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The present study was designed to evaluate in vitro and in vivo the potential anti-inflammatory and nephroprotective potential of ethyl acetate fraction extracted from Fumaria officinalis (EAF) against permethrin (PER). Male wistar rats were treated daily by gavage during 7 days as follows: group C: negative control rats received 2 mL/kg bw of corn oil, group EAF: positive control rats received EAF at a dose of 200 mg/kg bw dissolved in water, group PER: rats received PER at a dose of 34.05 mg/kg bw and group (PER + EAF): rats received PER (34.05 mg/kg bw) and EAF (200 mg/kg bw). In vitro study showed the ability of EAF to inhibit protein denaturation and heat-induced hemolysis confirming its anti-inflammatory activity. In vivo , PER treatment decreased calcium (Ca) and phosphorus (P) levels and increased lactate dehydrogenase (LDH) activity in plasma. It induced oxidative stress objectified by an increase in the lipid peroxidation and protein oxidation and a perturbation of antioxidant system in kidney and mitochondria. The activities of NADH–ubiquinone reductase, ubiquinol–cytochrome C reductase and cytochrome C oxidase activities were reduced. These alterations were confirmed by histopathological studies. Co-treatment with EAF improved the antioxidant status and mitochondrial bioenergetics. The nephroprotective effects of EAF could be attributed to its modulation of detoxification enzymes and/or free radical scavenging actions.

The present study explores the antioxidant, anti-microbial, and hepatoprotective potentials of flavonoid-rich fractions from Fumaria officinalis against permethrin-induced liver damage ex vivo/in vivo in rat. However, HPLC-DAD analysis revealed the richness of 6 components in ethyl acetate fraction (EAF) where ferulic acid, rosmarinic acid, and myricetin are the most abundant. The in vitro assays showed that EAFs have impressive antioxidant and anti-microbial properties. Ex vivo, permethrin (PER) (100 μM) induced a decrease of hepatic AST and ALT activities and 25-OH vitamin D and vitamin C levels and an increase of ALP and LDH activities, TBARS, and ϒ-GT levels with a disturbance of oxidative status. The hepatoprotective effect of EAF (1 mg/mL) against PER was confirmed by the amelioration of oxidative stress profile. In vivo, permethrin was found to increase absolute and relative liver weights, plasma transaminase activities, lactate-to-pyruvate ratio, hepatic and mitochondrial lipid peroxidation, and protein oxidation levels. This pesticide triggered a decrease of Ca 2+ and Mg 2+ -ATPases and mitochondrial enzyme activities. The co-treatment with EAF reestablished the hepatic and mitochondrial function, which could be attributed to its richness in phenolic compounds.

Vanadium has been shown to catalyze the generation of reactive oxygen species. Since free radical production and lipid peroxidation are potentially important mediators in testicular physiology and pathophysiology, the present study was conducted to elucidate vanadium-induced oxidative damage in rat testis and the ameliorative role of Salvia officinalis essential oil (SEO) against the adverse effects of this heavy metal. Adult male Wistar rats were treated daily during 10 days either with ammonium metavanadate (5 mg/kg bw, intraperitoneally), SEO (15 mg/kg bw, orally) or their combination. A group of rats receiving daily a saline solution served as a negative control. Vanadium treatment induced a significant decrease in body and reproductive organ weights, serum testosterone level and sperm number and motility. An increase in lipid peroxidation and protein oxidation as well as a marked inhibition in the activities of antioxidant enzymes in the testes and seminal vesicles indicated the occurrence of oxidative stress after vanadium toxicity. Histopathological changes in testis and seminal vesicles were also observed following vanadium administration. However, co-administration of SEO to vanadium-treated rats resulted in an appreciable improvement of these parameters, emphasizing the therapeutic effects of SEO. It can be suggested that SEO mitigates vanadium-induced reproductive damage due to its antioxidant capacity. Thus, we can hypothesize that SEO supplementation could protect against vanadium poisoning.