Endogenous Antioxidant Enzyme Activities Research Articles

Effect of Moderate Wine Consumption on Oxidative Stress Markers in Coronary Heart Disease Patients.

Evidence from research studies reports that wine consumption is associated with lower cardiovascular disease risk, partly through the amelioration of oxidative stress. The aim of the present study was to examine the effect of regular light to moderate wine consumption from coronary heart disease (CHD) patients compared to the effect induced by alcohol intake without the presence of wine microconstituents, on oxidation-induced macromolecular damage as well as on endogenous antioxidant enzyme activity. A randomized, single-blind, controlled, three-arm parallel intervention was carried out, in which 64 CHD patients were allocated to three intervention groups. Group A consumed no alcohol, and Group B (wine) and Group C (ethanol) consumed 27 g of alcohol/day for 8 weeks. Blood and urine samples were collected at baseline and at 4 and 8 weeks. Urine oxidized guanine species levels, protein carbonyls, thiobarbituric acid substances (TBARS) levels, as well as superoxide dismutase (SOD) and glutathione peroxidase (GPx) activities, were measured. Oxidized guanine species and protein carbonyl levels were significantly increased in the ethanol group during the intervention and were significantly decreased in the wine group. These results support the idea that wine’s bioactive compounds may exert antioxidant actions that counteract the macromolecular oxidative damage induced by alcohol in CHD patients.

Effect of salt stress on the photosynthetic characteristics and endogenous hormones, and: A comprehensive evaluation of salt tolerance in Reaumuria soongorica seedlings

ABSTRACT Salinity is a major limiting factor in desert ecosystems, where Reaumuria soongarica is a dominant species. It is crucial to study the growth and physiological response mechanisms of R. soongorica under salt stress for the protection and restoration of the desert ecosystems. However, the effects of salt concentration and stress duration on endogenous hormonal content and photosynthetic efficiency and salt injury index of R. soongorica leaves have not been reported. Currently, there is no systematic evaluation system to determine physiological adaptation strategies of R. soongorica seedlings in response to salt stress. In this study, simulation experiments were performed with NaCl solution mixed with soil. Enzyme-linked immunosorbent assay and LI-6800 portable photosynthesis analyzer were used to measure indole acetic acid (IAA), corn nucleoside hormone (ZR), abscisic acid (ABA), and photosynthesis-related parameters in leaves of R. soongorica seedlings at 0 (24–48 h after salt treatment), 3, 6, and 9 days. At the same time, growth indicators (salt injury index, root-to-shoot ratio), reactive oxygen species content, superoxide dismutase enzyme (SOD) activity, osmolyte content, membrane peroxidation, and leaf pigment content were measured at different salt concentrations and treatment times. Finally, principal component analysis and membership function method were used to comprehensively evaluate the salt tolerance of seedlings. The results showed that treatment with 200 mM NaCl for 3 days significantly increased SOD activity, the content of osmotic adjustment substances (proline, soluble protein), endogenous hormone content (ABA, ZR), root-to-shoot ratio, and Chla/Chlb values but decreased malondialdehyde content (MDA) in the leaves of R. soongorica seedlings. Leaf water content (LRWC), net photosynthetic rate (Pn), transpiration rate (Tr), water use efficiency (WUE), and IAA content in R. soongorica seedlings were lower than those in the control, when exposed to 400 and 500 mM NaCl solutions. Finally, the principal component analysis revealed endogenous hormone content and antioxidant enzyme activity to be useful for the comprehensive evaluation of salt tolerance in R. soongorica seedlings. The R. soongorica seedlings showed the strongest salt tolerance when exposed to 200 mM NaCl for 3 days. This study provides a theoretical foundation for gene mining and breeding of salt-tolerant species in the future.

Prophylactic Protective Action of Aqueous Extract of Green Oak Acorns on Ethanol-Induced Acute Injury to Rat Gastroduodenal Mucosa.

Quercus ilex fruit is widely used in the treatment of various gastrointestinal disorders, including diarrhea, for its bioactive compounds and astringent property. The current study focuses on the phytochemical characterization of the Q. ilex-aqueous extract (QIAE) and its protective effect against gastroduodenal (GD) ulcer (GDU) produced by absolute ethanol (EtOH) intoxication in adult male Wistar rats. Experimental rats were divided into six groups (n = 6): control, EtOH [95%, 4 g/kg body weight (b.w.)], EtOH + different doses of QIAE (100, 200, and 400 mg/kg, b.w.), and EtOH + Famotidine (FAM, 10 mg/kg, b.w.). Animals were orally pretreated (p.o.) with QIAE for 15 days and intoxicated with a single oral administration of EtOH for 2 h. The findings showed that the QIAE is rich in phenolic-astringent compounds and fibers, and it exhibited a significant scavenging activity on DPPH/ABTS free-radicals with half maximal inhibitory concentration (IC50) values of 177.00 ± 5.11 and 203.9 ± 2.23 μg/mL, respectively. In vivo part, QIAE significantly reduced the GD mucosal injury revealed by edema and leukocyte infiltration of the submucosal layer. GD mucosal homogenates revealed a remarkable increase in endogenous antioxidant enzyme activities (catalase, superoxide dismutase, and glutathione peroxidase) and a decrease in the lipid peroxidation levels (malondialdehyde) in animals pretreated with QIAE compared with the ulcer control group. QIAE exerted significant and dose-dependent anti-GDU protection in the rat model with a more effective action than FAM. The GD protective effect of the QIAE might be related to a direct radical scavenging activity, increased antioxidant enzymes, and depression of lipid peroxidation.

Saikosaponin-D Mitigates Oxidation in SH-SY5Y Cells Stimulated by Glutamate Through Activation of Nrf2 Pathway: Involvement of PI3K.

Alzheimer's disease (AD) is a typical neurodegenerative disease.Well-established studies have shown an elevated level of ROS (reactive oxygen species) that induces oxidative stress in AD.Saikosaponin-D exhibited significant therapeutic effects on neurodegenerative diseases. However, its in-depth molecular mechanisms against neurotoxicity remain not fully uncovered.Herein, the possible protective effects of saikosaponin-D on glutamate-induced neurotoxicity in SH-SY5Y cells and the underlying mechanism were elucidated. Saikosaponin-D pretreatment could ameliorate glutamate-induced cytotoxicity according to MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and depress apoptosis according to Hoechst 33,342 staining and Annexin V-FITC/PI double staining in SH-SY5Y cells. Additionally, saikosaponin-D administration suppressed oxidative stress in response to glutamate indicated by diminished intracellular ROS formation and reduced MDA (malondialdehyde) content in SH-SY5Y cells. These phenomena, appeared to correlate with the recovered cellular antioxidant enzyme activities and inducted HO-1 (heme oxygenase-1) expression accompanying the nuclear translocation of Nrf2 conduct by saikosaponin-D preconditioning which had been altered by glutamate, were correlated with its neuroprotective. Furthermore, addition of LY294002, a selective inhibitor of PI3K (phosphatidylinositol 3 kinase), blocked saikosaponin-D-caused Nrf2 nuclear translocation and reversed the protection of saikosaponin-D against glutamate in SH-SY5Y cells. Moreover, saikosaponin-D exhibited antioxidant potential with high free radical-scavenging activity as confirmed by a DPPH (2,2-diphenyl-1-picrylhydrazyl) and TEAC (Trolox equivalent antioxidant capacity) in a cell-free system in vitro. Taken together, our results indicated that saikosaponin-D enhanced cellular antioxidant capacity through not only intrinsic free radical-scavenging activity but also induction of endogenous antioxidant enzyme activities and HO-1 expression mediated, at least in part, by activating PI3K and subsequently Nrf2 nuclear translocation, thereby protecting the SH-SY5Y cells from glutamate-induced oxidative cytotoxicity. In concert, these data raise the possibility that saikosaponin-D may be an attractive candidate for prevention and treatment of AD and other diseases related to oxidation in the future.

Myrtenal mitigates streptozotocin-induced spatial memory deficit via improving oxido inflammatory, cholinergic and neurotransmitter functions in mice

The occurrence of chronic neurodegenerative disorders is on the rise, but with no effective treatment due to the paucity of information on the pathological mechanism underlying these disorders. Thus, this study investigated the role of oral administration of myrtenal in mitigating memory deficits and neuro-biochemical alterations in streptozotocin-demented mice model. Mice (n ​= ​35) were randomly allocated into five cohorts consisting of 7 mice each; Group I: Control mice received vehicle alone; Group II: streptozotocin; Group III: streptozotocin + 100 ​mg/kg myrtenal; Group IV: streptozotocin +200 ​mg/kg myrtenal; and Group V: streptozotocin ​+ ​donepezil 0.5 ​mg/kg. Data from this study demonstrated that the administration of streptozotocin (STZ) impaired spatial memory and induced alterations in markers of oxido-inflammatory response, cholinergic function, cytoarchitecture, and neurotransmitter levels in mice hippocampus. Notably, administration of myrtenal enhanced spatial memory performance in STZ-demented mice by improving the activities of endogenous antioxidant enzymes to protect the brain from oxido-inflammatory stress. Treatment with myrtenal also restored cholinergic function and stabilized the homeostasis of neurotransmitters in STZ-demented mice. The authors infer that fruits rich in myrtenal may be beneficial for treating patients living with dementia associated with Alzheimer's disease.

Anti-insecticides activity in cell-lines model of Thunbergia laurifolia leaf extract aiming for functional drink

Thunbergia laurifolia has been used for folklore medicine and consumed as an herbal tea in Thailand ancient times. The aim of this study was to determine the influence of aqueous crude extracts of T. laurifolia leaves on endogenous antioxidant enzyme activity, lipid peroxidation indicated by malondialdehyde (MDA) production, and anti-insecticides property using three types of cells. Murine macrophage (RAW264.7), human embryonic kidney (HEK293), and human hepatocellular carcinoma (HepG2) cells, were treated with crude extract either combined, pre, and post-treatment exposure to chlorpyrifos (CP) and methomyl (MT). Cell viability was determined using MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) test to find out anti-insecticide properties. Results indicated that crude extract increased catalase (CAT) and glutathione peroxidase (GPx) activities while decreasing malondialdehyde (MDA) levels in HEK293 and HepG2 cells and improved cells viability in all cell types induced by CP and MT toxins. The crude extract provided a protection and recovery effect on CP and MT insecticides better than atropine sulfate (AS) standard drug especially in HepG2 and HEK293 cells. Therefore, it was concluded that crude extract can improve antioxidant enzymes level and can be used as anti-insecticides. However, more investigation is needed to play it safe for functional drinks by processing in animal model further.

Harpephyllum caffrum stimulates glucose uptake, abates redox imbalance and modulates purinergic and glucogenic enzyme activities in oxidative hepatic injury

Objective: To investigate the antioxidative and antidiabetic effects of Harpephyllum caffrum bark infusion as well as its effects on glucogenic and nucleotide hydrolyzing enzyme activities in FeSO4- induced oxidative stress in rat hepatic tissue. Methods: Harpephyllum caffrum infusion was prepared from dried plant materials (40 g) infused in boiling water (400 mL) for 20 min at room temperature. The antioxidative and inhibitory activities against carbohydrate digestive enzymes of the infusion were determined using established protocols. The liver tissues of rats were used for glucose uptake assay and to evaluate the infusion's effect on endogenous antioxidant, glucogenic, and nucleotide hydrolyzing enzyme activities in FeSO4-induced hepatic injury. Results: The Harpephyllum caffrum infusion significantly reduced ferric iron (FRAP) and free radicals (OH• and DPPH) in a dose- dependent manner. It inhibited α-amylase and α-glucosidase activities and increased glucose uptake in hepatic tissues. FeSO4 significantly decreased glutathione concentration, catalase, and superoxide dismutase activities while increasing malondialdehyde level, glycogen phosphorylase, fructose-1,6-bisphosphatase, and adenosine triphosphatase activities. However, treatment with Harpephyllum caffrum infusion reversed FeSO4-induced changes. Characterization of the infusion revealed the presence of catechol, O-pyrocatechuic acid, mequinol, maltol, and glycoside derivatives. Conclusions: The Harpephyllum caffrum infusion demonstrates antidiabetic and antioxidative potentials in in vitro models of type 2 diabetes as depicted by its ability to inhibit carbohydrate digestive enzymes, mitigate oxidative imbalance, and regulate glucogenic and nucleotide hydrolyzing enzyme activities in oxidative hepatic injury.

Flight and Dietary Antioxidants Influence Antioxidant Expression and Activity in a Migratory Bird.

SynopsisEcologically relevant factors such as exercise and diet quality can directly influence how physiological systems work including those involved in maintaining oxidative balance; however, to our knowledge, no studies to date have focused on how such factors directly affect expression of key components of the endogenous antioxidant system (i.e., transcription factors, select antioxidant genes, and corresponding antioxidant enzymes) in several metabolically active tissues of a migratory songbird. We conducted a three-factor experiment that tested the following hypotheses: (H1) Daily flying over several weeks increases the expression of transcription factors NRF2 and PPARs as well as endogenous antioxidant genes (i.e., CAT, SOD1, SOD2, GPX1, GPX4), and upregulates endogenous antioxidant enzyme activities (i.e., CAT, SOD, GPx). (H2) Songbirds fed diets composed of more 18:2n-6 PUFA are more susceptible to oxidative damage and thus upregulate their endogenous antioxidant system compared with when fed diets with less PUFA. (H3) Songbirds fed dietary anthocyanins gain additional antioxidant protection and thus upregulate their endogenous antioxidant system less compared with songbirds not fed anthocyanins. Flight training increased the expression of 3 of the 6 antioxidant genes and transcription factors measured in the liver, consistent with H1, but for only one gene (SOD2) in the pectoralis. Dietary fat quality had no effect on antioxidant pathways (H2), whereas dietary anthocyanins increased the expression of select antioxidant enzymes in the pectoralis, but not in the liver (H3). These tissue-specific differences in response to flying and dietary antioxidants are likely explained by functional differences between tissues as well as fundamental differences in their turnover rates. The consumption of dietary antioxidants along with regular flying enables birds during migration to stimulate the expression of genes involved in antioxidant protection likely through increasing the transcriptional activity of NRF2 and PPARs, and thereby demonstrates for the first time that these relevant ecological factors affect the regulation of key antioxidant pathways in wild birds. What remains to be demonstrated is how the extent of these ecological factors (i.e., intensity or duration of flight, amounts of dietary antioxidants) influences the regulation of these antioxidant pathways and thus oxidative balance.

The Potential of A Balinese Traditional Medicine Kelor Leaves (Moringa oleifera) For Male Infertility Treatment : A Mini Review

Infertility is one of the causes of reproductive welfare disorders of married couples around the world.One of the causes of infertility at the molecular level is Oxidative Stress (OS) because the products ofReactive Oxygen Species (ROS), both endogenous and exogenous, exceed the levels of antioxidants inthe body. The aims of this review is to find out the potential of traditional medicinal from Bali, Indonesiawith local name Kelor (Moringa oleifera) leaves in preventing the occurrence of potential infertilityin men based on the results of research in vivo using animal trials. The method used by the writer is aliterature study.The results of this literature review found that kelor/moringa had a positive effect onsexual behavior, especially an increase in libido. In addition, it has a positive effect on spermatogenesis,the quality of spermatozoa especially increases sperm motility, sperm count/volume, germ cell count,renews endogenous antioxidant enzyme activity, reduces levels of ROS, and provides a protectiveeffect on the testes from damage. Moringa oleifera contains many free radical blocking molecules.Some phytochemical test results show that moringa contains powerful antioxidants, including alkaloids,flavonoids, saponins, triterpenoids/steroids, tannins.

A Comparison of the Antioxidant Effects Between Hydrogen Gas Inhalation and Vitamin C Supplementation in Response to a 60-Min Treadmill Exercise in Rat Gastrocnemius Muscle.

The reactive oxygen species (ROS) produced during exercise act as a double-edged sword because they may cause oxidative damage but also play a role in the signaling pathways. A supplementation of exogenous antioxidants can reduce the total amount of ROS during exercise while it may also affect the ROS’ role in the signaling pathways of mitochondrial biogenesis. It has been suggested that hydrogen gas, as an antioxidant, can selectively scavenge hydroxyl radicals but does not affect superoxide anion’s signal transduction. The aim of this study was to compare the effects of 1-h hydrogen gas inhalation 30min prior to a treadmill exercise on the key biomarkers of mitochondrial biogenesis and related signaling pathways, and the activities of endogenous antioxidant enzymes, with those of vitamin C, in the rat skeletal muscle. Eighty-one 8-week-old male Sprague–Dawley (SD) rats were randomly assigned to three interventions (exercise-only, exercise+4%H2, and exercise+vitamin C at 500mg/kg weight, with 27 rats under each intervention), and sampled at pre-, immediately post and 4h post a 60-min treadmill exercise at speed of 27m/min and flat inclination, with nine rats in each sub-group. Expression of mitochondrial biogenetic markers and related signaling molecules in gastrocnemius muscle, and concentrations of oxidative stress markers in serum were measured. Two-way ANOVA or Kruskal–Wallis analyses showed that both hydrogen inhalation and vitamin C supplementation significantly reduced serum levels of MDA immediately after exercise and AGEs 4h after exercise. The pre-exercise supplement of vitamin C significantly reduced mitochondrial complex IV concentrations and PGC-1α, NRF-1, TFAM gene expression levels compared to the pre-exercise group, but the hydrogen gas intervention did not result in a reduction in these measurements. Unlike vitamin C, hydrogen inhalation did not blunt post-exercise mitochondrial biogenetic signals, but resulted in an increase in complex IV concentration, activation of PGC-1α, and TFAM and NRF-2 gene transcription, and up-regulation of PGC-1α protein expression. The findings indicated that hydrogen gas inhalation could play the role as an effective antioxidant in response to the exercise, whilst it did not significantly affect mitochondrial biogenesis. The dose–response relationship and antioxidant effects in different types of exercise for hydrogen inhalation require further investigation.

Astaxanthin Inhibits Diabetes-Triggered Periodontal Destruction, Ameliorates Oxidative Complications in STZ-Injected Mice, and Recovers Nrf2-Dependent Antioxidant System.

Numerous studies highlight that astaxanthin (ASTX) ameliorates hyperglycemic condition and hyperglycemia-associated chronic complications. While periodontitis and periodontic tissue degradation are also triggered under chronic hyperglycemia, the roles of ASTX on diabetes-associated periodontal destruction and the related mechanisms therein are not yet fully understood. Here, we explored the impacts of supplemental ASTX on periodontal destruction and systemic complications in type I diabetic mice. To induce diabetes, C57BL/6 mice received a single intraperitoneal injection of streptozotocin (STZ; 150 mg/kg), and the hyperglycemic mice were orally administered with ASTX (12.5 mg/kg) (STZ+ASTX group) or vehicle only (STZ group) daily for 60 days. Supplemental ASTX did not improve hyperglycemic condition, but ameliorated excessive water and feed consumptions and lethality in STZ-induced diabetic mice. Compared with the non-diabetic and STZ+ASTX groups, the STZ group exhibited severe periodontal destruction. Oral gavage with ASTX inhibited osteoclastic formation and the expression of receptor activator of nuclear factor (NF)-κB ligand, 8-OHdG, γ-H2AX, cyclooxygenase 2, and interleukin-1β in the periodontium of STZ-injected mice. Supplemental ASTX not only increased the levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and osteogenic transcription factors in the periodontium, but also recovered circulating lymphocytes and endogenous antioxidant enzyme activity in the blood of STZ-injected mice. Furthermore, the addition of ASTX blocked advanced glycation end products-induced oxidative stress and growth inhibition in human-derived periodontal ligament cells by upregulating the Nrf2 pathway. Together, our results suggest that ASTX does not directly improve hyperglycemia, but ameliorates hyperglycemia-triggered periodontal destruction and oxidative systemic complications in type I diabetes.

Purple sweet potato extract maintains intestinal homeostasis and extend lifespan through increasing autophagy in female Drosophila melanogaster.

Purple sweet potatoes extract (PSPE) have been used as a natural food antioxidant with high anthocyanin concentrations. Research investigated the lifespan and the mechanisms of PSPE on female Drosophila melanogaster. Supplementation of PSPE extended the lifespan by 16.3% and had a protective effect on injury by oxidative stress. PSPE treatment enhanced the endogenous antioxidant enzyme activity and reduced malondialdehyde (MDA) content. Furthermore, PSPE significantly up-regulated foxo-related genes, inhibited mTOR mRNA expression, and activated autophagy to maintain intestinal homeostasis. Meanwhile, PSPE improved intestinal barrier dysfunction by 22.86%, decelerated the abnormal proliferation rate of intestinal stem cell (ISCs) by 23.77%, and improved intestinal integrity in geriatric D. melanogaster. In conclusion, PSPE may maintain intestinal homeostasis, and improve the antioxidant and stress resistance capacity through the insulin and rapamycin pathway, thereby extending the lifespan. Therefore, it provides active support to the development and application of PSPE in functional food. PRACTICAL APPLICATIONS: In recent years, with the increase of age, age-related complications have generally increased and seriously affected people's healthy life. Purple sweet potato is a nutrient-rich substance, which not only has a unique color but also contains rich anthocyanins, so it has many potential biological and pharmacological functions. Our results showed that the PSPE had a good effect of maintaining the intestinal homeostasis of the older adult, and provided a favorable theoretical basis for the development of PSPE functional products and scientific academic research.

Supplementation of Morin Restores the Altered Bone Histomorphometry in Hyperglycemic Rodents via Regulation of Insulin/IGF-1 Signaling.

Pathological mechanisms underlining diabetic bone defects include oxidative damage and insulin/IGF-1 imbalance. Morin is a bioflavonoid with antioxidant and anti-diabetic effects. This study evaluates morin’s protective effects against altered bone histomorphometry in diabetic rats through assessing insulin/IGF-1 pathway as a potential mechanism. Diabetic animals were administered two morin doses (15 and 30 mg/kg) for 5 weeks. Different serum hepatic and renal functions tests were assessed. Bone density and histomorphometry in cortical and trabecular tissues were evaluated histologically. The expressions of insulin, c-peptide and IGF-1 were estimated. In addition, the enzymatic activities of the major antioxidant enzymes were determined. Diabetic-associated alterations in serum glucose, aminotransferases, urea and creatinine were attenuated by morin. Diabetic bone cortical and trabecular histomorphometry were impaired with increased fibrosis, osteoclastic functions, osteoid formation and reduced mineralization, which was reversed by morin; particularly the 30 mg/kg dose. Insulin/IGF-1 levels were diminished in diabetic animals, while morin treatment enhanced their levels significantly. Diabetes also triggered systemic oxidative stress noticeably. The higher dose (30 mg/kg) of morin corrected the endogenous antioxidant enzymatic activities in diabetic rats. Findings indicate the potential value of morin supplementation against hyperglycemia-induced skeletal impairments. Activation of insulin/IGF-1 signaling could be the underlining mechanism behind these effects.

Raspberry Consumption Increases Cardiac NRF2 Transcriptional Products in Angiotensin II-Infused Rats

Abstract Objectives To determine whether raspberry consumption mitigates cardiac oxidative stress induced by angiotensin (Ang) II in rats. Methods Eight-week-old male Sprague-Dawley rats were fed AIN-93M (4% corn oil) diets with or without a 10% w/w raspberry freeze-dried powder for seven weeks. At week 4, rats were implanted with subcutaneous osmotic minipumps that delivered 0.9% saline (control) or Ang II (270 ng/kg body weight/day). At week 7, hearts were excised for protein analysis via western blot. Protein expression of NRF2 and its transcriptional products, HO-1 and NQO1, were quantified in the left ventricle. Data are normalized to control and presented as mean ± standard deviation. Results were analyzed with one-way ANOVA followed by Tukey post hoc test if data were normally distributed. Otherwise, non-parametric Kruskal-Wallis test was conducted. Results The expression of the antioxidant transcription factor NRF2 was significantly increased by raspberry consumption compared with Ang II alone (2.41 ± 0.62, n = 5 vs 1.31 ± 0.20-fold, n = 5, P = 0.002) and compared to control (1.00 ± 0.19-fold, n = 5, P = 0.0003). Additionally, the expression of NRF2 transcriptional product NQO1 was significantly increased by raspberry consumption compared to control (1.70 ± 0.52, n = 5 vs 1.00 ± 0.41-fold, n = 5, P = 0.05) but not compared to Ang II (1.30 ± 0.25-fold, n = 5, P = 0.3). Lastly, HO-1 was significantly increased in rats consuming raspberries compared to control (3.04 ± 1.80, n = 5 vs 1.00 ± 0.23-fold, n = 5, P = 0.02), but not compared to Ang II alone (1.92 ± 1.06-fold, n = 5, P = 0.8). Conclusions Raspberries directly increase NRF2 and its transcriptional products in the hearts of rats infused with Ang II. These findings may translate to cardio-protection from neurohumoral insult due to reduced oxidative stress and increased endogenous antioxidant enzyme activity. Funding Sources This work was supported by the Agriculture and Food Research Initiative (grant no. 2019–67,017-29,257/project accession no. 1,018,642) from the USDA National Institute of Food and Agriculture.

Comparative evaluation of cardioprotective activity of Gala and Fuji apple juice against isoprenaline-induced cardiotoxicity in rats.

Comparative evaluation of cardioprotective activity of Gala and Fuji apple juice against isoprenaline induced cardiotoxicity in rats. Rats (125-150g) were orally administered Gala (GA) and Fuji (FA) apple juice (3mL/day, per oral) for 13days. Myocardial injury was inducted on 14th and 15th day by the administration of Isoprenaline (85mg/kg/day, subcutaneous). In treated group i.e. GA and FA, aspartate aminotransferase (AST), alanine transaminase (ALT), lactate dehydrogenase (LDH), creatine kinase (CK), Troponin-I level and malondialdehyde (MDA) content was reduced while glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) level was significantly increased. Marked reduction in cholesterol, triglyceride, phospholipids, low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) was observed while high-density lipoprotein (HDL) level increased significantly. In tissue and serum total serum protein (TSP) level, Albumin, Globulin and A/G ratio increased very significantly in the treated group while the level of white blood corpuscles (WBC), haemoglobin (Hb), erythrocyte sedimentation rate (ESR), total fibrinogen (TF), bleeding time (BT), c-reactive protein (C-rP), red blood corpuscles (RBC), clotting time (CT) and prothrombin time (PT) showed a significant rise in the level. The level of Sialic acid, hexose, fucose and hexosamine was highly significantly increased, there was an increase in the level of K+ and glycogen while a significant reduction in electrolyte and glucose level was observed when all these parameters were compared to Isoprenaline (ISO) group. The above findings were supported by histopathological examination of hearts. Cardioprotective activity was compared with standard drug, metoprolol. On comparative analysis of both juices, GA juices have found more effective when compared to FA juice. The study was concluded that Gala and Fuji apple possessed significant prophylactic and protective effects against Isoprenaline-induced cardiotoxicity in rats through maintaining inhibiting lipid peroxidation, endogenous antioxidant enzyme activities and cytokine levels.

Quantification and verification of temperature effect on the duality of alleochemical role in boreal forest regeneration

By designing and conducting a series of temperature-controllable experiments in greenhouse, this work emphatically investigated how the positive or negative allelochemical effects of a key metabolic compound 3,4-dihydroxyacetophenone (DHAP) from the needles of Picea schrenkiana would vary with environmental temperature. It was found that the alleochemical effect of DHAP on the germination, seedling growth, root development, endogenous plant hormone content and antioxidant enzyme activity of P. schrenkiana demonstrated an orientation duality identified by the existence of a compensation concentration at a certain temperature, which set up a boundary between promotional and inhibitory effect. As temperature increased from 10/2 °C up to 12/4, 14/6, 16/8, and 18/10 °C in turn, the compensation point of DHAP concentration would correspondingly shift from 0.32mM down to 0.28, 0.24, 0.21 and 0.19mM, respectively. Overall, this work will deepen and enrich the understandings to the uncertainty of allelochemical effects on P. schrenkiana regeneration due to climate warming, and provide some helpful suggestions to develop a scientific management strategy for boreal forest.

Polyphenol-rich leaf of Aphanamixis polystachya averts liver inflammation, fibrogenesis and oxidative stress in ovariectomized Long-Evans rats

Aphanamixis polystachya (Wall.) R.Parker, locally known as Pithraj, is a medicinal herb having enormous traditional applications. However, the scientific rationale underlying the ethnomedicinal claims was not well-founded. The current investigation aimed to explore the mechanistic insights of protective effects of ethanol extract of A. polystachya leaf (PT), given orally, on the chemical-intoxicated hepatic inflammation and fibrosis in Long-Evans female overiectomized rats. The GC-MS and HPLC-DAD analysis of PT revealed the presence of several bioactive metabolites, including polyphenolic compounds. Catechin hydrate, caffeic acid, syringic acid, epicatechin and p-coumaric acid have been identified and quantified in the ethanol extract of PT leaf. Intoxication with CCl4 developed the oxidative stress, fibrosis and inflammation in liver of rats. Moreover, thiobarbituric acid reactive substances (TBARS), nitric oxide (NO), advanced protein oxidation product (APOP) level were found increased; whereas superoxide dismutase (SOD) and catalase activities in the plasma and liver were decreased in CCl4 administered rats. Treatment with PT prominently mitigated the oxidative stress (TBARS, NO, APOP), and inflammatory (MPO) markers and improved the endogenous antioxidant enzymes (catalase and SOD) activities in CCl4-intoxicated rats. Additionally, histological assessment confirmed the clear manifestation of inflammation and fibrosis in the liver of CCl4-intoxicated rats, which was prevented by PT and silymarin treatment. In conclusion, PT treatment may protect the liver in CCl4-administered rats, probably by mitigating oxidative stress, inflammation and fibrosis, and also augmenting the function of the antioxidant enzymes.

Mesoporous Polydopamine Nanoparticles Attenuate Morphine Tolerance in Neuropathic Pain Rats by Inhibition of Oxidative Stress and Restoration of the Endogenous Antioxidant System.

Oxidative stress resulting from reactive oxygen species (ROS) is known to play a key role in numerous neurological disorders, including neuropathic pain. Morphine is one of the commonly used opioids for pain management. However, long-term administration of morphine results in morphine antinociceptive tolerance (MAT) through elevation of ROS and suppression of natural antioxidant defense mechanisms. Recently, mesoporous polydopamine (MPDA) nanoparticles (NPS) have been known to possess strong antioxidant properties. We speculated that morphine delivery through an antioxidant nanocarrier might be a reasonable strategy to alleviate MAT. MPDAs showed a high drug loading efficiency of ∼50%, which was much higher than conventional NPS. Spectral and in vitro studies suggest a superior ROS scavenging ability of NPS. Results from a rat neuropathic pain model demonstrate that MPDA-loaded morphine (MPDA@Mor) is efficient in minimizing MAT with prolonged analgesic effect and suppression of pro-inflammatory cytokines. Additionally, serum levels of liver enzymes and levels of endogenous antioxidants were measured in the liver. Treatment with free morphine resulted in elevated levels of liver enzymes and significantly lowered the activities of endogenous antioxidant enzymes in comparison with the control and MPDA@Mor-treated group. Histopathological examination of the liver revealed that MPDA@Mor can significantly reduce the hepatotoxic effects of morphine. Taken together, our current work will provide an important insight into the development of safe and effective nano-antioxidant platforms for neuropathic pain management.

Potassium bromate-induced cell model of age-related macular degeneration in vitro.

Age‑related macular degeneration (AMD) progression occurs due to oxidative stress in retinal pigment epithelium(RPE) cells. To develop a new model of AMD, the present study investigated the effects of potassium bromate(KBrO3) on ARPE‑19 cells. Incubation with KBrO3 for 24h significantly decreased ARPE‑19 cell viability in a concentration‑dependent manner compared with the control group. The MTT and lactate dehydrogenase assay results indicated that KBrO3 induced cell apoptosis. Compared with the control group, KBrO3 treatment significantly decreased the Bcl2/Bax ratio, as determined via western blotting, and caspase‑3 mRNA expression levels. Fluorescence microscopy indicated the increased ROS levels in cells treated with KBrO3. Endogenous antioxidant enzyme activities, including superoxide dismutase and glutathione peroxidase, were significantly inhibited by KBrO3 compared with the control group. Moreover, the antioxidants tiron and phloroglucinol inhibited KBrO3‑mediated effects on ARPE‑19 cells in a dose‑dependent manner. Additionally, GPR109A is the binding site of 4‑hydroxynonenal(4‑HNE). KBrO3 displayed cytotoxic effects in 293cells, which naturally lack the GPR109A gene, but these effects were not observed in 4‑HNE‑treated 293cells, suggesting that KBrO3 induced apoptosis without increasing endogenous 4‑HNE levels in cells. Moreover, the results suggested that KBrO3‑induced oxidative stress may activate STAT3 to increase VEGF expression in ARPE‑19 cells. Collectively, the results of the present study supported the potential use of KBrO3 to induce an invitro model of AMD in ARPE‑19 cells.

Functional relevance of Gedunin as a bona fide ligand of NADPH oxidase 5 and ROS scavenger: An in silico and in vitro assessment in a hyperglycemic RBC model

Clinical evidence suggests that type 2 diabetes therapy can greatly benefit from the suppression of reactive oxygen species generation and the activation or restoration of cellular antioxidant mechanisms. In human, NADPH oxidase (NOX) is the main producer of reactive oxygen species (ROS) that supress the activity of endogenous antioxidant enzymes. In the present study, the antioxidant potential of Gedunin was studied. In silico findings reveal its strong binding affinity with NOX5 C terminal HSP90 binding site that disrupts NOX5 stability and its ability to generate ROS, leading to restoration antioxidant enzymes activities. It was found that Gedunin suppressed hyperglycaemia induced oxidative stress in an in vitro RBC model and markedly reversed glucose induced changes including haemoglobin glycosylation and lipid peroxidation. A significant restoration of activities of cellular antioxidant enzymes; superoxide dismutase, catalase and glutathione peroxidase in the presence of Gedunin revealed its ability to reduce oxidative stress. These results substantiated Gedunin as a bona fide inhibitor of human NOX5 and a ROS scavenging antioxidant with promising therapeutic attributes including its natural origin and inhibition of multiple diabetic targets.