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(A) Alanine aminotransferase (ALT). (B)—aspartate aminotransferase (AST), and (C)—alkaline phosphatase (ALP) in castor oil–induced experimental rat model treated with Psidium guajava extract for 28 days. Bars were significantly different at *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001
Source publication
The present study evaluated the therapeutic potential of root extracts of Psidium guajava—a medicinal plant used by the indigenous people of Nigeria to treat hepatitis and other health conditions. Thirty male rats were divided into six groups of five rats. Group 1 received 20mL/kg body weight of distilled water (normal control). Group 2 was induce...
Citations
... These factors lead to tissue damage and a redox imbalance state (Jedidi et al., 2022a;Sahin et al., 2018). Overproduction of ROS induced with alcohol/castor oil produces lipid peroxidation and it generates cellular alterations that lead to liver/renal toxicities (Amujiri et al., 2021;Farzaei et al., 2018). ...
... More impressively, subacute SF-AE pretreatment protected all these deregulations. However, the results of the present study are consistent with those published by Amujiri et al. (2021) who suggested that Psidium guajava extract has an important potential hepatoprotective against castor oil-induced damage. The same hepatonephroprotection role has been observed with other plant species such as Lavandula stoechas (Selmi et al., 2015) and Ceratonia siliqua (Rtibi et al., 2016). ...
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.
