H2O2 Group Research Articles

Assessing the Efficacy and Outcomes Following Irrigation with Streptokinase VersusHydrogen Peroxide in Necrotizing Pancreatitis: A Randomized Pilot Study.

Percutaneous catheter drainage (PCD's) are prone to blockage because of necrosum. To improve the efficacy of PCD, necrolytic agents have been used. The present study compared the use of Streptokinase with H2O2 in saline irrigation. This is a single-center randomized pilot study (from July 2018 to Dec 2019). Patients with infected pancreatic necrosis not showing response to PCD and saline irrigation were included in the study. Patients received either Streptokinase (Streptokinase group 50,000IU in 100ml normal saline) or 3% H2O2 (3% H2O2 in 100ml normal saline in 1:10 dilution). Primary endpoints were the need for surgery and mortality while secondary endpoints were hospital stay and complications attributable to necrolytic agents. There were 30 patients in the study, 15 in each arm. Organ failure was seen in 23 (76.6%), single organ failure was present in 11 (47%), and multi-organ failure in 12 (53%). Bleeding complications (20% in H2O2 vs 6.6% in Streptokinase), need for surgery (73% in H2O2 vs 33.3% in Streptokinase) and mortality (60% in H2O2 vs 33% in Streptokinase) were higher in H2O2 group but the difference was not significant statistically. Post-irrigation hospital stay was lesser in the Streptokinase group compared to H2O2 group but the difference did not reach statistical significance (14.1 ± 7.7 vs 19.2 ± 11.7, p = 0.09) CONCLUSIONS: Streptokinase irrigation led to a trend for reduced need for necrosectomy and mortality. H2O2 group had more bleeding complications. Post-irrigation hospital stay was lesser in Streptokinase group.

Expression profile of miRNAs involved in the hepatoprotective effects of curcumin against oxidative stress in Nile tilapia.

Curcumin is a polyphenol with antioxidant activity that has been used to protect the health of fish livers. Our previous studies about comparative transcriptome have shown that curcumin can enhance the Nrf2-Keap1 signaling pathway and induce downstream anti-stress genes to maintain cell viability. However, the possible role of miRNAs in the protective mechanism of curcumin is not understood. In this study, the tilapia hepatocyte H2O2 stress model was used, and the miRNA expression profile for four groups (control group, curcumin group, H2O2 group, and protection group) were established by high-throughput sequencing. In our results, 278-333 types of Oreochromis niloticus miRNAs, 309-543 types of conserved miRNAs, and 535-746 types of novel miRNAs were identified in different samples. Differentially expressed miRNAs were identified by comparing miRNA expression profiles among the four groups. The expression levels were confirmed by q-PCR. The target genes of these differentially expressed miRNAs were predicted, and their functional annotations were enriched by GO and KEGG analysis, which revealed that many target genes were involved in "response to stimulus" and "antioxidant activity" in each pair of groups. Several miRNAs related to oxidative stress showed differential expression. For example, in the H2O2 group, the expression of miR-122wasdecreased, and the expression of miR-21 and miR-489 increased significantly. In the curcumin group, the expression of miR-153b wasdecreased, and the expression of miR-200a and miR-29 was increased significantly. miR-153b, miR-200a, and miR-29 may be involved in the regulation of the Nrf2-Keap1 signaling pathway by curcumin. This work might provide insights into the molecular mechanisms of miRNA regulation of curcumin on the prevention and alleviation of liver diseases in fish.

Management of walled-off necrosis with nasocystic irrigation with hydrogen peroxide versus biflanged metal stent: randomized controlled trial.

Background and study aims Walled-off necrosis (WON) is a known complication of acute necrotizing pancreatitis (ANP). There is no study comparing nasocystic irrigation with hydrogen peroxide (H 2 O 2 ) versus biflanged metal stent (BMS) in the management of WON. The aim of this study was to compare the clinical efficacy of both the treatment strategies. Patients and methods This study was conducted on patients with symptomatic WON who were randomized to nasocystic irrigation with H 2 O 2 (Group A) and BMS placement (Group B). Primary outcomes were clinical and technical success while secondary outcomes were procedure time, adverse events, need for additional procedures, duration of hospitalization, and mortality. Results Fifty patients were randomized into two groups. Group A (n = 25, age 37.8 ± 17.6 years, 16 men) and Group B (n = 25, age 41.8 ± 15.2 years, 17 men). There were no significant differences in baseline characteristics between the two groups. The most common etiology of pancreatitis was alcohol, observed in 27 (54 %) patients. Technical success (100 % vs 96 %, P = 0.98), clinical success (84 % vs 76 %, P = 0.76), requirement of additional procedures (16 % vs 24 %, P = 0.70) and adverse events (4 vs 7, P = 0.06) were comparable in both the groups. The duration to clinical success (34.4 ± 12 vs 14.8 ± 10.8 days, P = 0.001) and procedure time (36 ± 15 vs 18 ± 12 minutes, P = 0.01) were longer in Group A compared to Group B. Conclusions Nasocystic irrigation with H 2 O 2 and BMS are equally effective in the management of WON but time to clinical success and procedure time is longer with nasocystic irrigation.

Piceatannol alleviate ROS-mediated PC-12 cells damage and mitochondrial dysfunction through SIRT3/FOXO3a signaling pathway.

Oxidative stress-associated mitochondrial dysfunction has been identified as a major mechanism in multiple neurodegenerative diseases. This study aims to investigate the cytoprotective effects of piceatannol on ROS-mediated PC-12 cells damage and related mitochondrial dysfunction. Piceatannol treatment could significantly attenuate PC-12 cells oxidative damage and ROS-mediated cells apoptosis. Moreover, pretreatment with piceatannol effectively decreased mitochondrial membrane depolarization, cleaved-caspase 3, and increased Bcl-2 and Bcl-2/Bax compared with control H2 O2 group. Meanwhile, piceatannol treatment improved mitochondrial respiration function which led to an enhancement in the maximal respiration and spare respiratory capacity. Further mechanisms analysis showed that the protein expression of SIRT3 and its downstream protein FOXO3a were significantly increased after piceatannol addition in a dose-dependent manner. Whereas the cytoprotective role of piceatannol was markedly abolished by the SIRT3 inhibitor 3-TYP, suggesting that SIRT3/FOXO3a signaling pathway played a vital role in mediating the neuronal cytoprotective effects of piceatannol. PRACTICAL APPLICATIONS: The results of our study provide a novel insight that piceatannol could be potentially used as a promising bioactive component against oxidative damage and neurocyte apoptosis. The findings may provide theoretical basis for brain health of piceatannol consumption in some extent.

Protective effect of dexmedetomidine on neuronal hypoxic injury through inhibition of miR-134.

To explore the mechanism of dexmedetomidine (DEX)-mediated miR-134 inhibition in hypoxia-induced damage in PC12 cells. Hydrogen peroxide (H2O2)-stimulated PC12 cells were divided into control, H2O2, DEX + H2O2, miR-NC/inhibitor + H2O2, and miR-NC/ mimic + DEX + H2O2 groups. Cell viability and apoptosis were assessed by the 3-(4,5-dimethylthiazol(-2-y1)-2,5-diphenytetrazolium bromide (MTT) assay and Annexin V-FITC/PI staining, while gene and protein expression levels were detected by qRT-PCR and western blotting. Reactive oxygen species (ROS) levels were tested by 2',7'-dichlorodihydrofluorescein diacetate (DCFH-DA) staining, and malondialdehyde (MDA) content was determined with a detection kit. DEX treatment decreased H2O2-elevated miR-134 expression. H2O2-induced PC12 cell damage was improved by DEX and miR-134 inhibitor; additionally, cell viability was increased, while cell apoptosis was reduced. In addition, both DEX and miR-134 inhibitor reduced the upregulated expression of cleaved caspase-3 and increased the downregulated expression of Bcl-2 in H2O2-induced PC12 cells. However, compared to that in the DEX + H2O2 group, cell viability in the mimic + DEX + H2O2 group was decreased, and the apoptotic rate was elevated with increased cleaved caspase-3 and decreased Bcl-2 expression. Inflammation and oxidative stress were increased in H2O2-induced PC12 cells but improved with DEX or miR-134 inhibitor treatment. However, this improvement of H2O2-induced inflammation and oxidative stress induced by DEX in PC12 cells could be reversed by the miR-134 mimic. DEX exerts protective effects to promote viability and reduce cell apoptosis, inflammation, and oxidative stress in H2O2-induced PC12 cells by inhibiting the expression of miR-134.

Palm Tocotrienol-Rich Fraction Protects Neonatal Rat Cardiomyocytes from H2o2-Induced Oxidative Damage

Oxidative stress plays an important role in the pathogenesis of heart disease. Tocotrienol-rich fraction (TRF) is an antioxidant and that has the potential to reduce the risk of heart disease. This study is to determine the protective effects of palm TRF against H2O2-induced oxidative damage in neonatal rat cardiomyocytes (NRCM). The NRCM were divided into control, treated with TRF (10 µg/mL), H2O2 (0.5 mM) and treated with TRF prior to H2O2 induction (pre-treatment). Cell viability was determined by the MTS assay,while the presence of reactive oxygen species (ROS) was determined using fluorescent dihydroethidium (DHE) and 5-(and-6)-carboxy-2′,7′-dichlorodihydrofluorescein diacetate (carboxy-H2DCFDA) dye. Mitochondrial integrity and cell death were determined using JC-1 and Annexin V-FITC staining, respectively. Lactate dehydrogenase (LDH) and superoxide dismutase (SOD) activity were determined by colorimetric assay kit. The concentration of H2O2 from 0.5 to 5 mM reduced the cell viability and the H2O2 IC50 value of 0.5 mM was used in the experiment. H2O2 induction increased the intensity of carboxy-H2DCFDA and DHE-stains; and also the intensity of green fluorescence of J-monomers in JC-1 staining compared to the control group. The activity of LDH increased while the activity of SOD decreased in the H2O2 group. Pre-treatment with TRF reduced the intensities of carboxy-H2DCFDA and DHE-stains, as well as the green fluorescence of J-monomers in JC-1. Meanwhile, the LDH activity was reduced in the pre-treatment group but no changes were recorded in SOD activity compared to the H2O2 group. Palm TRF protects cardiomyocytes from oxidative damage by reducing ROS production and maintaining the mitochondrial membrane integrity thus reducing cell death.

Physiological and histological protective role of Astragalus spinosus root alcoholic extract against oxidative stress induced by H2O2 in rabbits

This study amid to evaluate the role of plant’s root (Astragalus spinosus), in biochemical parameters and histological sections effect in reduce the oxidative stress induced by hydrogen peroxide in rabbits Oryctalagus cuniculus, 7-9 months age and (1300-1500 g) of weight. Animals were distributed to three groups, every group were included five rabbits; group (1) control received water and diet. Group (2): animals treated with H2O2 (0.05) and drinking water. Group (3): animals treated with H2O2 and alcoholic extract of the plant root (5mg/kg body weight) for period one month. Study showed high significant increasing in Creatinine and ALP, LDH concentrations of animals treated with H2O2 alone (1.74±0.40) (9.900±1.058), (260.40±26.66) respectively, in compared with control (0.838±0.08) (8.420±1.132), (154.0±49.79) respectively while the concentration of Creatinine, ALP and LDH had been decreased with high significant (P≤ 0.05) in group treated with H2O2 and extract of the plant roots (0.79±0.09), (9.220±0.801) and (166.2±36.08) respectively in compared with H2O2 group. And the result of histological sections of liver, kidneys and heart, which showed an improvement of cells in group treated with the extract of the plant which had been induced by oxidative stress.

The Antioxidant Effects of Calligonum Extract on Oxidative Stress in Spermatogonial Stem Cells Culture

Background: Spermatogenesis is a programmed route of germ cell proliferation and differentiation that could produce abundant numbers of spermatozoa. The antioxidants play a vital role in decreasing ROS production in cells, therefore plants extract administration with antioxidant property can prevent of cell damage. In the present study, antioxidant effects of Calligonum extract on proliferation and colonization rate of spermatogonial cells was assessed. Materials and Methods: After isolation and culture of spermatogonial stem cells (SSCs) from neonatal mice (4-5 day old) and identification by PLZF and Oct4 markers, the therapeutic effect of Calligonum comosum extract was measured on the cells treated with H2O2. Induced oxidative stress cells were treated with 10 μg/ml extract for 3 weeks. ROS levels were assessed by flow cytometry, proliferation by cell count and TAC by FRAP assay. Also, the apoptosis rate was measured with P53 and Bax genes by real time PCR method. Results: After three weeks of treatment, the Calligonum group showed significantly lower ROS level relative to the H2O2 group. Antioxidants levels were in Calligonum group significantly higher than the H2O2 group (P≤0.05). There was a strong inverse relationship between the two groups. Proliferation and colonization rate were in Calligonum + H2O2 group significantly higher than H2O2 group alone (P≤0.05). Finally, the results of the study indicated that P53 and Bax expression decreased in Calligonum + H2O2 group compared to H2O2 group. Conclusion: The results of present study expressed that Calligonum as a plant with antioxidant effect could reduce the level ofROS, and increase proliferation and colonization rate and TAC. In other hand, 30 μM doses of H2O2increased oxidative stress and apoptosiswhile decreased proliferation of SSCs.

SS-31 protect retinal pigment epithelial cells from H2 O2 -induced cell injury by reducing apoptosis.

Evidence has shown that effects from oxidative stress induced damage of retinal or human retinal pigment epithelial (RPE) cells. Antioxidant supplementation is a plausible strategy to avoid oxidative stress and maintain the function of retina. d‐Arg‐2,6‐dimethyltyrosine‐Lys‐Phe‐NH2 (SS‐31) has been used in the treatment of many diseases. In this study, we found that SS‐31 attenuated hydrogen peroxide (H2O2)‐induced loss of cell viability, reduced oxidative damage and cell apoptosis in RPE cells. HO‐1, Trx‐1 and Nrf‐2 expression levels significantly increased on pre‐treatment with SS‐31 compared with the H2O2 group. SS‐31 inhibited apoptosis through the downregulation of Bax and the upregulation of Bcl‐2. Our results suggest that SS‐31 had a protective effect against H2O2 treatment in ARPE‐19 cells by enhancing the antioxidative enzymes expression and decreasing apoptosis, which could be considered a promising therapeutic intervention for retinal degeneration.

Dietary taurine attenuates hydrogen peroxide-impaired growth performance and meat quality of broilers via modulating redox status and cell death signaling

Oxidative stress seriously affects poultry production. Nutritional manipulations have been effectively used to alleviate the negative effects caused by oxidative stress. This study investigated the attenuating effects and potential mechanisms of dietary taurine on the growth performance and meat quality of broiler chickens challenged with hydrogen peroxide (H2O2). Briefly, a total of 192 male Arbor Acres broilers (28 d old) were randomly categorized into three groups: non-injection of birds on basal diets (control), 10.0% H2O2 injection of birds on basal diets (H2O2), and 10.0% H2O2 injection of birds on basal diets supplemented with 5 g/kg taurine (H2O2 + taurine). Each group consisted of eight cages of eight birds per cage. Results indicated that H2O2 administration significantly reduced growth performance and impaired breast meat quality by decreasing ultimate pH and increasing shear force value (P < 0.05). Dietary taurine improved the body weight gain and feed intake and decreased feed/gain ratio of H2O2-challenged broilers. Meanwhile, oxidative stress induced by intraperitoneal injection of H2O2 suppressed the nuclear factor-κB (NF-κB) signaling and initiated autophagy and apoptosis. Compared with the H2O2 group, taurine supplementation restored the redox status in the breast muscle by decreasing levels of reactive oxygen species and contents of oxidative products and increasing antioxidant capacity (P < 0.05). Moreover, upregulated mRNA expression of NF-κB signaling-related genes, including NF-κB subunit 1 (p50) and B-cell CLL/lymphoma 2 (Bcl-2), and enhanced protein expression of NF-κB were observed in the H2O2 + taurine group (P < 0.05). Additionally, dietary taurine decreased the expression of caspase family, beclin1, and microtubule-associated protein 1light chain 3 beta (LC3-II; P < 0.05), thereby rescuing autophagy and apoptosis in breast muscle induced by H2O2. Collectively, dietary supplementation with taurine effectively improves growth performance and breast meat quality of broilers challenged with H2O2, possibly by protecting against oxidative injury and modulating cell death signaling.

Grape seed proanthocyanidins protect PC12 cells from hydrogen peroxide-induced damage via the PI3K/AKT signaling pathway

Grape seed proanthocyanidins (GSP) are natural flavonoids with strong antioxidant and anti-apoptotic effects. Oxidative stress and neuronal apoptosis are major contributors to spinal cord injury (SCI). In this study, we assessed the potential protective effects of GSP on hydrogen peroxide (H2O2)-damaged pheochromocytoma-12 (PC12) cells in an in vitro model of SCI as well as the putative mechanism of action. We established a model using PC12 cells with oxidative damage induced by H2O2. Cells were treated with various concentrations of GSP (control group, 200 μmol/L H2O2 group, 5 μM GSP + H2O2 group, 10 μM GSP + H2O2 group, and 25 μM GSP + H2O2 group). The CCK-8 assay was used to determine cell activity. Dichloro-dihydro-fluorescein diacetate was used to detect intracellular reactive oxygen species (ROS), and flow cytometry was used to determine apoptosis rate. Western blot analysis was used to detect the expression of caspase-3, Bax, Bcl-2, and PI3K/AKT proteins. The results showed that GSP reduced H2O2-induced intracellular ROS and inhibited apoptosis. Furthermore, GSP inhibited the expression of caspase-3 and Bax, while promoting the expression of Bcl-2. In addition, GSP promoted the phosphorylation of PI3K and AKT. Moreover, a PI3K inhibitor (LY294002) weakened the protective effects of GSP on H2O2-induced PC12 cells. In conclusion, GSP pretreatment can protect PC12 cells from oxidative damage induced by H2O2 via the PI3K/AKT signaling pathway.

Protective Effect of Mitochondrially Targeted Peptide Against Oxidant Injury of Cone Photoreceptors Through Preventing Necroptosis Pathway

Retinopathy is an eye disease caused by the death of retinal cells in the macular area and the surrounding choroid. As the retinal rod cell dysfunction and death lead to the loss of night vision, the disease will lead to visual dysfunction and blindness as the disease progresses. Because of the irreversible nature of cell death, gene therapy has become a research hotspot in the field of retinopathy. But the technology is still in animal studies or clinical trials, and more research is needed to prove its feasibility. In this study, oxidative damage cell model was established and divided into a control group, H₂O₂ group, SS31 +NEC1 group, SS31 +H₂O₂ group, and SS31 +NEC1 +H₂O₂ group, for different interventions. The cell survival rate of the H₂O₂ group was significantly increased compared with those of the SS31 + H₂O₂ group, SS31 +NEC1 +H₂O₂ group, and NEC1 +H₂O₂ group. Nec1 combined treatment significantly reduced reactive oxygen species (ROS) production compared with that in the H₂O₂ group. The level of MDA in the SS31 group, Nec-1 group and combined treatment of SS31 +NEC1 group decreased significantly compared with the H₂O₂ group. The proportion of cells with decreased mitochondrial membrane potential in the H₂O₂ group significantly increased, and the rate of positivity for propidium iodide (PI) of 661W cells in the H₂O₂ group and the control group significantly increased. Nine hours after H₂O₂ treatment of 661W cells, the RIP3 expression level began to increase, and peaked at 24 h. The level of RIP3 in the H₂O₂ group was significantly increased, while this level was downregulated in the SS31 and NEC1 treatment groups. Therefore, this study suggests that SS31 has a partial protective effect on 661W cells by inhibiting necrosis, which has certain guiding significance for the treatment of retinal diseases.

Influence of preprocedural antiseptic mouthrinses against COVID-19 on enamel/dentin bond strength of a universal adhesive

The aim of the study was to determine the effect of preprocedural mouthrinses used against COVID-19 on enamel/dentin shear bond strength (SBS) of a universal adhesive with different application strategies. Three hundred sound human mandibular anterior teeth were used for the study. The teeth were distributed according to the tooth substrates; enamel and dentin. After obtaining flat enamel/dentin surfaces, each substrate group was divided into a control and four experimental groups (n = 30): Group I (Control) – distilled water; Group II – 1.5% hydrogen peroxide (H2O2) (30 s); Group III – 1.5% H2O2 (60 s); Group IV – 0.2% povidone-iodine (PVP-I) (30 s); Group V – 0.2% PVP-I (60 s). Each group was then assigned into two subgroups according the application strategy of the universal adhesive, Prime & Bond Universal (n = 15); a-etch and rinse (ER) and b-self-etch (SE). The resin composite bonded assemblies were subjected to SBS testing after 24 h. The failure modes and SEM investigations were evaluated. Statistical analysis involved four-way ANOVA with pair-wise comparisons using Bonferroni correction test (p < 0.05). On enamel, the highest SBS in ER application strategy were determined for the control group, followed by PVP-I and H2O2 group, respectively (p < 0.05). For self-etch strategy, no significant difference was detected among the groups (p > 0.05). The ER application mode showed higher SBS on enamel (p < 0.05) except for group H2O2 for 30 s. There was no difference between the dentin SBS of control and mouthrinse groups regardless of application mode (p > 0.05). In comparison between the rinsing times, 60 s rinsing significantly improved the enamel SBS when ER mode was used(p < 0.05). Neither rinsing period, nor adhesive strategy affected the dentin SBS (p > 0.05). The preprocedural usage of antiseptic mouthrinses and their rinsing times affect the bonding performance of the universal adhesive only on enamel surfaces in ER mode.

Effect of surface treatment on roughness and bond strength of CAD‐CAM multidirectional glass fiber‐reinforced composite resin used for implant‐supported prostheses

AbstractThe study evaluated the effect of different surface treatments on the surface roughness of a new‐generation fiber‐reinforced CAD‐CAM composite resin (FRC) and its bond strength to veneered composite resin. Fifty specimens (10 mm × 10 mm × 1 mm) were prepared from FRC blocks (Trinia; Shofu) and embedded in acrylic resin. The specimens were divided into five groups (n = 10) for different surface treatments: nontreated (control), Al2O3 airborne particle abrasion, silica coating (Cojet), acid etching (H2SO4) and hydrogen peroxide (H2O2) application. Surface roughness (Ra) of the specimens was measured using a profilometer. A veneering composite resin (3 mm in diameter by 4 mm in length) was applied on the specimens. The shear bond strength between the FRC and the veneering resin was measured. A one‐way analysis of variance was used to analyze the data. The differences among the groups were analyzed with Dunn post hoc tests (α = 0.05). Surface treatments increased the surface roughness, and Al2O3 airborne particle abrasion resulted in the highest Ra value followed by H2SO4, Cojet, H2O2 and control group (P &lt; 0.05). The highest shear bond strength was achieved with Al2O3 application (P &lt; 0.05). Cojet and H2O2 applications resulted in higher shear bond strength than the control (P &lt; 0.05). H2SO4 application resulted in lower bond strength than the control (P &lt; 0.05). Surface treatments increased the surface roughness of FRC. Al2O3 and silica coating increased the surface roughness more than the chemical applications. The tested surface treatments can be used to increase the bond strength except for the H2SO4 application. © 2021 Society of Chemical Industry

Effect of main ingredients of Danhong Injection against oxidative stress induced autophagy injury via miR-19a/SIRT1 pathway in endothelial cells

BackgroundAutophagy plays an important role in cellular homeostasis. Oxidative stress stimulated endothelial excessive autophagy has been proposed as a major risk factor for cardiovascular diseases (CVD). Danhong injection (DHI), the most prescribed traditional Chinese medicine for the treatment of CVD, has been shown to elicit vascular protective effects. However, its underlying mechanisms remain poorly defined. This study aimed to uncover the protective effects of DHI and its main bioactive components on autophagy injury of human umbilical vein endothelial cells (HUVECs) induced by H2O2 and reveal the possible mechanisms. MethodsHUVECs were treated with different concentrations of DHI or its components, after exposed to H2O2. The protective effects of DHI and its components in H2O2-induced HUVECs were examined via a cytotoxicity assay and western blot. Apoptosis was evaluated with flow cytometry. Autophagy flux was assessed by transmission electron microscopy and LC3 plasmid transfection. Besides, the role miR-19a and SIRT1 in DHI and components-mediated anti-autophagy responses were validated with inhibitors transfection. ResultsOur results showed that DHI and its components do have different effects on different aspects. In terms of HUVECs survival rate, Salvianolic acid B (Sal B) and danshensu (DSS) performed better than DHI, Hydroxysafflor yellow A (HSYA) and Tanshinone IIA (DST-IIA). As for the proliferation effect on HUVECs, only Sal B has the most obvious performance as same as 3MA. Besides, DHI and its components are sensitive and superior in regulating and balancing ROS concentration. Among the GSH/GSSG indicators, DSS and HSYA performed better. In terms of SOD content and apoptotic rate, the SOD level showed the opposite trend compared with H2O2 group. For the expression of LC3, Beclin-1 and P62, DHI and its components all had significant effects. When miR-19a or SIRT1 was inhibited, Sal B (0.5 μg/ml) can not decrease autophagy-related protein effectively. ConclusionDHI and its components all had anti-autophagy effects. And Sal B (0.5 μg/ml) inhibited HUVECs autophagy via miR-19a/SIRT1 pathway.

L-Arginine inhibits hydrogen peroxide-induced oxidative damage and inflammatory response by regulating antioxidant capacity in ovine intestinal epithelial cells

Little is known how L-arginine (Arg) affects the ovine intestinal epithelial cells (IOECs) redox status induced by hydrogen peroxide (H2O2). This study aimed to examine the impact of Arg on IOECs subjected to H2O2-induced oxidative damage, intestinal barrier injury, and inflammatory response. The IOECs were incubated for 16 h then classified as four groups (n = 6/group) and cultured in corresponding media including (1) control (CON) group, in which IOECs were cultured in Arg-free Dulbecco’s modified Eagle’s F12 Ham medium (DMEM) containing 100 μM Arg; (2) Arg group, in which IOECs were cultured in Arg-free DMEM containing 350 μM Arg; (3) H2O2 group, in which IOECs were cultured in CON group plus 150 μM H2O2; (4) Arg + H2O2 group, in which IOECs were cultured in Arg group plus150 μM H2O2. After culturing for 24 h in media, some characteristics of cells in the four groups were measured. Arg administration decreased the H2O2-induced reactive oxygen species (ROS) production compared with the H2O2 group (p < .05). Compared with H2O2, adding Arg to H2O2 increased (p < .05) transepithelial electrical resistance (TEER), but decreased (p < .05) tumour necrosis factor α (TNF-α) within the IOECs. Compared with H2O2, adding Arg to H2O2-induced injured IOECs increased (p < .05) glutathione peroxidase 1 (GPx1), zonula occludens-1 (ZO-1), and epithelial nitric oxide (NO) synthase (eNOS) protein levels, and decreased (p < .05) TNF-α levels within cells. Arg inhibits H2O2-induced oxidative damage, intestinal barrier injury, and inflammatory response by NO pathway within IOECs. HIGHLIGHTS Arg inhibits H2O2-induced oxidative damage of IOECs. Arg inhibits H2O2-induced barrier injury of IOECs. Arg inhibits H2O2-induced inflammatory of IOECs. Arg modulates the antioxidant activity by a NO pathway in IOECs.

Resveratrol protects human luteinised granulosa cells against hydrogen peroxide-induced oxidative injury through the Sirt1.

Granulosa cells (GCs) control follicular development and are important for female reproduction. Resveratrol (Res) was considered as an antioxidant and Sirt1 inducer. Hydrogen peroxide (H2O2) is the classical reagent to study oxidative stress. The study was conducted to investigate the role of Res against H2O2 in human luteinised granulosa cells (LGCs). The LGCs in the H2O2 group were treated with 100μmol/L H2O2 for 24h. The LGCs in the Res group were treated with 50μmol/L Res for 2h, followed by H2O2. The LGCs in the Sirt1 blockage group were treated with 2.5μmol/L EX527+50μmol/L Res for 2h, followed by H2O2. Results showed that Res significantly increased LGCs viability in H2O2-induced LGCs. The apoptotic rate and ROS in the H2O2 group was higher and the antioxidant enzyme activity was lower compared with other groups. Following the Res, the apoptotic rate and ROS level were reduced and the antioxidant enzyme activity were increased. In the Res blockage group, no significant alterations in the cell apoptosis, ROS and antioxidant enzyme activity were observed compared with the H2O2 group. The Res group had a Caspase-3 downregulation and Sirt1 upregulation compared with the other groups. In conclusion, Res had a protective effect against the H2O2-induced LGCs, and the mechanism may be associated with Sirt1.

Preadministration of yerba mate (Ilex paraguariensis) helps functional activity and morphology maintenance of MC3T3-E1 osteoblastic cells after in vitro exposition to hydrogen peroxide.

Natural substances with antioxidant effects may benefit prevention and treatment of people with or prone to bone diseases after menopause, such as osteoporosis. This study aimed to evaluate the in vitro effect of preadministration of yerba mate extract (YM) in the metabolism of MC3T3-E1 osteoblasts exposed to hydrogen peroxide (H2O2). The cells (MC3T3-E1) were cultured in 24-well plates with the concentration of 1μg/mL yerba mate extract dissolved in culture medium throughout the culture period. Four hours before each experiment, 400μmol/L H2O2 was added per well to simulate oxidative stress. There were evaluated cell adhesion and proliferation, in situ detection of alkaline phosphatase (ALP), mineralized nodules, and immunolocalization of osteocalcin (OCN), bone sialoprotein (BSP) and alkaline phosphatase (ALP) proteins. The results showed that YM preadministration to H2O2 exposition significatively increased cell adhesion after 3days as well as proliferation and in situ ALP detection after 10 and 7days respectively, when compared to H2O2 group. Besides, staining of OCN and BSP proteins was less intense and scattered in poor spread cells with cytoskeletal changes in H2O2 group when compared to control and YM H2O2 group. ALP staining was restrained to intracellular regions and similar in all experimental groups. Our results suggest that preadministration of yerba mate extract may prevent deleterious effects in the morphology and functional activity of osteoblasts exposed to H2O2, which could enable the maintenance of extracellular matrix in the presence of oxidative stress.

The Protective Effect of Aspirin Eugenol Ester on Oxidative Stress to PC12 Cells Stimulated with H2O2 through Regulating PI3K/Akt Signal Pathway.

Aspirin eugenol ester (AEE) is a new pharmaceutical compound esterified by aspirin and eugenol, which has anti-inflammatory, antioxidant, and other pharmacological activities. This study is aimed at identifying the protective effect of AEE against H2O2-induced apoptosis in rat adrenal pheochromocytoma PC12 cells and the possible mechanisms. The results of cell viability assay showed that AEE could increase the viability of PC12 cells stimulated by H2O2, while AEE alone had no significant effect on the viability of PC12 cells. Compared with the control group, the activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) were significantly decreased, and the content of malondialdehyde (MDA) was significantly increased in the H2O2 group. By AEE pretreatment, the level of MDA was reduced and the levels of SOD, CAT, and GSH-Px were increased in H2O2-stimulated PC12 cells. In addition, AEE could reduce the apoptosis of PC12 cells induced by H2O2 via reducing superoxide anion, intracellular ROS, and mitochondrial ROS (mtROS) and increasing the levels of mitochondrial membrane potential (ΔΨm). Furthermore, the results of western blotting showed that compared with the control group, the expression of p-PI3K, p-Akt, and Bcl-2 was significantly decreased, while the expression of Caspase-3 and Bax was significantly increased in the H2O2 group. In the AEE group, AEE pretreatment could upregulate the expression of p-PI3K, p-Akt, and Bcl-2 and downregulate the expression of Caspase-3 and Bax in PC12 cells stimulated with H2O2. The silencing of PI3K with shRNA and its inhibitor-LY294002 could abrogate the protective effect of AEE in PC12 cells. Therefore, AEE has a protective effect on H2O2-induced PC12 cells by regulating the PI3K/Akt signal pathway to inhibit oxidative stress.

Dietary phytogenic feed additives supplementation as potential ameliorating agent for control of hydrogen peroxide induced oxidative stress in rats

The study assessed the impact of the phytogenic feed additives (PFA) of either powder meal or crude extract form on hydrogen peroxide (H2O2) induced sub-clinical stress rats. Adult wistar rat (n=40), distributed into 4 groups, and exposed to H2O2 alone (H2O2) or along with supplementation of PFA in powder meal, pH2O2 and crude extract form, eH2O2 at the rate of 1.5% and 0.15%, respectively, of total DMI along with an appropriate non-H2O2 control (CONT) during an eight weeks period of study. The weekly body weight was conducted with fortnightly blood collection to assess the ameliorating effect of PFA on peroxide induced oxidative stress of rats. The dietary interventions had significant decreasing impact (P<0.05) on the activity of SOD, GST and catalase after exposure to hydrogen peroxide indicative of an oxidative stress situation. However, this decrease was not observed in the pH2O2 (72.79±1.80 U/mg Hb) and eH2O2 (74.91±2.17 U/mg Hb) group which, in turn, indicate the effectiveness of the chosen PFA both as powder or extract form in neutralizing the oxidative stress. Further, the significant (P<0.05) increase in lipid peroxidation indices (nmol MDA/mg Hb) upon H2O2 exposure was found to be neutralized by the use of the PFA, as could be ascertained from the lower values recorded in the pH2O2 and eH2O2 groups with respect to positive control H2O2 group. There was no (P>0.05) significant different observed for protein bound sulfhydryl groups and remain comparable among the different dietary groups. H2O2 exposure to animals suppressed (P<0.05) the levels of vitamin A and E however, dietary PFA in both form of powder (pH2O2) and extract (eH2O2) did significantly (P<0.05) improve this depression and play role as and antioxidative vitamin sparing. The results indicated that peroxide exposure at selected dose level impart significant increase of pro-oxidant molecules and supplementation of the PFA formulation either in powder meal or crude extract form was effective in reducing the hydrogen peroxide induced oxidative stress.