Brain Antioxidant Enzymes Research Articles

Unpredictable chronic mild stress induced anxio-depressive disorders and enterobacteria dysbiosis: Potential protective effects of Detariummicrocarpum

Ethnopharmacological relevanceDetarium microcarpum Guill. & Perr. is used traditionally in Far North Cameroun to treat stomach aches, anxiety, epilepsy, and other mental disorders. Aim of the studyEvaluate the anxiolytic and antidepressant-like effects of D. microcarpum (DM) in unpredictable chronic mild stress (UCMS) model of depression in male rats and its impact on fecal enterobacteria of stressed rats. Materials and methodsRats were handled daily (control) or subjected to the UCMS procedure for 42 days. Anxiety-like behaviors were assessed using the light and dark box test (LBD) and the open field test (OFT). Depressive-like behaviors were assessed using the forced swimming test (FST), the sucrose preference test (SPT), and the novelty suppressed feeding test (NSFT). Feces were then collected, followed by blood, brain, and duodenum sections after sacrifice. Monoamine levels, pro-inflammatory cytokines, oxidative stress factors, and nitrosative stress were assessed. Feces were introduced into Hectoen enteric agar for the identification of enterobacteria. An in vitro growth test was performed. ResultsThe DM ethanolic extract has significantly increased the time spent in the light box, in the LBD, and in the center area of the OFT. Moreover, the extract has significantly reduced the preference for sucrose in the SPT, the time of immobility in the FST, and the latency period to consume the pet in the NSFT. DM extract has significantly reduced serum cortisol levels. It also significantly decreased the pro-inflammatory cytokines TNF-α and Il-1β in both brain and duodenum homogenate. DM has increased the brain's serotonin, GABA, and dopamine levels. The DM extract also decreased the MDA and nitrite levels. It also increased the SOD and CAT activities in both brain and duodenal homogenate. Histologically, the DM extract restored the cell's density in hippocampi sections and prevented gut inflammation and peroxidation characterizing leaky gut syndrome. DM extract has no effect on the growth of enterobacteria species isolated in vitro. ConclusionThe ethanolic extract of DM would have anxiolytic and antidepressant effects via the modulation of the HPA axis, brain antioxidant enzyme activities, inflammation, and nitrosative stress. Moreover, it could act by preventing leaky gut syndrome.

High-concentration hydrogen inhalation mitigates sepsis-associated encephalopathy in mice by improving mitochondrial dynamics.

Sepsis-associated encephalopathy (SAE) is a neuronal injury with poor prognosis. Mitochondrial dysfunction is critical in SAE development, and hydrogen gas (H2) has a protective effect on septic mice. This study aimed to investigate the effect of high concentration (67%) of H2 on SAE and whether it is related to mitochondrial biogenesis and mitochondrial dynamics. A mouse sepsis model was induced by cecal ligation and puncture. The mice inhalated 67% H2 for 1 h at 1 and 6 h post-surgery, respectively. The 7-day survival rate was recorded. Cognitive function was assessed using the Y-maze test and Morris water maze test. Serum inflammatory factors, antioxidant enzymes, as well as mitochondrial function indexes including mitochondrial membrane potential (MMP) and ATP in the hippocampal tissue were evaluated 24 h after surgery. Mitochondrial dynamic proteins (DRP1 and MFN2) and biosynthetic proteins (PGC-1α, NRF2, and TFAM) in the hippocampal tissue were detected. Moreover, the morphology of mitochondria was observed by transmission electron microscopy. Inhalation of 67% H2 improved the 7-day survival rates and recognition memory function of septic mice, alleviated brain antioxidant enzyme activity (SOD and CAT), and reduced serum proinflammatory cytokine levels. H2 inhalation also enhanced the expression of MFN2 and mitochondrial biogenesis-related factors (PGC-1α, NRF2, and TFAM) and decreased the expression of fission protein (DRP1), leading to improvement in mitochondrial function, as evidenced by MMP and ATP levels. Inhalation of high concentration (67%) of H2 in septic mice improved the survival rate and reduced neuronal injury. Its mechanism might be mediated by enhancing mitochondrial biogenesis and mitochondrial dynamics.

Preliminary monosodium glutamate-induced changes in mammary gland receptors and gene expression, water channel, oxidative stress, and some lactogenic biomarkers in lactating rats

BackgroundChanges induced by monosodium glutamate (MSG) can negatively impact milk production and secretion, among other adverse effects. This study aimed to investigate the effects of MSG consumption on receptor gene expression and quantification of hormones and receptors, as well as oxidative stress biomarkers and other lactogenic parameters in lactating animals. Twenty-four female Wistar rats, nine weeks of age, were randomly assigned to four groups, each containing six rats, at parturition. The rats in groups II, III, and IV were given varying doses of monosodium glutamate (MSG); while, group I was given distilled water and served as the control. The experimental period lasted two (2) weeks.ResultsThe groups administered with MSG showed a significant decrease in mammary PRLR gene expression (p < 0.05), as well as a marked reduction (p < 0.05) in mammary PRLR, OXT receptor, AQP-3, brain antioxidant enzymes (SOD, GPx, and CAT), and pituitary SOD compared to the control group (p < 0.05). Furthermore, there was a significant increase (p < 0.05) in reactive oxygen species levels in the serum and mammary gland homogenates, erythrocyte osmotic fragility, and elevated (p < 0.05) brain and pituitary MDA levels in the MSG-administered groups compared to the control group. Daily milk yields were significantly decreased (p < 0.05) in the MSG-administered groups between days 10 and 14 of lactation.ConclusionThe findings of this study suggest that prolonged consumption of MSG could interfere with lactation-associated functions via increased ROS production, reduced antioxidants, decreased AQP-3, mammary prolactin and oxytocin receptors, and prolactin receptor mRNA in lactating Wistar rats.Graphical

Naringin mitigates testicular injury and associated neuronal toxicity in lead-exposed cockerel chicks.

Lead (Pb) poisoning affects multiple organs including the reproductive system. The experiment was performed to explore the protective effect of naringin on testicular apoptosis, neuronal dysfunction and markers of stress in cockerel chicks. Thirty-six cockerel chicks were used for this study, and randomly grouped into six chicks per group viz. control, Pb only (600 ppm), Pb and naringin (80 mg/kg), Pb and Naringin (160 mg/kg), naringin only (80 mg/kg) and naringin only (160 mg/kg), respectively, for eight weeks. Pb was administered via drinking water while naringin was administered via oral gavage. Oxidative stress indices in the brain and testes were assessed, and immunohistochemistry of TNF-α and caspase 3 was done in the brain and testes, respectively. Lead administration induced inflammatory and testicular apoptosis cascade accompanied with increased oxidative stress and upregulation of brain and testicular antioxidant enzymes in comparison to the control and Pb-only-treated cockerels. Immunohistochemistry showed significant immunoreactivity of testicular caspase 3 and TNF-α in the brain. Treatment of Pb-exposed chickens with naringin offered protection to Pb acetate-induced testicular oxidative stress, apoptosis, and neuroinflammation in cockerel chicks.

Effect of Momordica cochinchinensis extract on locomotor function and brain antioxidant enzyme activity in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated zebrafish Parkinson’s disease model

BACKGROUND: Gac fruit (Momordica cochinchinensis) belongs to the Cucurbitaceae family. The red aril of Gac fruit contains high concentrations of carotenoids, including lycopene and beta-carotene. OBJECTIVE: This study aimed to investigate the effect of Gac fruit aril extract on locomotor activities in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced zebrafish model and measure antioxidant enzyme activities in the zebrafish brain. METHODS: This study used adult male zebrafish (Danio rerio) as an animal model. MPTP was used as a toxin to induce movement dysfunction in zebrafish, while the standard drug selegiline acted as a monoamine oxidase-B inhibitor. Locomotion was recorded on day 7 after MPTP induction using a digital video tracking system, and parameters related to zebrafish swimming, including total distance, velocity, and immobility, were observed. The brain tissue of the zebrafish was collected for antioxidant enzyme activity analysis. RESULTS: The results showed that Gac fruit extract at doses of 200 and 400 mg/kg improved locomotor functions in MPTP-induced Parkinsonism in zebrafish. However, antioxidant enzyme activities, such as catalase and superoxide dismutase activities, in the zebrafish brain showed no significant differences among all groups. CONCLUSIONS: These findings provide insights into the further research of Gac fruit extract as a nutraceutical for preventing Parkinson’s disease.

Evaluation of Helianthus annuus Flower Extract on Biomarkers of Alzheimer’s Disease

AbstractBackgroundAlzheimer’s disease (AD) is a slowly progressive disease of the brain that is characterized by the impairment of memory and eventually by disturbances in reasoning, planning, language, and perception. Amyloid β‐peptide (Aβ) is main source of oxidative stress in AD because it can acquire a free‐radical state that contributes to its toxic effects. Aβ‐induced cytotoxicity is caused by intracellular accumulation ofreactive oxygen species, which leads to lipid peroxidation and cell death. Helianthus annuus flower is known for its nutritional value and having many medicinal benefits as well. Helianthus annuus flower contain many medicinally essential phytoconstituents, such as phenol, flavonoid, and carotenoid.MethodSTZ administration through route such as intracebroventricular or intraperitoneal injection produces reduced cognition and increased cerebral aggregated Aβ fragments, total tau protein, and Aβ deposits. These changes were accompanied with decreased glycogen synthase kinase (GSK‐3) alpha/beta ratio (phosphorylated/total) in the brain. Administration of STZ in a rodent’s brain has been shown to produce neuroinflammation, oxidative stress and biochemical alterations, which is considered to be a valid experimental model of the early pathophysiological changes in neurodegenerative disease.ResultTwo doses (100 and 200 mg/kg) of the flower extract from Helianthus annuus were given over the course of seven days. The standard agent utilised was piracetam (120 mg/kg). Oral administration of Helianthus annuus flower extract resulted in a considerable reduction in A1‐40 58 0.21 (100mg/kg) and 53 0.79 (200mg/kg) and A1‐42 17 0.89 (100mg/kg) and 15 1.02 (200mg/kg). Helianthus annuus flower extract increased the levels of the following brain antioxidant enzymes at 100 mg/kg and 200 mg/kg, respectively: CAT (15.5 2.8** and 14.0 1.12**), SOD (13.5 1.4** and 18.3 1.7**, GSH (203.3 15.3** and 218.0 13.5**), TBARS (200.3 7.3** and 208.0 11.0**). AChE activity was significantly decreased when Helianthus annuus flower extract was taken orally at doses of 100 mg/kg and 200 mg/kg, respectively.ConclusionData of the present study revealed that Helianthus annuus flower significantly decreased the brain Amyloid β 1‐42 and AChE activity in rats. Data revealed that administration of both Helianthus annuus flower (100mg/kg) and Helianthus annuus flower (200mg/kg) increased the activity of SOD and CAT.

Modulatory effects of Cannabis sativa co-administration with tramadol and codeine on cognitive function in male rats

Most teenagers mix up various psychoactive cocktail substances in combinations to get intoxicated. The role of the mixture combination of codeine (CDE), tramadol (TMD), and Cannabis sativa (CNB) on brain cognition, purinergic, cholinergic, and antioxidant enzyme activities remains unknown. This study sought to assess the mechanism of action of combinations of CDE+ TMD+ CNB on the function and activities of the brain of male Wistar rats. Forty-eight male Wistar rats were divided into 8 groups, n = 6. Group 1 served as a control, groups 2, 3, and 4 were exposed to CDE (2 mg/kg bw), TMD (10 mg/kg bw), and CNB (200 mg/kg bw), while groups 5, 6, 7, and 8 were co-administered with CDE+TMD, CNB+ TMD, CNB+CDE, and CNB+TMD+CDE orally for 28 days. This study revealed the effect of prolonged administration of CNB, TMD, and CDE on the suppression of cognitive function, acetyl-cholinesterase (AChE), butyl-cholinesterase (BChE), monoamine oxidase (MAO) enzyme activities, and antioxidant enzyme activities in rats’ brains when compared against control rats (P < 0.05). However, the activities of ectonucleosides (NTPdase), adenosine deaminase (ADA), and malondialdehyde levels produced in the brain of rats were significantly elevated (P < 0.05). This study reported the mechanism behind the neurotoxicity of CNB, TMD, and CDE on rats’ cognitive, cholinergic, purinergic, and antioxidant enzymes as a consequence of the drastic reduction in cholinesterase enzyme activities leading to neurotransmitter poisoning.

Assessment of Anti-Alzheimer Pursuit of Jambolan Fruit Extract and/or Choline against AlCl3 Toxicity in Rats

Jambolan fruit extract and choline were investigated for Aluminum tri chloride (AlCl3)-induced Alzheimer’s disease in rats. Thirty-six male “Sprague Dawley” rats weighing (150 ± 10 g) were allocated into six groups; the first group was fed a baseline diet and served as a negative control. Alzheimer’s disease (AD) was induced in Group 2 rats by oral administration of AlCl3 (17 mg/kg body weight) dissolved in distilled water (served as a positive control). Rats in Group 3 were orally supplemented concomitantly with both 500 mg/kg BW of an ethanolic extract of jambolan fruit once daily for 28 days and AlCl3 (17 mg/kg body weight). Group 4: Rivastigmine (RIVA) aqueous infusion (0.3 mg/kg BW/day) was given orally to rats as a reference drug concomitantly with oral supplementation of AlCl3 (17 mg/kg body weight) for 28 days. Group 5 rats were orally treated with choline (1.1 g/kg) concomitantly with oral supplementation of AlCl3 (17 mg/kg body weight). Group 6 was given 500 mg/kg of jambolan fruit ethanolic extract and 1.1 g/kg of choline orally to test for additive effects concurrently with oral supplementation of AlCl3 (17 mg/kg bw) for 28 days. Body weight gain, feed intake, feed efficiency ratio, and relative brain, liver, kidney, and spleen weight were calculated after the trial. Brain tissue assessment was analyzed for antioxidant/oxidant markers, biochemical analysis in blood serum, a phenolic compound in Jambolan fruits extracted by high-performance liquid chromatography (HPLC), and histopathology of the brain. The results showed that Jambolan fruit extract and choline chloride improved brain functions, histopathology, and antioxidant enzyme activity compared with the positive group. In conclusion, administering jambolan fruit extract and choline can lower the toxic impacts of aluminum chloride on the brain.

Fluoride exposure causes behavioral, molecular and physiological changes in adult zebrafish (Danio rerio) and their offspring

Fluoride exposure through drinking water, foods, cosmetics, and drugs causes genotoxic effects, oxidative damage, and impaired cognitive abilities. In our study, the effects of fluoride on anxiety caused by the circadian clock and circadian clock changes in a zebrafish model were investigated at the molecular level on parents and the next generations. For this purpose, adult zebrafish were exposed to 1.5 ppm, 5 ppm, and 100 ppm fluoride for 6 weeks. At the end of exposure, anxiety-like behaviors and sleep/wake behaviors of the parent fish were evaluated with the circadian rhythm test and the novel tank test. In addition, antioxidant enzyme activities and melatonin levels in brain tissues were measured. In addition, morphological, physiological, molecular and behavioral analyzes of offspring taken from zebrafish exposed to fluoride were performed. In addition, histopathological analyzes were made in the brain tissues of both adult zebrafish and offspring, and the damage caused by fluoride was determined. The levels of BMAL1, CLOCK, PER2, GNAT2, BDNF and CRH proteins were measured by immunohistochemical analysis and significant changes in their levels were determined in the F- treated groups. The data obtained as a result of behavioral and molecular analyzes showed that parental fluoride exposure disrupts the circadian rhythm, causes anxiety-like behaviors, and decreases the levels of brain antioxidant enzymes and melatonin in parents. In addition, delay in hatching, increase in death and body malformations, and decrease in blood flow velocity, and locomotor activity was observed in parallel with dose increase in offspring. On the other hand, an increase in offspring apoptosis rate, ROS level, and lipid accumulation was detected. As a result, negative effects of fluoride exposure on both parents and next generations have been identified.

Neuroprotective potential of Moringa oleifera mediated by NF-kB/Nrf2/HO-1 signaling pathway: A review.

Moringa oleifera is a traditional Indian herb belonging to the Moringaceae family, it is commonly known as the horse-radish tree, drumstick, or sahajna. In developing countries, Moringa is used as feed for both humans and animals due to its well-known antioxidant, anti-inflammatory, and anti-apoptotic properties owing to its several phytoconstituents including β-carotene, quercetin, kaempferol, ascorbic acid, flavonoids, phenolic acid, rhamnose, glycosylates, glucomoringin, and isothiocyanates. These constituents help to maintain the brain antioxidant enzyme levels, mitochondrial functions, and neurogenesis, showing neuroprotective effects in several neurodegenerative disorders including Parkinson's Disease, Alzheimer's Disease, Huntington's Disease, and Amyotrophic lateral sclerosis. This review discusses various phytoconstituent of moringa and their therapeutic potential in various neurological disorders. Additionally, we also concise the safety and toxicity profile, of different molecular pathways involved in the neuroprotective effect of M. oleifera including M. oleifera nanoparticles for better therapeutic value. PRACTICAL APPLICATIONS: Several clinical and preclinical studies on Moringa oleifera have been conducted, and the outcomes indicate moringa could be used in the treatment of brain disorders. As a result, we conclude that moringa and its nanoformulations could be employed to treat neurological problems. In the future, M. oleifera phytoconstituents could be evaluated against specific signaling pathways, which could aid researchers in discovering their mechanism of action. Furthermore, the use of moringa as a nutraceutical owing to its myriad pharmacological potential will go a long way in boosting the economy of countries that grow moringa on a large scale.

Biochemical regulatory processes in the control of oxidants and antioxidants production in the brain of rats with iron and copper chronic overloads.

Iron [Fe(II)] and copper [Cu(II)] overloads in rat brain are associated with oxidative stress and damage. The purpose of this research is to study whether brain antioxidant enzymes are involved in the control of intracellular redox homeostasis in the brain of rats male Sprague-Dawley rats (80-90g) that received drinking water supplemented with either 1.0g/L of ferrous chloride (n = 24) or 0.5g/L cupric sulfate (n = 24) for 42days. Nicotinamide adenine dinucleotide phosphate(NADPH) oxidase, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and glutathione transferase (GT) activities in brain were determined by spectrophotometric methods and NO production by the content of nitrite concentration in the organ. Chronic treatment with Fe(II) and Cu(II) led to a significant decrease of nitrite content and SOD activity in brain. Activity of NADPH oxidase increased with Cu(II) treatment. Concerning Fe(II), catalase and GT activities increased in brain after 28 and 4days of treatment, respectively. In the case of Cu(II), catalase activity decreased whereas GT activity increased after 2 and 14days, respectively. The regulation of redox homeostasis in brain involves changes of the activity of these enzymes to control the steady state of oxidant species related to redox signaling pathways upon Cu and Fe overload. NO may serve to detoxify cells from superoxide anion and hydrogen peroxide with the concomitant formation of peroxynitrite. However, the latest is a powerful oxidant which leads to oxidative modifications of biomolecules. These results suggest a common pathway to oxidative stress and damage in brain for Cu(II) and Fe(II).

Hibernation with Rhythmicity in the Retina, Brain, and Plasma but Not in the Liver of Hibernating Giant Spiny Frogs (Quasipaa spinosa).

Simple SummaryAquatic ectotherms experience hypoxia under water during hibernation, which enables them to move denoting some level of consciousness, unlike terrestrial hibernators. However, how aquatic ectotherms modulate their clocks and clock-controlled genes in different tissues and plasma melatonin and corticosterone in light-dark cycles under natural environments before and during hibernation, remains to be largely unexplored. To achieve these, in this study, we investigated circadian clock genes, circadian clock-controlled genes, antioxidant enzyme genes, and related hormones in giant spiny frog (Quasipaa spinosa). Our results demonstrated that, despite the hypometabolic state of hibernation, the retina and the brain displayed some circadian rhythms of clock and antioxidant genes, as well as melatonin, while the liver was inactive. These novel findings may contribute to an understanding of how aquatic ectotherms use their circadian system differentially to modulate their physiology in escaping hypoxia during hibernation and preparing for arousal.Hibernation in ectotherms is well known, however, it is unclear how the circadian clock regulates endocrine and antioxidative defense systems of aquatic hibernators. Using the giant spiny frog (Quasipaa spinosa), we studied mRNA expression levels of (1) circadian core clock (Bmal1, Clock, Cry1 and Per2), clock-controlled (Ror-α, Mel-1c and AANAT), and antioxidant enzyme (AOE) (SOD1, SOD2, CAT and GPx) genes in retina, brain, and liver; and (2) plasma melatonin (MT) and corticosterone (CORT) levels, over a 24-hour period at six intervals pre-hibernation and during hibernation. Our results showed that brain Bmal1, Cry1, Per2 and Mel-1c were rhythmic pre-hibernation and Clock and Ror-α during hibernation. However, the retina Bmal1, Clock and Mel-1c, and plasma MT became rhythmic during hibernation. All brain AOEs (SOD1, SOD2, CAT and GPx) were rhythmic pre-hibernation and became non-rhythmic but upregulated, except SOD1, during hibernation. However, plasma CORT and liver clocks and AOEs were non-rhythmic in both periods. The mRNA expression levels of AOEs closely resembled those of Ror-α but not plasma MT oscillations. In the hibernating aquatic frogs, these modulations of melatonin, as well as clock and clock-controlled genes and AOEs might be fundamental for them to remain relatively inactive, increase tolerance, and escape hypoxia, and to prepare for arousal.

Angelica purpurascens (Avé-Lall.) Gilli. Essential Oil Improved Brain Function via Cholinergic Modulation and Antioxidant Effects in the Scopolamine-Induced Zebrafish (Danio rerio) Model.

Angelica purpurascens (Avé-Lall.) Gilli. is a medicinal plant that displays antioxidant, anticholinesterase, and neuroprotective properties. The effect of A. purpurascens essential oil (APO) on memory impairments and brain oxidative stress in zebrafish (Danio rerio) treated with scopolamine (Sco), as well as the underlying mechanism involved, were investigated in this study. Exposure to Sco (100 μM) resulted in anxiety in zebrafish, as assessed by the novel tank diving test (NTT), whereas spatial memory and novelty response dysfunctions, as evidenced by the Y-maze test and novel object recognition test (NOR), were noticed. When zebrafish were given Sco and simultaneously given APO (25 and 150 μL/L, once daily for 13 days), the deficits were averted. An increase in brain antioxidant enzymes, a reduction of lipid peroxidation, and protein oxidation were linked to this impact. Furthermore, acetylcholinesterase (AChE) activity was significantly reduced in the brains of APO-treated zebrafish. The main detected components in the APO composition were β-phellandrene (33.80%), sabinene (6.80%), α-pinene (5.30%), germacrene-D (4.50%), α-phellandrene (4.20%), and p-cymene (3.80%) based on gas chromatography–mass spectrometry (GC-MS) investigations. Our findings show that APO’s beneficial effect in a zebrafish model of Sco-induced memory impairment is mediated through multiple mechanisms, including the restoration of cholinergic system function and the improvement of the brain antioxidant state. As a result, APO could be employed as a potential source of bioactive molecules with useful biological properties and medicinal uses.

Assessment of In Vitro Tests as Predictors of the Antioxidant Effects of Insulin, Metformin, and Taurine in the Brain of Diabetic Rats.

Hyperglycemia-induced oxidative stress is an intrinsic feature of diabetes mellitus and a recognized causative factor of complications associated with the disease. As a result, compounds possessing antioxidant properties are commonly investigated as possible ways of minimizing and even preventing diabetes-related oxidative stress. On these premises, the present study was carried out to investigate the antioxidant properties of metformin (MET), a common oral hypoglycemic agent, of taurine (TAU), a sulfonic acid compound with known antioxidant benefits in diabetes, and of insulin (INS), a standard antidiabetic serving as a reference compound, by using in vitro and in vivo tests. A battery of seven in vitro tests was used to assess antioxidant/antiradical activity. The addition of a treatment compound led to a meanpercentage decrease of values for free radical/lipid peroxidation (LPO) that ranged from very high (82%) with INS to moderate (43%) with MET) and to low (31%) with TAU. Combining MET with TAU leads to an improvement of the effect seen with MET alone (46%). By contrast, under the same conditions, N-acetylcysteine, a known antioxidant, was more potent (92%) than any of the test compounds. In vivo studies were conducted using rats made diabetic with streptozotocin and treated with daily doses of INS, MET, TAU, and MET-TAU for 6weeks. Among the test compounds, the greatest hypoglycemic effect was attained with INS (>90% decrease), followed by MET (~70% decrease), with TAU providing only a modest effect (-30% decrease). Unexpectedly, however, all three compounds reduced the diabetic values for brain LPO, nitric oxide, antioxidant enzymes, glutathione, and glutathione-related enzymes to values that varied in extent within a narrow range (<12% from one another). On the other hand, pairing MET with TAU led to a small enhancement (<10%) of the effects seen with MET alone. In short, while in vitro tests for antioxidant/antiradical activity suggest marked differences in potency for INS, MET, and TAU as a result of different structures, changes in the values of indices of oxidative stress affected by these compounds in the brain of diabetic rats varied within a rather narrow range. Also, the present results suggest that although hyperglycemia is an important determinant of the oxidative stress of diabetes, other factors may be involved since a weak hypoglycemic like TAU demonstrated in vivo antioxidant actions that were comparable to those of more potent hypoglycemic agents like INS and MET.

Influence of Moringa (Moringa oleifera) enriched ice creams on rats’ brain: Exploring the redox and cholinergic systems

The broad application of Moringa oleifera leaves in the treatment of numerous diseases is prevalent globally where it extends to the management of diabetes, hypertension, inflammation, hypercholesterolemia and neurodegenerative diseases. This study provides findings on the role of Moringa oleifera leaves (MO) [MO leaves] formulated ice creams on brain cholinergic enzymes [acetylcholinesterase (AChE) and butyrylcholinesterase (BChE)], antioxidant enzymes, glycemic index and blood lipid profile of rats. Thirty (30) adult male rats acclimatized for 2 weeks were divided into five groups: Group 1 rats received commercial ice cream, Group 2 rats were received plain ice-cream, Group 3, 4 and 5 received 0.5 g, 1.0 g and 2.0 g of MO-formulated ice creams. Rats were fed on normal pellets and exposed to ice creams produced from whipping cream, skimmed milk and Moringa oleifera leaves for 30 consecutive days. Following administration, results from this study revealed that rats that received Moringa formulated ice-creams had reduced brain butyrylcholinesterase (BChE) and acetylcholinesterase (AChE) enzymes activities, glycemic index (GI), total cholesterol (TC), triglycerides (TG) and low-density lipoprotein cholesterol (LDL-C) levels and significantly increased high-density lipoprotein-cholesterol (HDL-C) level in the plasma while revealing elevated brain antioxidant status (Superoxide dismutase (SOD) and Catalase (CAT)) when compared against rats consuming commercial ice creams. Therefore, results from this study attests to the intake of ice creams made from blends of Moringa leaves in the reduction of rats’ body weight, glycemic index and lipid profile (TC, TG, LDL-C), inhibition of brain cholinergic enzymes (AChE and BChE) while increasing brain antioxidant enzymes activities (SOD and CAT).

Stress and steroid interaction modulates expression of estrogen receptor alpha in the brain, pituitary, and testes of immature Gallus gallus domesticus

In nature, food availability stimulates hypothalamo-pituitary-gonadal (HPG) axis while its scarcity induces stress, which further stimulates hypothalamo-pituitary-adrenal (HPA) axis producing a detrimental effect on the avian reproductive physiology. The present experiment was designed to examine the interaction of stress like food restriction and estradiol on male reproductive physiology with special emphasis on estrogen receptor alpha (ERα) as these play crucial role in reproduction. To achieve this, 60 day old White Leghorn immature cockrels were taken and divided into four groups (n = 8 per group). One group was provided with food and water ad libitum. Second group was food restricted (FR) for 9 h/day after 5 days, third and fourth were administered with estradiol benzoate (EB 0.5 mg/100g/day) for 12 days. Fourth group was FR for 9 h/day after 5 days of EB treatment till last day of experiment (EB + FR). Immunofluorescent localization of ERα was principally in the pre-optic area and paraventricular nuclei of hypothalamus and in anterior pituitary gland. ERα expression was highly reduced (from 40 AU to 20 AU) after FR in testis but it increased (50 AU) after EB administration, EB + FR reflects a diminishing pattern in the increment after EB. FR decreased plasma estradiol while EB increased it. Increased plasma corticosterone, hydrogen peroxide, malondialdehyde, and decreased anti-oxidant enzymes in brain and testis of all groups indicate oxidative stress in the HPG axis. The increased ERα after EB and a decrease with FR and EB + FR support their reproductive function. Estrogen and its receptor alpha are responsible for maintaining epithelial morphology but FR along with EB administration modulates the testicular development by significantly decreasing its size (p<.0001) and seminiferous tubules (p<.0001) and no sperm formation via highly reduced expression of ir-ERα in HPG axis. Our findings led us to conclude that stress like FR and estradiol induces testicular regression immature male chickens by modulating ir-ERα expression in the HPG axis thereby resulting in reduction in reproductive physiology

Protective Effect of Vernonia Cinerea Against Sunset Yellow Induced Anxiogenic Behaviour in Mice Model: Counteract Oxidative Damage based Approach

Background: Sunset yellow is a commonly used synthetic food additive in various food beverages. Over usage of this colorant induces the anxiogenic behaviour in mice through oxidative stress. Vernonia cinerea reverses anxiogenic behaviour by counteracting oxidative stress. Objective: The study was designed to screen the protective effect of Vernonia cinerea extract against sunset yellow induced anxiogenic behaviour in mice through counteracting oxidative damage. Methods: The anxiogenic behaviour was induced by the administration of sunset yellow (20 mg/kg, p.o) for 30 days. Ethanol extract of aerial parts of Vernonia cinerea (EEVC) (400 mg/kg, p.o) was administered after 1 hour of sunset yellow treatment. Diazepam (1 mg/kg, p.o) was used as a reference drug for comparisons. Results: FT-IR studies of the extract were done by comparing with standards to determine the presence of phenols and flavonoids. Vernonia cinerea significantly improved the altered anxiogenic behaviour of sunset yellow treated animals. Significant increase in the brain antioxidant enzymes catalase (CAT), superoxide dismutase (SOD) and neurotransmitter Gamma-aminobutyric acid (GABA) level and decrease in the lipid peroxidation and glutamate neurotransmitter were observed in Vernonia cinerea treated group and also this extract reversed the hippocampus CA3 region abnormalities such as perivascular oedema, haemorrhage and severe vocalisation in sunset yellow group. Conclusion: The Vernonia cinerea possesses significant antioxidant, antiradical and GABA enhancing effects against sunset yellow induced anxiogenic animals.

Dimethyl Fumarate, an Approved Multiple Sclerosis Treatment, Reduces Brain Oxidative Stress in SIV-Infected Rhesus Macaques: Potential Therapeutic Repurposing for HIV Neuroprotection.

Dimethyl fumarate (DMF), an antioxidant/anti-inflammatory drug approved for the treatment of multiple sclerosis, induces antioxidant enzymes, in part through transcriptional upregulation. We hypothesized that DMF administration to simian immunodeficiency virus (SIV)-infected rhesus macaques would induce antioxidant enzyme expression and reduce oxidative injury and inflammation throughout the brain. Nine SIV-infected, CD8+-T-lymphocyte-depleted rhesus macaques were studied. Five received oral DMF prior to the SIV infection and through to the necropsy day. Protein expression was analyzed in 11 brain regions, as well as the thymus, liver, and spleen, using Western blot and immunohistochemistry for antioxidant, inflammatory, and neuronal proteins. Additionally, oxidative stress was determined in brain sections using immunohistochemistry (8-OHdG, 3NT) and optical redox imaging of oxidized flavoproteins containing flavin adenine dinucleotide (Fp) and reduced nicotinamide adenine dinucleotide (NADH). The DMF treatment was associated with no changes in virus replication; higher expressions of the antioxidant enzymes NQO1, GPX1, and HO-1 in the brain and PRDX1 and HO-2 in the spleen; lower levels of 8-OHdG and 3NT; a lower optical redox ratio. The DMF treatment was also associated with increased expressions of cell-adhesion molecules (VCAM-1, ICAM-1) and no changes in HLA-DR, CD68, GFAP, NFL, or synaptic proteins. The concordantly increased brain antioxidant enzyme expressions and reduced oxidative stress in DMF-treated SIV-infected macaques suggest that DMF could limit oxidative stress throughout the brain through effective induction of the endogenous antioxidant response. We propose that DMF could potentially induce neuroprotective brain responses in persons living with HIV.

Effect of Xenon on the Phosphorylation of Glycogen Synthase Kinase 3β and Antioxidant Enzymes in Rat Brain

Relevance. The increase in the number of severe brain injuries due to stroke and traumatic brain injury determines the need to study and develop effective strategies for neuroprotection. The article highlights new mechanisms of the neuroprotective action of the inhalation anesthetic xenon based on the data of our own experimental studies.Aim of study. To assess the effect of anesthesia with xenon at a concentration of 0.5 MAC (minimum alveolar concentration) on the phosphorylation of glycogen synthase kinase 3β (GSK-3β) and the content of antioxidant defense enzymes in the rat brain.Material and methods. The effect of inhalation anesthesia with xenon on the phosphorylation of the GSK-3β enzyme in comparison with lithium chloride, as well as on the content of heme oxygenase, catalase, and Mn-superoxide dismutase in rat brain homogenates was studied by immunoblotting.Results. The use of xenon at a concentration of 0.5 MAA causes an almost twofold increase in the content of the phosphorylated form of the GSK-3β enzyme in comparison with the control (p&lt;0.05) and significantly increases the pool of antioxidant defense enzymes: heme oxygenase by 50% (p &lt;0.05) and Mn-superoxide dismutase by 60% (p&lt;0.05).Conclusion. The conducted experimental study revealed new molecular mechanisms of action of the inhalation anesthetic xenon. The effect of xenon on the pool of enzymes involved in the protection of the brain from oxidative distress was found. The data obtained indicate the prospects for using xenon and require further research in this direction. The use of xenon at a concentration of 50 vol.% (0.5 MAA) for 30 minutes does not affect the content of the glycogen synthase-3β enzyme, at the same time causing an almost twofold increase in its phosphorylated form, the glycogen synthase-3β enzyme, and is accompanied by a significant increase the content of heme oxygenase, Mn-superoxide dismutase and a slight increase in the content of catalase in rat brain homogenates. Thus, the results of the study suggest that one of the possible mechanisms of the neuroprotective effect of xenon is the phosphorylation of glycogen synthase-3β, which prevents the opening of the mitochondrial pore, inhibiting the death of mitochondria-mediated apoptosis of neurons and increasing the level of antioxidant protection in them.

Non-steroidal anti-inflammatory drug Ibuprofen modulates brain lipid peroxidation and anti-oxidant enzymes in rat

Ibuprofen (IBU) is a non-steroidal anti-inflammatory analgesic drug used widely in medicine. The present study evaluated the effects of IBU on lipid peroxidation (LPO), catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and reduced glutathione (GSH) in Rattus norvegicus. Sixty male albino rats were divided into four groups (A, B, C, and D), and the groups were further sub-divided into three sub-groups containing five rats. Rats in groups B, C, and D were orally given standard therapeutic dose equivalents of 10, 20, and 30 mg/kg IBU respectively for 21 days and allowed to recover for 7 days. Group A which served as the control was not administered any form of the drug but were given equal volume of distilled water. The results indicate that LPO, SOD, and CAT activities all significantly increased compared with the control. The GSH and GPx values however did not follow consistent pattern. After the 7-day withdrawal from the drug, CAT and LPO returned to the control values. The present study indicates that IBU alters the oxidative parameters in albino rats. Further studies on the pharmacokinetics of the drug and the effects of its metabolites in different species are needed.