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Natural plant extracts contain a variety of phenolic compounds which are assigned various biological activities. Our work aims to make a quantitative and qualitative characterization of the Zest (ZL) and the Flesh (FL) of lemon (Citrus limon), to valorize the pharmacological uses of lemon, by evaluating in vitro activities (DPPH, free radical scavenging and reducing power). The antibacterial, antifungal, and antiproliferative activities were sought in the ability of Citrus limon extracts to protect DNA and protein. We found that the ZL contains high amounts of phenolics responsible for the important antioxidant properties of the extract. However, the FL is richer in flavonoids than the ZL. The FL extract was also found to be more effective than the ZL in protecting plasmid DNA against the strand breakage induced by hydroxyl radicals. We also concluded that the FL extract exhibited potent antibacterial activity unlike ZL. Analysis by LC/MS-MS identified 6 compounds (Caffeoyl N-Tryptophan, Hydroxycinnamoyl-Oglucoside acid, Vicenin 2, Eriocitrin, Kaempferol-3-O- rutinoside, and Quercetin-3-rutinoside). These preliminary results showed that Citrus limon has antibacterial and antioxidant activity in vitro. It would be interesting to conduct further studies to evaluate the in vivo potential in an animal model.

Background Flavonoids, which existed nearly in all fruits and vegetables, are considered as a class of plant-secondary metabolites with a polyphenolic structure and have properties with health-improving potential. Yet, not so many experimental focus on the benefits of flavonoid in vivo after external application. Here we assessed the impacts of naringin in vitro and in vivo in the human glioma U-87 cells implanted into athymic mice. Methods Tumor size and animal survival time were followed in naringin-treated mice bearing subcutaneous gliomas. To define the effects of naringin on angiogenesis, in vitro, tube formation and migration were assayed using endothelial HUVEC cell line. Results Low concentration of naringin remarkably inhibited tubulogenesis and reduced cell invasion. Moreover, naringin has been shown to have a toxicity effect on U-87 cells in a dose-dependent way. Furthermore, naringin administration (120 mg/kg/day) applies serious anti-cancer belongings on glioblastoma, as demonstrated by a slow cancer progression. Conclusions Our study has provided the first evidence on the antitumor effect of naringin, which is somehow due to the inhibition of invasion and angiogenesis.

Natural polyphenols are widely reported to have a large range of pharmacological properties, especially antioxidant activities and free radical scavenging capacities. In this study, we investigate the effects of naringin, chlorogenic acid, and quercetin mixtures (NCQ) on renal fibrosis in streptozotocin (STZ)-induced diabetic aged rats and its underlying mechanisms for ten consecutive weeks. The oxidative defense system in the kidneys of treated rats was found to be improved. Several biomarkers were investigated including the blood urea nitrogen, creatinine, and uric acid. Moreover, antioxidant parameters were evaluated and we found that superoxide dismutase, catalase, glutathione peroxidase, Na+-K+-ATPase activities, the nitric oxide production, the protein carbonyl, the advanced oxidation protein products, lipid peroxidation, and reduced glutathione levels were all significantly balanced and close to control values. In addition, NCQ restored renal injuries and fibrosis as assessed by histological method and molecular biology investigation of the matrix metalloproteinase, the transforming growth factor-beta TGF-β, the tumor necrosis factor TNFα, and p53 expression. Our study proposes the NCQ combination as potential plant-derived bioactive compounds to prevent diabetic nephropathy.

The increase in the usage of silica nanoparticles (SiNPs) in the industrial and medical fields has raised concerns about their possible adverse effects on human health. The present study aimed to investigate the potential adverse effects of SiNPs at daily doses of 25 and 100 mg/kg body weight intraperitoneally (i.p.) for 28 consecutive days on markers of liver damage in adult male rats. Results revealed that SiNPs induced a marked increase in serum markers of liver damage, including lactate dehydrogenase (LDH), alanine aminotransferase (ALAT), and aspartate aminotransferase (ASAT). SiNPs also induced an elevation of reactive oxygen species (ROS) production in liver, along with an increase in oxidative stress markers (NO, MDA, PCO, and H2O2), and a decrease in antioxidant enzyme activities (CAT, SOD, and GPx). Quantitative real-time PCR showed that SiNPs also induced upregulation of pro-apoptotic gene expression (including Bax, p53, Caspase-9/3) and downregulation of anti-apoptotic factors Bcl-2. Moreover, histopathological analysis revealed that SiNPs induced hepatocyte alterations, which was accompanied by sinusoidal dilatation, Kupffer cell hyperplasia, and the presence of inflammatory cells in the liver. Taken together, these data showed that SiNPs trigger hepatic damage through ROS-activated caspase signaling pathway, which plays a fundamental role in SiNP-induced apoptosis in the liver.

Background Pyrethroids, such as bifenthrin (BF), are among the most widely used class of insecticides that pose serious risks to human and wildlife health. Pyrethroids are proposed to affect astrocytic functions and to cause neuron injury in the central nervous system (CNS). Microglia are key cells involved in innate immune responses in the CNS, and microglia activation has been linked to inflammation and neurotoxicity. However, little information is known about the effects of BF-induced toxicity in primary microglial cells as well as in organotypic hippocampal slice cultures (OHSCs). Methods Oxidative stress and inflammatory responses induced by BF were evaluated in primary microglial cells and OHSCs incubated with different concentrations of BF (1–20 μM) for 4 and 24 h. mRNA and protein synthesis of cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), nuclear erythroid-2 like factor-2 (Nrf-2), and microsomal prostaglandin synthase-1 (mPGES-1) was also studied by qPCR and Western blot. Cell viability was analyzed by MTT-tetrazolio (MTT) and lactate dehydrogenase (LDH) assays. Neurotoxicity in OHSCs was analyzed by propidium iodide (PI) staining and confocal microscopy. Results Exposure of microglial cells to BF for 24 h resulted in a dose-dependent reduction in the number of viable cells. At sub-cytotoxic concentrations, BF increased reactive oxygen species (ROS), TNF-alpha synthesis, and prostaglandin E 2 (PGE 2 ) production, at both 4- and 24-h time points, respectively. Furthermore, BF incubation decreased superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities and increased lipid peroxidation, protein oxidation, and H 2 O 2 formation. In addition, BF significantly induced protein synthesis and mRNA expression of oxidative and inflammatory mediators after 4 and 24 h, including Nrf-2, COX-2, mPGES-1, and nuclear factor kappaB (NF-kappaB). A 24-h exposure of OHSCs to BF also increased neuronal death compared to untreated controls. Furthermore, depletion of microglia from OHSCs potently enhanced neuronal death induced by BF. Conclusions Overall, BF exhibited cytotoxic effects in primary microglial cells, accompanied by the induction of various inflammatory and oxidative stress markers including the Nrf-2/COX-2/mPGES-1/NF-kappaB pathways. Moreover, the study provided evidence that BF induced neuronal death in OHSCs and suggests that microglia exert a protective function against BF toxicity.

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.

Cadmium (Cd) is a highly toxic heavy metal. It accumulates in biological tissues, especially in fish which constitutes a first rank food for humans, particularly in the coastal areas. This study investigates the effect of long-term exposure to low Cd concentration (17 μg/kg/day) in rat striatum and hippocampus. In this study, the neurobehavioral ability changes were assessed by applying cognitive standard testing at the end of the rats’ exposure period. In addition, the examination of mitochondrial swelling was performed at the same time of evaluation of its redox status in the brain regions studied through stress parameters (GSH, MDA, GST, and CAT). This study examined also whether this long-term exposure can modify the apoptotic signaling pathway via assessment of apoptotic markers (caspase-8 and 9, Bax, Bcl-2, and Cyt-c) in cell lysates. The results of this study showed changes in neurobehavioral abilities of animals and a stronger mitochondrial swelling associated with a significant decrease in antioxidant systems (GSH, GST, and CAT) and conversely an increase in the lipoperoxidation end product (MDA) in both the striatal and hippocampal mitochondria. In addition, the results revealed a significant increase in pro-apoptotic intracellular components such as caspase-9, Cyt-c, and Bax, and showed also an evident decrease in Bcl-2 levels. In conclusion, our results reported that chronic exposure to Cd produces behavioral and cognitive perturbations, enhances oxidative stress associated with mitochondrial edema and Cyt-c leakage, and, ultimately, potentiates apoptosis signaling pathway in both brain regions in rats.

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.

Selenium nanoparticles (SeNPs) have gained importance due to their potential biological properties. The present work is the first study to investigate the protective effect of selenium nanoparticles (SeNPs) synthesized using L. seed extract on stomach ulcers in adult rats. The formation of SeNPs was confirmed by Ultraviolet-visible (UV), Fourier Transform Infrared Spectroscopy (IR), Thermal-gravimetric analysis (TGA-DTA coupled system), X-ray diffraction analysis (XRD) and scanning electron microscope (SEM) analysis. Animals were classified into 4 distinct groups. Group 1, serving as controls; group 2, serving as ulcer-group where rats received a single oral dosage of 96% ethanol (5 mL/Kg BW). Rats in Group 3 were given orally 0.5 mg/kg BW of SeNPs 1 hour before ethanol-induced gastric ulcer. Group 4 received SeNPs only (0.5 mg/kg BW) by intragastric way and served as a positive control. Green synthesis was confirmed via UV-Vis spectroscopy (230 nm peak), FTIR revealed functional groups (O-H, C=O, Se-O or Se-Se). XRD pattern shows an average crystallite sizes of nanoparticles were around 26 (4) and 268 (4) nm for β-SeO2 and g-SeO2 forms, respectively. SEM examination indicated that SeNPs have a predominantly spherical to sub-spherical morphology. TG-DTA analysis demonstrates the good thermal stability of selenium nanoparticles, evidenced by initial moisture loss, controlled degradation of organic stabilizers and the formation of a stable inorganic selenium core. SeNPs' protective effects were assessed by evaluating the ulcer index, conducting histological analysis, measuring oxidative stress markers and antioxidant defenses, as well as examining key factors involved in gastric mucosal protection. Our results demonstrated that SeNPs reduced malondialdehyde (MDA), and advanced oxidation protein product (AOPP) levels, nitric oxide (NO) levels in stomach of ethanol-induced gastric ulcer, as well as the activities of Catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD); while glutathione (GSH) and non-protein thiols (NPSH) levels were restored reaching control values. Moreover, the gastric healing effect of SeNPs pretreatment was associated with an improvement in hematological parameters and a reduction in CRP levels. These findings underscore the potential of SeNPs to enhance the antioxidant defense system of gastric mucosal cells and prevent ethanol-induced gastric damage in rats.

Background Opuntia ficus-indica is recognised for its anti-inflammatory effects and potential health benefits. Its different parts are rich in bioactive compounds and are consumed in various traditional diets. However, its cellular and molecular targets are not well known. In this study, we evaluated the effects of hydroethanolic cladode extract (HECE) on human neutrophil functions. Methods High-performance liquid chromatography (HPLC) was employed to characterise and identify the bioactive compounds of the hydroethanolic extract of Opuntia ficus - indica cladode, neutrophil chemotaxis was assessed via agarose assay, and neutrophil degranulation was assessed by the release of myeloperoxidase (MPO) and neutrophil gelatinase-associated lipocalin (NGAL) via western blotting. Neutrophil ROS production was evaluated by chemiluminescence, and superoxide anion generation was determined via a cytochrome C reduction assay. Results HPLC analysis revealed that the extract contains flavonoids and polyphenols involved in oxidative stress inhibition. HECEs significantly inhibited neutrophil chemotaxis, reduced MPO degranulation, and strongly reduced ROS production in phorbol 12-myristate 13-acetate (PMA)- or N-formyl-methionyl-leucyl-phenylalanine (FMLP)-stimulated neutrophils. The extract reacted with superoxide anions and inhibited hydrogen peroxide production. Conclusions Opuntia ficus-indica hydroethanolic cladode extract modulates major neutrophil functions and has antioxidant effects. These results could explain the anti-inflammatory properties of this plant and may lead to future therapeutic applications in inflammatory diseases.