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

Saber JedidiKais RtibiHoucine SelmiFoued AlouiHichem Sebai
Published in: Physiological reports (2023)
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.
Keyphrases
  • oxidative stress
  • dna damage
  • gene expression
  • fatty acid
  • ischemia reperfusion injury
  • liver failure
  • diabetic rats
  • mouse model
  • cell proliferation
  • breast cancer cells
  • reactive oxygen species
  • cell cycle arrest