Mitochondrial bioenergetics and redox dysfunction in nephrotoxicity induced by pyrethroid permethrin are ameliorated by flavonoid-rich fraction.

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.

Flavonoid-rich fraction attenuates permethrin-induced toxicity by modulating ROS-mediated hepatic oxidative stress and mitochondrial dysfunction ex vivo and in vivo in rat.

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 Ca2+ and Mg2+-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.

Anti-oxidant and hepatoprotective effects of Salvia officinalis essential oil against vanadium-induced oxidative stress and histological changes in the rat liver.

The present study was designed to evaluate the protective effects of Salvia officinalis essential oil (SOEO) against vanadium-induced hepatotoxicity in Wistar rats. Animals were divided into three groups: the first group served as the control (C), where rats received daily 0.5 mL of saline solution (0.9%) given by intraperitoneal (i.p.) way. Rats in the second group (V) received daily by i.p. way 5 mg/kg BW of NH4VO3 (V). Rats in the third group (SV) received daily V (5 mg/kg BW) by i.p. way and SOEO (15 mg/kg BW) by gavage. Animals were sacrificed after 4 or 10 days of treatment. Administration of V increased plasma ALT, AST, ALP, and LDH activities, and cholesterol, bilirubin, triglyceride, and NO levels in rats and reduced anti-oxidant enzyme activities in the liver. Treatment with SOEO significantly attenuated these changes. Moreover, the histopathological changes and the overexpression of Hsp72/73 proteins induced by V were significantly improved by SOEO. Therefore, our results suggested that SOEO could protect against V-induced oxidative damage in rat livers. The hepatoprotective effect of SOEO might be attributed to its modulation of detoxification enzymes and/or to its anti-oxidant and free radical scavenging effects.

Microwave extraction of Salvia officinalis essential oil and assessment of its GC-MS identification and protective effects versus vanadium-induced nephrotoxicity in Wistar rats models.

In this study, we assess the impact of Salvia officinalis essential oil on renal toxicity induced by vanadium in rats. The animals were exposed to either ammonium metavanadate (5 mg/kg body weight) or the combination of vanadium and S. officinalis essential oil (15 mg EO/kg body weight) for 10 days. Vanadium induced significant renal damage, demonstrated by increased plasma levels of urea and creatinine. A marked increase in lipid peroxidation markers and carbonyl protein levels with a significant decrease in enzymatic antioxidants (SOD), catalase (CAT), and glutathione peroxidase (GPx) was also observed in vanadium-treated rats. Histopathological studies also showed vanadium-induced alterations. Concomitant administration of sage essential oil significantly restored biochemical markers and pathological lesions. This protective effect seems to be due to the richness of this extract in ß-caryophyllene, limonene, carvacrol, caryophyllene, borneol and α-pinene, and α-pinene and α-thujene. These rates are determined by GC MS.