Low-level laser irradiation protects the chick embryo chorioallantoic membrane from UV cytotoxicity

Low-level laser therapy or photobiomodulation is the medical use of a very low intensity light in the red to near infrared (wavelengths in the range of 630-940 nm). The present work was conducted to explore the effects of both UV and low-level laser irradiation (LLLI) on microcirculation using the in vivo model of the chick embryo chorioallantoic membrane (CAM). The effects were assessed by measuring lipid peroxidation and antioxidant enzyme activity. Cell cytotoxicity, survival and intracellular reactive oxygen species (ROS) of the CAM were also evaluated. We found that UV irradiation induced alterations of the vessels, leading to bleeding and extravasation. This effect was intensified after 60 min of exposure to UV irradiation, leading to marked edema. UVA irradiation increased cell cytotoxicity as assessed by lactate dehydrogenase (LDH) release (56.23% of control) and reduced cell viability as assessed by decreased fluorescein diacetate (FDA) fluorescence (56.23% of control). Pretreatment with LLLI prior to UV exposure protected the CAM tissue from UV-mediated cell death. This protective effect was supported by the observation of significantly inhibited lipid peroxidation (from 0.3±0.004 for UV, to 0.177±0.012 after LLLI pretreatment), ROS and O2 -production, as indicated by respective dihydrorhodamine (DHR) and dihydroethidium (DHE) intensities (from 132.78% of control for UVA, to 95.90% of control for L-UV (DHR), and from 127.34% of control for UVA, to 82.03% of control for L-UV (DHE)), and by preventing the increase in oxidative activities. LLLI efficiently protected CAM cells from UV-induced oxidative stress and appeared as a safe protective pretreatment against UV irradiation

Protective effect of grape seed extract and orlistat co-treatment against stroke: Effect on oxidative stress and energy failure

Ischemic stroke is a major health concern and a leading cause of mortality worldwide. Oxidative stress is an early event in the course of stroke inducing neuro-inflammation and cell death. Grape seed extract (GSE) is a natural phytochemical mixture exhibiting antioxidant, anti-inflammatory and neuroprotective properties. Orlistat (ORL) is an anti-obesity agent and a gastro-intestinal lipase inhibitor which showed recently beneficial effects on brain lipotoxicity. Recent studies reported the increase of lipase activity upon stroke which led us to investigate the neuroprotective effect of ORL on rat brain I/R injury as well as the putative synergism with GSE. I/R insult infarcted the brain parenchyma as assessed by TTC staining, induced an oxidative stress as revealed by increased lipoperoxidation along with alteration of antioxidant enzymes activities which was corrected using the cotreatment of ORL + GSE. I/R also disturbed the main metabolic pathways involved in brain fueling as glycolysis, neoglucogenesis, glycogenolysis, TCA cycle and electron transfer chain (ETC) complexes. These disturbances were also corrected with the cotreatment ORL + GSE which maintained energetic activities near to the control level. I/R also disrupted transition metals distribution, along with associated enzymes as tyrosinase, LDH or glutamine synthetase activities and induced hippocampal inflammation as revealed by glycogen depletion from dentate gyrus area along with depressed anti-inflammatory IL1β cytokine and increased pro-inflammatory CD68 antigen. Interestingly almost all I/R-induced disturbances were corrected either partially upon ORL and GSE on their own and the best neuroprotection was obtained in the presence of both drugs (ORL + GSE) enabling robust neuroprotection of the sub granular zone within hippocampal dentate gyrus area

Effect of garlic’s mode of administration on erythrocytes and plasma parameters in Wistar rat

Garlic preparations are recognized as hypolipidemic, cardioprotective and antihypertensive agents. However, there are some discrepancies about the beneficial effects of garlic according to dosage and mode of administration. We aimed to determine the ability of high dosage garlic (5 g/kg bw) to modulate erythrocytes and plasma parameters when administered orally (p.o.) or via intraperitoneal (i.p.) route. With regard to erythrocytes parameters, p.o. garlic treatment was found to have beneficial effects as it increased hemoglobin and hematocrit levels. Garlic i.p. treatment showed detrimental activity as it decreased these parameters. Our results reveal that garlic administered by p.o. does not involve any significant variation on mean cell volume (MCV), mean cell hemoglobin (MCH) and mean cell hemoglobin concentration (MCHC). Nevertheless, garlic i.p. increased MCV but reduced the MCH. The MCHC remained invariable even in intraperitoneal way. Concerning plasma parameters, our data show that garlic did not induce any variation on glycaemia and plasma electrolytes whatever its mode of administration. High garlic dosage was found to be relatively safe when administered orally.Keywords: Garlic, erythrocytes, hemoglobin, hematocrit, glycaemia, plasmatic electrolytes, administration mod

Protective effect of grape seed and skin extract on high dosage garlic-induced renal oxidative stress

In this study, the protective role of grape seed and skin extract (GSSE) against high garlic dose-induced renal toxicity has been evaluated. Rats were intraperitoneally injected with garlic (5 g/kg bw) or GSSE (500 mg/kg bw) or a combination of garlic and GSSE at the same doses daily for one month. Renal oxidative stress markers and antioxidant status were evaluated. We also measured plasma creatinine and urea. Data showed that high garlic dose induced renal toxicity by increasing creatinine and urea and a pro-oxidative status characterized by increased malondialdehyde, carbonyl protein, calcium and H2O2, but decreased free iron. Unexpectedly garlic increased catalase but decreased peroxidase and superoxide dismutase activities. GSSE co-treatment counteracted almost all garlic-induced deleterious effects. In conclusion, high garlic dose induced a pro-oxidative state characterized by the Fenton reaction between H2O2 and free iron, inducing Ca2+ depletion, while GSSE exerted antioxidant properties and Ca2+ repletion

Antioxidant effect of grape seed extract corrects experimental autoimmune encephalomyelitis behavioral dysfunctions, demyelination, and glial activation

International audienceBackground and purpose Multiple sclerosis (MS), a multifactorial autoimmune disease of the central nervous system (CNS), is characterized by demyelination and chronic inflammation, as well as axonal and neuronal loss. There is no cure for MS, and despite a significant improvement in the therapeutic management of patients during the last 20 years, some symptoms are still resistant to treatment, and the evolution of the disease to progressive form seems still ineluctable. The etiology of MS is complex and still not fully understood. However, inflammation is a major driver of physiopathology and oxidative stress contributes to CNS lesions and promotes existing inflammatory response. Plant polyphenols are endowed with many therapeutic benefits through alleviating oxidative stress and inflammation, thus providing neuroprotection in MS. We presently evaluated the curative effect of grape seed extract (GSE) in an experimental autoimmune encephalomyelitis (EAE) mouse model of MS. Experimental approach Six-week-old C57Bl/6J females were subjected to the EAE paradigm (using myelin oligodendrocyte glycoprotein peptide fragment (35-55), complete Freund’s adjuvant, and pertussis toxin) and then chronically treated with GSE from day 10 to day 30 post-induction. Clinical score and body weight were monitored daily, while evaluation of sensitive, motor, cognitive, and anxiety-related behaviors was performed weekly. Then, the GSE effect was evaluated on whole brain and spinal cord samples through the evaluation of oxidative stress damage, antioxidant capacities, myelin alteration, astroglial and microglial proliferation, and sirtuin expression. Key results Grape seed extract curative chronic treatment corrected the clinical course of EAE, as well as the mechanical hypersensitivity, and avoided the development of EAE mouse thermal cold allodynia. The neuropathological evaluation showed that GSE reduced oxidative stress in the brain and spinal cord by decreasing the lipid and protein oxidation through correction of the three main antioxidant enzyme activities, namely, superoxide dismutase, catalase, and glutathione peroxidase, as well as restoring normal myelin protein expression and correcting microglial and astroglial protein overexpression and sirtuin downregulation. Conclusion and implications These data strongly support GSE as an effective therapeutic approach in MS treatment

Neuroprotective effect of grape seed extract on brain ischemia: a proteomic approach

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