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Salvia officinalis flowers extract ameliorates liver and kidney injuries induced by simultaneous intoxication with ethanol/castor oil

The current study investigated the possible mechanisms of aqueous extract Salvia officinalis flowers (SF‐AE) and its protective effects against hepatorenal toxicities produced by simultaneous acute administration of ethanol (EtOH)/castor oil (CO). Healthy male rats (N = 50) were separated into five...

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Detalles Bibliográficos
Autores principales: Jedidi, Saber, Rtibi, Kais, Selmi, Houcine, Aloui, Foued, Sebai, Hichem
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10643985/
https://www.ncbi.nlm.nih.gov/pubmed/37960994
http://dx.doi.org/10.14814/phy2.15854
Descripción
Sumario:The current study investigated the possible mechanisms of aqueous extract Salvia officinalis flowers (SF‐AE) and its protective effects against hepatorenal toxicities produced by simultaneous acute administration of ethanol (EtOH)/castor oil (CO). Healthy male rats (N = 50) were separated into five equal groups: control, Ethanol (EtOH) + Castor oil (CO), doses of increasing orders of SF‐AE (50, 100, and 200 mg/kg, b.w., p.o.) during 15 days. Liver and kidney injuries were induced by EtOH (4 g/kg, b.w., p.o.) combined with CO (5 mL/kg, b.w., p.o.). Compared to the control group, SF‐AE pretreatment protected against simultaneous administration of EtOH and CO‐caused serious histological alterations in liver and kidney tissues. SF‐AE also reversed liver and kidney biochemical parameters and lipid profile alterations. More importantly, SF‐AE significantly reduced the malondialdehyde (MDA) level and counteracted the depletion of both enzymatic and non‐enzymatic antioxidants. SF‐AE also prevents against inflammation induced by EtOH combined with CO, expressed by the rise of inflammation biomarkers (C‐reactive protein: CRP and alkaline phosphatase: ALP). Additionally, combined EtOH intoxication and CO poisoning exerted an increase in H(2)O(2), free iron and calcium levels. Impressively, SF‐AE treatment regulated levels of these studied intracellular mediators in a dose‐dependent manner. In conclusion, SF‐AE can potentially improve liver and kidney injuries associated with biochemical parameter deregulations, possibly by controlling oxidative stress and inflammation.