristina Kelma Loiola Ponte |
|---|---|
| Přispěvatelé: | Lima Júnior, Roberto César Pereira |
| Jazyk: | portugalština |
| Rok vydání: | 2016 |
| Předmět: | |
| Zdroj: | Repositório Institucional da Universidade Federal do Ceará (UFC) Universidade Federal do Ceará (UFC) instacron:UFC |
| Popis: | Hemorrhagic cystitis (HC) is an important side effect of acrolein (ACR), a metabolite of the anticancer agents oxazaphosphorines. Amifostine (AMF) is a cytoprotective agent, which protects normal tissues from anticancer chemotherapy-associated toxic effects. Recent studies reported the involvement of hydrogen sulfide (H2S) in various physiological and pathological conditions, as well as the constitutive production in mammalian tissues. This study aimed to investigate the protective effect of Amifostine and H2S in IFO-induced HC in mice. Swiss male mice were injected with either ACR (75 mcg, ive) or IFO (400 mg/kg, ip), and were killed 3 or 12 hours, respectively. Another group of animals received Amifostine (AMF, 50mg/kg) 30 minutes before the ACR or IFO. Cell apoptosis, in vivo and in vitro bladder motor function, expression of pro-inflammatory cytokines and enzymes were measured. To investigate the protective effect of H2S, the mice were treated with L-cysteine (25. 50 or 100 mg/kg, po) or Lawesson's reagent (9, 27 or 81 mmol/kg, po) or glibenclamide (10 mg/kg, po) + L-cysteine (50 mg/kg, po). The in silico analysis showed the likely chemical interaction between AMF and acrolein. In in vivo studies, ifosfamide induced significant (P |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|