Journal of ethnopharmacology · 2020
Protective effects of Glycyrrhiza glabra supplementation against methotrexate-induced hepato-renal damage in rats: An experimental approach.
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Chauhan Prerna, Sharma Himanshu, Kumar Uma, Mayachari Anand, Sangli Gopalkrishna, Singh Surender
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: In traditional medicine, Glycyrrhiza glabra, commonly known as liquorice, is known to possess promising pharmacological properties including anti-oxidative, anti-inflammatory, gastro, hepato and nephro-protective activities.
AIM: The present study investigated the protective effects of Glycyrrhiza glabra rhizome extract (GGE) on MTX-induced hepato-renal damage in Wistar albino rats.
MATERIALS AND METHODS: Rats were pre-treated with GGE (100, 200 or 400 mg/kg) from day 1 to 15 and administered MTX (20 mg/kg) on day 4. Methotrexate-induced hepato-renal damage was assessed by serum toxicity biomarkers (AST, ALT, BUN and creatinine), oxidative stress estimation (MDA, GSH, SOD, CAT, peroxidase and glutathione reductase), interleukins profiling (TNF-α, IL-1β, IL-6 and IL-12), tissue histopathology and immunohistochemical (caspase-3 and NFkB) examination.
RESULTS: MTX induced hepato-renal damage resulted in elevated serum levels of AST, ALT, BUN and creatinine, increased pro-inflammatory cytokines concentration and accumulation of MDA and reduced levels of GSH, SOD, CAT, peroxidase and glutathione reductase. Conversely, co-treatment with GGE dose-dependently ameliorated oxidative stress, serum interleukins, hepato-renal toxicity biomarkers (p < 0.001), preserved tissue architecture and downregulated both caspase-3 and NFkB expression in hepato-renal tissue.
CONCLUSION: The above results suggested that GGE can alleviate MTX-induced hepato-renal damage by decreasing oxidative stress and suppressing the ensuing activation of pro-apoptotic and pro-inflammatory pathways.
AIM: The present study investigated the protective effects of Glycyrrhiza glabra rhizome extract (GGE) on MTX-induced hepato-renal damage in Wistar albino rats.
MATERIALS AND METHODS: Rats were pre-treated with GGE (100, 200 or 400 mg/kg) from day 1 to 15 and administered MTX (20 mg/kg) on day 4. Methotrexate-induced hepato-renal damage was assessed by serum toxicity biomarkers (AST, ALT, BUN and creatinine), oxidative stress estimation (MDA, GSH, SOD, CAT, peroxidase and glutathione reductase), interleukins profiling (TNF-α, IL-1β, IL-6 and IL-12), tissue histopathology and immunohistochemical (caspase-3 and NFkB) examination.
RESULTS: MTX induced hepato-renal damage resulted in elevated serum levels of AST, ALT, BUN and creatinine, increased pro-inflammatory cytokines concentration and accumulation of MDA and reduced levels of GSH, SOD, CAT, peroxidase and glutathione reductase. Conversely, co-treatment with GGE dose-dependently ameliorated oxidative stress, serum interleukins, hepato-renal toxicity biomarkers (p < 0.001), preserved tissue architecture and downregulated both caspase-3 and NFkB expression in hepato-renal tissue.
CONCLUSION: The above results suggested that GGE can alleviate MTX-induced hepato-renal damage by decreasing oxidative stress and suppressing the ensuing activation of pro-apoptotic and pro-inflammatory pathways.