Antioxidant and Cytoprotective Role of Citral-Rich Essential Oils in In Vitro Animal Cell Models.

Almond skins are known for their antioxidative and anti-inflammatory properties, which are mainly due to the presence of polyphenols. The aim of the present study was to evaluate the antioxidant and anti-inflammatory effects of almond skin extract (ASE) obtained from the Sicilian cultivar "Fascionello" and to evaluate the possible mechanisms of action using an in vitro model of human monocytic U937 cells as well as an in vivo model of carrageenan (CAR)-induced paw edema. The in vitro studies demonstrated that pretreatment with ASE inhibited the formation of ROS and apoptosis. The in vivo studies showed that ASE restored the CAR-induced tissue changes; restored the activity of endogenous antioxidant enzymes, such as superoxide dismutase, catalase, and glutathione; and decreased neutrophil infiltration, lipid peroxidation, and the release of proinflammatory mediators. The anti-inflammatory and antioxidant effects of ASE could be associated with the inhibition of the pro-inflammatory nuclear NF-κB and the activation of the nuclear factor-erythroid 2-related factor 2 (Nrf2) antioxidant pathways. In conclusion, almond skin could reduce the levels of inflammation and oxidative stress and could be beneficial in the treatment of several disorders.

The study aimed to investigate the therapeutic efficacy of S. dulcamara extract (SDE) in managing type II diabetes‐related parameters, including blood glucose levels, α‐amylase activity, and modulation of endogenous antioxidant enzymes (SOD, GPx, CAT). Diabetes was induced in rats using streptozocin, and the anti‐diabetics effect was evaluated by the administration of S. dulcamara extract at different doses. Blood glucose levels, α‐amylase activity, and endogenous antioxidants were estimated and found to be significant (P<0.05) in the rats treated with the extract of S. dulcamara at a dose of 200 mg/kg. The extract showed dose‐dependent inhibition of α‐amylase suggesting the potential benefits in glycemic control. Moreover, the study demonstrated a modulation in the activity of endogenous antioxidant enzymes (SOD, GPx, CAT). Importantly, the fruit extract showed no significant hemolysis or acute toxicity at varying concentrations (12.5 and 25 mg/mL) indicating the safe and biocompatible nature, as confirmed by normal biochemical parameters and histopathological examination. In conclusion, the methanolic fruit extract of S. dulcamara shows significant anti‐diabetic activity by alleviating oxidative stress associated with type II diabetes and its complications.

To investigate whether protective effect of tacrolimus postconditioning on rats' spinal cord ischemia-reperfusion injury is mediated by up-regulation of activity of endogenous antioxidant enzymes and down-regulation of production of oxygen free radicals. Ninety male Sprague-Dawley rats were randomly divided into ischemia-reperfusion (IR) group, tacrolimus postconditioning (TP) group and sham operation (SO) group. The model of spinal cord ischemia was prepared by means of catheterization through femoral artery and balloon dilatation. IR group underwent reperfusion 20 min after spinal cord ischemia. TP group experienced a single injection of tacrolimus (0.5 mg/kg) through the left common carotid artery at the onset of reperfusion. SO group received femoral artery catheterization only. Fluoro spectro photometry was employed to detect the level of reactive oxygen species (ROS) in injured spinal cord segment at 15 minutes after reperfusion. The content of malondialdehyde (MDA) and activity of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-PX) were determined at 15 minutes, 1, 6, and 24 hours after reperfusion respectively. BBB scale was conducted to evaluate hindlimb motor function at 14 days after reperfusion. The level of ROS in TP group was significantly lower than that in IR group at 15 minutes after reperfusion. The activity of SOD was significantly higher in TP group than in IR group at all observational time points, while the activities of CAT and GSH-PX were significantly higher in TP group than in IR group at 1 and 6 hours after reperfusion. The content of MDA in TP group was significantly less than that in IR group at all observational time points. The motor function score of TP group was significantly superior to that of IR group at 14 days after reperfusion. Tacrolimus post conditioning can improve activity of endogenous antioxidant enzymes, decrease production of oxygen free radicals, suppress lipid peroxidation, and thereby promote functional recovery after spinal cord ischemia-reperfusion injury in rats.

Antioxidant effects of zinc-oxide nanoparticles on post-thaw quality and in vivo fertility of Beetal buck spermatozoa

Triptolide Alleviates Hepatic Ischemia/Reperfusion Injury by Attenuating Oxidative Stress and Inhibiting NF-κB Activity in Mice

Sirtuins (Sirt) are a family of phylogenetically conserved nicotinamide adenine nucleotide (NAD(+))-dependent protein deacetylases, among which Sirt3 resides primarily in the mitochondria and serves as a stress responsive deacetylase, playing a role in protecting cells from damage under stress conditions. The present study aimed to investigate the role of Sirt3 in hydrogen peroxide (H(2)O(2))-induced oxidative neuronal injury in HT22 mouse hippocampal cells. Treatment with H(2)O(2) increased the expression of Sirt3 in a dose- and time-dependent manner, and the knockdown of Sirt3 using specific small interfering RNA (siRNA) exacerbated the H(2)O(2)-induced neuronal injury. The overexpression of Sirt3 induced by lentiviral transfection significantly reduced the generation of reactive oxygen species (ROS) and lipid peroxidation following injury, whereas the activities of endogenous antioxidant enzymes were not affected. Further experiments revealed that the H(2)O(2)-induced inhibition of mitochondrial complex activity and adenosine triphosphate (ATP) synthesis, the decrease in mitochondrial Ca(2+) buffering capacity and mitochondrial swelling were all partly reversed by Sirt3. Furthermore, the overexpression of Sirt3 attenuated the release of cytochrome c, the increase in the Bax/Bcl-2 ratio, as well as caspase-9/caspase-3 activity induced by H(2)O(2), and eventually inhibited apoptotic neuronal cell death. These results suggest that Sirt3 acts as a prosurvival factor, playing an essential role in protecting HT22 cells under H(2)O(2)-induced oxidative stress, possibly by inhibiting ROS accumulation and the activation of the mitochondrial apoptotic pathway.

Neuroprotective effects of Abacopterin E from Abacopteris penangiana against oxidative stress-induced neurotoxicity

Maerua angolensis has been used traditionally in the management of pain, arthritis, and rheumatism in Ghana and Nigeria but no scientific evidence is currently available to give credence to its folkloric use. The aim of this study was therefore to evaluate the anti-inflammatory effects of a stem bark extract of Maerua angolensis DC (MAE) in acute inflammatory models. The effects of MAE (30-300 mg kg−1) on neutrophil infiltration, exudate volume, and endogenous antioxidant enzymes in lung tissues and lung morphology were evaluated with the carrageenan induced pleurisy model in Sprague Dawley rats. The effects of MAE (30-300 mg kg−1) on vascular permeability were also evaluated in the acetic acid induced vascular permeability in ICR mice. MAE significantly reduced neutrophil infiltration, exudate volume, and lung tissue damage in carrageenan induced pleurisy. MAE increased the activities of antioxidant enzymes glutathione, superoxide dismutase, and catalase in lung tissues. The extract was also able to reduce myeloperoxidase activity and lipid peroxidation in lung tissues in carrageenan induced rat pleurisy. Vascular permeability was also attenuated by the extract with marked reduction of Evans blue dye leakage in acetic acid induced permeability assay. The results indicated that Maerua angolensis is effective in ameliorating inflammation induced by carrageenan and acetic acid. It also has the potential of increasing the activity of endogenous antioxidant enzymes.

D-003 and policosanol (CAS 557-61-9), specific and distinct mixtures of high molecular weight primary aliphatic acids and alcohols, respectively, have shown to inhibit lipid peroxidation in vivo, but comparative studies between their effects on lipid peroxidation processes had not been conducted before. To compare the effects of D-003 and policosanol on markers of lipid peroxidation in vivo in rats. Male Wistar rats were distributed into 9 groups: a control group treated with acacia gum/water vehicle, 4 with policosanol and 4 with D-003, both treatments at 5, 25, 100 and 250 mg/kg. Treatments were administered during 4 weeks. Both treatments significantly and dose-dependently reduced plasma malondyaldehide (MDA) and total peroxides. Nevertheless, while D-003 was effective from 5 mg/kg, the lowest effective dose of policosanol was 25 mg/kg. The maximal effects of both treatments were obtained with 100 mg/kg, but greater in D-003 than in policosanol group, and the same occurred across all doses tested. MDA concentrations generated with the enzymatic system in liver homogenates were also significantly and dose-dependently inhibited with both treatments. The lowest effective doses of D-003 and policosanol were 5 and 100 mg/kg, respectively, and the highest inhibitions of about 80% (D-003) and 11% (policosanol). D-003 was more effective than policosanol in all comparisons. D-003 was also more effective than policosanol for lowering MDA concentrations generated with the no enzymatic system, but in these conditions policosanol was effective from 25 mg/kg and produced an inhibition somewhat greater (about 29%) than on MDA-generated by the enzymatic system. Both policosanol and D-003 did not modify the activity of endogenous antioxidant enzymes compared with the controls. D-003 (5-250 mg/kg) orally administered for 4 weeks was more effective than policosanol for lowering all the lipid peroxidation markers assessed, like plasma MDA and total peroxides, and MDA concentrations generated by the enzymatic and non-enzymatic oxidant systems of liver homogenates. The inhibitions with D-003 were marked and dose-dependent. Neither D-003 nor policosanol modified the activity of enzymes involved in the endogenic antioxidant defensive system.

1. The aim of this work was to study potential mechanisms participating in postischemic protection of selectively vulnerable CA1 neurons in the hippocampus. Experiments were focused on measuring changes in endogenous antioxidant enzyme activity. 2. Forebrain cerebral ischemia was induced in a rat by four-vessel occlusion. Ten minutes of ischemia induces so-called delayed neuronal death in selectively vulnerable CA1 region 3 days later. After 7 days of reperfusion, 71.6% of neurons succumb to neurodegeneration. When 5 min of ischemia was used as postconditioning, 2 days after 10 min of cerebral ischemia, delayed neuronal death in CA1 was almost completely (89.9%) prevented. 3. Searching for mechanisms of protection, we measured the activity of endogenous antioxidant enzymes. Activities of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT) were measured in the hippocampus, striatum and cortex by spectrophotometric methods after 10 min of ischemia used as the preconditioning. Two days after the preconditioning or the sham operation, second ischemia was induced for 5 min. We observed significant increase of total SOD activity in all studied regions of the brain 5 h after postconditioning (5 min of ischemia). SOD activity decreased to control values after 24 h. 4. In some experiments, we used intraperitoneal injections of norepinephrine (3.1 microM/kg) or 3-nitropropionic acid (20 mg/kg) as postconditioning, instead of ischemia. All three treatments resulted in significant increase of SOD activity, but norepinephrine was the most effective. The same effect as was seen for total SOD activity could be observed for CuZn-SOD as well as Mn-SOD activity. Similarly, considerable increase in the activity of catalase was detected 5 h after postconditioning (5 min of ischemia). It is interesting that the greatest changes were established in selectively vulnerable hippocampus and striatum. As in the case of SOD, the highest levels of CAT activity were induced by norepinephrine, while lower but significant increase in CAT activity was induced by 3-nitropropionic acid.5. Our results suggest that endogenous antioxidants SOD and CAT could play considerable neuroprotective role after postconditioning.

We previously reported that reduced platelet endogenous antioxidant enzymes activities are related to the low plasma zinc level in patients with end-stage renal failure (ESRF). In this study, we attempt to evaluate whether dietary zinc deprivation reduces the activities of endogenous antioxidant and then enhances oxidative stress in the unstimulated platelet of normal and 5/6 nephrectomized (Nx) rats because increased platelet oxidative stress is suggested to involve in the incidence of thrombotic and atherosclerotic diseases. Male Sprague-Dawley rats (n = 48) were fed a zinc-deficient diet and deionized distilled water for 1 week to induce reduction of plasma zinc level. Half of the rats continued on this diet for 4 weeks as zinc-deplete group, and the other half were maintained on the same diet but with zinc-supplemented water (120 mg/L zinc sulfate solution) to correct the reduction of plasma zinc level as zinc-replete group. Half of each group underwent 5/6 Nx, while the other half underwent sham operation. Another 12 normal rats were fed standard rat chow (containing 23.4% protein and 50 ppm zinc) and drank deionized distilled water as normal control rats. In zinc-deplete rats including sham-operated and 5/6 Nx rats exhibited lower endogenous antioxidant enzymes activities such as reduced glutathione (GSH), superoxide dismutase (SOD), and glutathione peroxidase (GPX) and higher malondialdehyde (MDA) levels than normal control rats in the unstimulated platelets. However, in zinc-replete rats including sham-operated and 5/6 Nx rats have a normal endogenous antioxidant enzymes activity and normal MDA levels in the unstimulated platelets. We suggest that in uremia, the low plasma zinc level may be a risk factor for thrombotic and atherosclerotic diseases because it reduces the activities of endogenous antioxidant enzymes and increases oxidative stress in the unstimulated platelet.

Bleomycin (BLM), an antineoplastic drug, is known to induce DNA strand breaks and is also mutagenic in mammalian cells; however, its mechanism of action is not well understood. It has been proposed that BLM cytotoxicity is mediated through the generation of reactive oxygen species. We have determined the effects of BLM on endogenous hepatic antioxidant enzymes such as glutathione peroxidase (GPx), glutathione reductase, and glucose‐6‐phosphate de‐hydrogenase in rats exposed to BLM in conjunction with dietary vitamins, vitamin C and β‐carotene (BC). Male Fischer 344 rats of two different age groups were treated with BLM in the presence or absence of antioxidant vitamins. In control animals, an age‐associated decrease in GPx activity was noted (p < 0.05). The decrease in GPx activity observed in BLM‐treated old animals given vitamin C was significant fp < 0.05) compared with BLM‐treated young animals fed vitamin C. BC moderately induced GPx and glutathione reductase activities in old BLM‐treated animals; however, the increase in GPx was statistically significant (p < 0.05) only compared with old controls. A similar increase was noted in the activities of all the enzymes examined in young animals. Our results indicate that BLM exposure was accompanied by alterations in the activities of endogenous antioxidant enzymes, with a profound increase in activities occurring in old animals. In addition, the observed enzyme activities were modulated by antioxidant vitamin administration. The observation that both vitamins displayed differential effects on the enzyme activities also suggests that vitamin C and BC exert their effects by separate mechanisms.

The preventive effect of Hyphaene thebaica fruit in colon carcinogenesis was evaluated in Wistar rats at 0, 2.5, 5 and 10% inclusion rates for twelve weeks with concomitant 72-h intra-rectal N-methyl-N-nitrosourea (MNU) instillations. Indices of antioxidant status and carcinogenesis were analyzed using spectrophotometric, ELISA, histological and immunohistochemical techniques. The fruit protected against lipid peroxidation and level of early biomarkers of colon carcinogenesis, accompanied by decrease in some endogenous antioxidant enzymes functionality. It also prevented colon tissues against MNU-induced severe inflammations and damage to the mutL-homolog 1 (MLH1) gene. There was significant negative correlation between endogenous antioxidant enzyme activities and carcinoembryonic antigen (CEA) as well as lipid peroxidation, but relationship between total polyphenols and percentage expression of MLH1 proteins as well as endogenous antioxidant enzyme activities was positive. These results validate the folkloric use of H. thebaica fruit in the management of colorectal disorders. PRACTICAL APPLICATIONS: Hyphaene thebaica fruit which is widely consumed in northern Nigeria and other countries of sub-Saharan Africa is rich in fiber and antioxidant polyphenols. These two classes of compounds have demonstrated capacity to prevent colorectal cancer and cancer of other sites. Therefore, the validated protective Hyphaene thebaica fruit suggests that it can be processed for inclusion in beverages/diets as functional foods for prevention and management of colorectal disorders.

Effect of feeding blended and interesterified vegetable oils on antioxidant enzymes in rats

Anti-inflammatory, antioxidant and photoprotective activity of standardised Gaultheria procumbens L. leaf, stem, and fruit extracts in UVA-irradiated human dermal fibroblasts