Nicorandil attenuates lithocholic acid-induced hepatotoxicity in mice through impeding oxidative stress, inflammation and apoptosis.
Tissue Cell
; 91: 102569, 2024 Sep 17.
Article
in En
| MEDLINE
| ID: mdl-39303437
ABSTRACT
This study was performed to explore the beneficial protective impact of nicorandil (Nico) against lithocholic acid (LCA)-induced hepatotoxicity. MATERIALS AND METHODS:
Mice received Nico (50 and 100â¯mg/kg. orally) for 7 days and LCA (125â¯mg/kg, i.p.) was injected for the last 4 days two times daily.RESULTS:
Nico improved both structural and functional abnormalities induced by LCA. Nico significantly decreased serum levels of transaminases, ALP, GGT and markedly elevated albumin levels. Additionally, Nico mitigated oxidative stress; it decreased contents of MDA and NO and increased GSH level and SOD activity. Moreover, Nico markedly decreased the elevated levels of TNF-α, JNK, Bax, Caspase-3 and iNOS, and increased the levels of eNOS in hepatic tissues. Furthermore, Nico substantially decreased the expression of NFκBp65 in hepatic tissues. Histopathological and transmission electron microscopy findings further supported these biomarkers.CONCLUSION:
Nico might be used as an adjuvant medication to prevent LCA-induced hepatotoxicity, pending further clinical research, through impeding oxidative stress, inflammation and apoptosis.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Language:
En
Journal:
Tissue Cell
Year:
2024
Document type:
Article
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