Molecular Characterization of Prdx Family and Response of Antioxidant Enzymes in Berberine Hydrochloride-Treated Charybdis japonica Infected With Aeromonas hydrophila

Berberine hydrochloride is an isoquinoline alkaloid, which has antitumoral, antibacterial, and antiviral activities in vivo and in vitro. Charybdis japonica is one of the main economic species of crab in Southeast Asia. We studied the molecular mechanism of oxidative stress in berberine hydrochloride-treated C. japonica infected with Aeromonas hydrophila. C. japonica were infected with A. hydrophila after being submerged in different concentrations (0, 100, 200, and 300 mg/L) of berberine hydrochloride for 48 h. The full-length cDNA of Prx6 and the ORFs of Prx5 and PXL2A were cloned. Prx6 and PXL2A each have one conserved domain, Cys44, and Cys81. The Prx5 conserved domain contains three important Cys loci, Cys75, Cys100, and Cys76. Prx6 was different from Prx5 and PXL2A in the Peroxiredoxin family. The transcription levels of PXL2A infected with A. hydrophila were all higher than the control. The transcription levels of C. japonica were further increased by adding berberine hydrochloride and were increased the highest at a concentration of 300 mg/L. The activities of glutathione peroxidase, superoxide dismutase, and catalase in the hepatopancreas of berberine hydrochloride-treated C. japonica infected with A. hydrophila were significantly increased compared with those only infected with A. hydrophila and the control group. The glutathione transferase activity in the hepatopancreas was significantly increased in berberine hydrochloride-treated C. japonica. The results of this study provide a new understanding of the potential role of berberine hydrochloride on the oxidative stress mechanisms of C. japonica.

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Schisandrin A protects intestinal epithelial cells from deoxynivalenol-induced cytotoxicity, oxidative damage and inflammation

Scientific Reports ◽

10.1038/s41598-019-55821-4 ◽

2019 ◽

Vol 9 (1) ◽

Cited By ~ 5

Author(s):

Murphy L. Y. Wan ◽

Paul C. Turner ◽

Vanessa A. Co ◽

M. F. Wang ◽

Khaled M. A. Amiri ◽

...

Keyword(s):

Oxidative Stress ◽

Intestinal Inflammation ◽

Health Concern ◽

Heme Oxygenase 1 ◽

Antioxidant Enzyme Activities ◽

Transferase Activity ◽

Nuclear Factor ◽

Ht 29

AbstractExtensive research has revealed the association of continued oxidative stress with chronic inflammation, which could subsequently affect many different chronic diseases. The mycotoxin deoxynivalenol (DON) frequently contaminates cereals crops worldwide, and are a public health concern since DON ingestion may result in persistent intestinal inflammation. There has also been considerable attention over the potential of DON to provoke oxidative stress. In this study, the cytoprotective effect of Schisandrin A (Sch A), one of the most abundant active dibenzocyclooctadiene lignans in the fruit of Schisandra chinensis (Turcz.) Baill (also known as Chinese magnolia-vine), was investigated in HT-29 cells against DON-induced cytotoxicity, oxidative stress and inflammation. Sch A appeared to protect against DON-induced cytotoxicity in HT-29 cells, and significantly lessened the DON-stimulated intracellular reactive oxygen species and nitrogen oxidative species production. Furthermore, Sch A lowered DON-induced catalase, superoxide dismutase and glutathione peroxidase antioxidant enzyme activities but maintains glutathione S transferase activity and glutathione levels. Mechanistic studies suggest that Sch A reduced DON-induced oxidative stress by down-regulating heme oxygenase-1 expression via nuclear factor (erythroid-derived 2)-like 2 signalling pathway. In addition, Sch A decreased the DON-induced cyclooxygenase-2 expression and prostaglandin E2 production and pro-inflammatory cytokine interleukin 8 expression and secretion. This may be mediated by preventing DON-induced translocation of nuclear factor-κB, as well as activation of mitogen-activated protein kinases pathways. In the light of these findings, we concluded that Sch A exerted a cytoprotective role in DON-induced toxicity in vitro, and it would be valuable to examine in vivo effects.

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Oxidative stress in proliferative lesions of parathyroid gland

Polish Journal of Surgery ◽

10.5604/01.3001.0012.7258 ◽

2018 ◽

Vol 90 (5) ◽

pp. 1-6

Author(s):

Mariusz Deska ◽

Oliwia Segiet ◽

Ewa Romuk ◽

Grzegorz Buła ◽

Joanna Polczyk ◽

...

Keyword(s):

Oxidative Stress ◽

Glutathione Transferase ◽

Antioxidant Defense System ◽

Stress Index ◽

Control Group ◽

Endocrine Disorders ◽

Transferase Activity ◽

Lipid Hydroperoxides ◽

Sod Activity ◽

Sh Groups

Background: Primary hyperparathyroidism (PHPT) is one of the most common endocrine disorders and defined as excessive secretion of parathormone. PHPT is a risk factor of several cardiovascular diseases, which could be caused by alterations in oxidant-antioxidant balance. Materials and methods: Blood serum collected from 52 consecutive patients with PHPT treated surgically constituted our study material, whereas 36 healthy volunteers were our control group. Oxidative stress was evaluated in both patients and control subjects by assessment of malondialdehyde (MDA) and lipid hydroperoxides (LHP). Antioxidants were evaluated by the measurement of superoxide dismutase (SOD), ceruloplasmin (CER), catalase (CAT), sulfhydryl (SH) groups, glutathione (GSH), glutathione peroxidase (GSH-Px), glutathione transferase activity (GST) and glutathione reductase (GR). Moreover total antioxidant capacity (TAC) and total oxidative status (TOS) were measured and oxidative stress index (OSI) was calculated. Results: OSI was increased in patients with PHPT when compared to normal controls, whereas TAC was lower in PHPT. The levels of CER, MnSOD, GR, SH groups and MDA were significantly decreased in PHPT. The levels of serum LHP, catalase and SOD were significantly higher in patients with PHPT than in healthy patients. The erythrocyte CAT activity and GST were significantly increased in patients after parathyroidectomy. The erythrocyte GR and GPx were up-regulated postoperatively, whereas SOD activity decreased. Conclusions: In PHPT there are several alterations in the balance between the production of reactive oxygen species and antioxidant defense system.

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Orosomucoid 1 Attenuates Doxorubicin-Induced Oxidative Stress and Apoptosis in Cardiomyocytes via Nrf2 Signaling

BioMed Research International ◽

10.1155/2020/5923572 ◽

2020 ◽

Vol 2020 ◽

pp. 1-13

Author(s):

Xiaoli Cheng ◽

Dan Liu ◽

Ruinan Xing ◽

Haixu Song ◽

Xiaoxiang Tian ◽

...

Keyword(s):

Oxidative Stress ◽

Caspase 3 ◽

Acute Phase Protein ◽

Control Group ◽

Heme Oxygenase 1 ◽

H9c2 Cells ◽

Phase Protein ◽

New Treatment

Doxorubicin (DOX) is an effective anticancer drug, but its therapeutic use is limited by its cardiotoxicity. The principal mechanisms of DOX-induced cardiotoxicity are oxidative stress and apoptosis in cardiomyocytes. Orosomucoid 1 (ORM1), an acute-phase protein, plays important roles in inflammation and ischemic stroke; however, the roles and mechanisms of ORM1 in DOX-induced cardiotoxicity remain unknown. Therefore, in the present study, we aimed to investigate the function of ORM1 in cardiomyocytes experiencing DOX-induced oxidative stress and apoptosis. A DOX-induced cardiotoxicity animal model was established in C57BL/6 mice by administering an intraperitoneal injection of DOX (20 mg/kg), and the control group was intraperitoneally injected with the same volume of sterilized saline. The effects were assessed after 7 d. Additionally, H9c2 cells were stimulated with DOX (10 μM) for 24 h. The results showed decreased ORM1 and increased oxidative stress and apoptosis after DOX stimulation in vivo and in vitro. ORM1 overexpression significantly reduced DOX-induced oxidative stress and apoptosis in H9c2 cells. ORM1 significantly increased the expression of nuclear factor-like 2 (Nrf2) and its downstream protein heme oxygenase 1 (HO-1) and reduced the expression of the lipid peroxidation end product 4-hydroxynonenal (4-HNE) and the level of cleaved caspase-3. In addition, Nrf2 silencing reversed the effects of ORM1 on DOX-induced oxidative stress and apoptosis in cardiomyocytes. In conclusion, ORM1 inhibited DOX-induced oxidative stress and apoptosis in cardiomyocytes by regulating the Nrf2/HO-1 pathway, which might provide a new treatment strategy for DOX-induced cardiotoxicity.

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Sulforaphane Attenuates Contrast-Induced Nephropathy in Rats via Nrf2/HO-1 Pathway

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/9825623 ◽

2016 ◽

Vol 2016 ◽

pp. 1-12 ◽

Cited By ~ 19

Author(s):

Zhihong Zhao ◽

Guixiang Liao ◽

Qin Zhou ◽

Daoyuan Lv ◽

Harry Holthfer ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Model ◽

Renal Tissue ◽

Antioxidant Defenses ◽

Control Group ◽

Heme Oxygenase 1 ◽

Contrast Induced Nephropathy ◽

Hk2 Cells

Background. Oxidative stress plays an important role in the pathogenesis of contrast-induced nephropathy (CIN). The aim of this study was to investigate the antioxidant effects of sulforaphane (SFN) in a rat model of CIN and a cell model of oxidative stress in HK2 cells.Methods. Rats were randomized into four groups (n=6per group): control group, Ioversol group (Ioversol-induced CIN), Ioversol + SFN group (CIN rats pretreated with SFN), and SFN group (rats treated with SFN). Renal function tests, malondialdehyde (MDA), and reactive oxygen species (ROS) were measured. Western blot, real-time polymerase chain reaction analysis, and immunohistochemical analysis were performed for nuclear factor erythroid-derived 2-like 2 (Nrf2) and heme oxygenase-1 (HO-1) detection.Results. Serum blood urea nitrogen (BUN), creatinine, and renal tissue MDA were increased after contrast exposure. Serum BUN, creatinine, and renal tissue MDA were decreased in the Ioversol + SFN group as compared with those in the Ioversol group. SFN increased the expression of Nrf2 and HO-1 in CIN rats and in Ioversol-induced injury HK2 cells. SFN increased cell viability and attenuated ROS level in vitro.Conclusions. SFN attenuates experimental CIN in vitro and in vivo. This effect is suggested to activate the Nrf2 antioxidant defenses pathway.

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In vitro and in vivo tenocyte-protective effectiveness of dehydroepiandrosterone against high glucose-induced oxidative stress

BMC Musculoskeletal Disorders ◽

10.1186/s12891-021-04398-z ◽

2021 ◽

Vol 22 (1) ◽

Author(s):

Shintaro Mukohara ◽

Yutaka Mifune ◽

Atsuyuki Inui ◽

Hanako Nishimoto ◽

Takashi Kurosawa ◽

...

Keyword(s):

Oxidative Stress ◽

Matrix Metalloproteinase ◽

Protein Expression ◽

Achilles Tendon ◽

Mrna Expression ◽

High Glucose ◽

Control Group ◽

Type I

Abstract Background Dehydroepiandrosterone (DHEA), an adrenal steroid, has a protective role against diabetes. This study aimed to investigate the in vitro and in vivo protective effects of DHEA against high glucose-induced oxidative stress in tenocytes and tendons. Methods Tenocytes from normal Sprague-Dawley rats were cultured in low-glucose (LG) or high-glucose (HG) medium with or without DHEA. The experimental groups were: control group (LG without DHEA), LG with DHEA, HG without DHEA, and HG with DHEA. Reactive oxygen species (ROS) production, apoptosis, and messenger RNA (mRNA) expression of NADPH oxidase (NOX) 1 and 4, and interleukin-6 (IL-6) were determined. Further, diabetic rats were divided into a control group and a DHEA-injected group (DHEA group). NOX1 and NOX4 protein expression and mRNA expression of NOX1, NOX4, IL-6, matrix metalloproteinase (MMP)-2, tissue inhibitors of matrix metalloproteinase (TIMP)-2, and type I and III collagens in the Achilles tendon were determined. Results In rat tenocytes, DHEA decreased the expression of NOX1 and IL-6, ROS accumulation, and apoptotic cells. In the diabetic rat Achilles tendon, NOX1 protein expression and mRNA expression of NOX1, IL-6, MMP-2, TIMP-2, and type III collagen were significantly lower while type I collagen expression was significantly higher in the DHEA group than in the control group. Conclusions DHEA showed antioxidant and anti-inflammatory effects both in vitro and in vivo. Moreover, DHEA improved tendon matrix synthesis and turnover, which are affected by hyperglycemic conditions. DHEA is a potential preventive drug for diabetic tendinopathy.

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Endometriosis Susceptibility to Dapsone-Hydroxylamine-Induced Alterations Can Be Prevented by Licorice Intake: In Vivo and In Vitro Study

International Journal of Molecular Sciences ◽

10.3390/ijms22168476 ◽

2021 ◽

Vol 22 (16) ◽

pp. 8476

Author(s):

Chiara Sabbadin ◽

Alessandra Andrisani ◽

Gabriella Donà ◽

Elena Tibaldi ◽

Anna Maria Brunati ◽

...

Keyword(s):

Oxidative Stress ◽

In Vitro Study ◽

Carbonic Anhydrase Activity ◽

Control Group ◽

Beneficial Effects ◽

Licorice Extract ◽

Anti Oxidant ◽

Gynecological Disease

Endometriosis, an estrogen-dependent chronic gynecological disease, is characterized by a systemic inflammation that affects circulating red blood cells (RBC), by reducing anti-oxidant defenses. The aim of this study was to investigate the potential beneficial effects of licorice intake to protect RBCs from dapsone hydroxylamine (DDS-NHOH), a harmful metabolite of dapsone, commonly used in the treatment of many diseases. A control group (CG, n = 12) and a patient group (PG, n = 18) were treated with licorice extract (25 mg/day), for a week. Blood samples before (T0) and after (T1) treatment were analyzed for: i) band 3 tyrosine phosphorylation and high molecular weight aggregates; and ii) glutathionylation and carbonic anhydrase activity, in the presence or absence of adjunctive oxidative stress induced by DDS-NHOH. Results were correlated with plasma glycyrrhetinic acid (GA) concentrations, measured by HPLC–MS. Results showed that licorice intake decreased the level of DDS-NHOH-related oxidative alterations in RBCs, and the reduction was directly correlated with plasma GA concentration. In conclusion, in PG, the inability to counteract oxidative stress is a serious concern in the evaluation of therapeutic approaches. GA, by protecting RBC from oxidative assault, as in dapsone therapy, might be considered as a new potential tool for preventing further switching into severe endometriosis.

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In Vitro and in Vivo Tenocyte-protective Effectiveness of Dehydroepiandrosterone Against High Glucose-induced Oxidative Stress

10.21203/rs.3.rs-154654/v1 ◽

2021 ◽

Author(s):

Shintaro Mukohara ◽

Yutaka Mifune ◽

Atsuyuki Inui ◽

Hanako Nishimoto ◽

Takashi Kurosawa ◽

...

Keyword(s):

Oxidative Stress ◽

Matrix Metalloproteinase ◽

Protein Expression ◽

Achilles Tendon ◽

Mrna Expression ◽

High Glucose ◽

Control Group ◽

Type I

Abstract BackgroundDehydroepiandrosterone (DHEA), an adrenal steroid, has a protective role against diabetes. The aim of this study was to investigate the in vitro and in vivo protective effects of DHEA against high glucose-induced oxidative stress in tenocytes and tendons. Methods In an in vitro study, tenocytes from normal Sprague-Dawley rats were cultured in low-glucose (LG) or high-glucose (HG) medium with or without DHEA. The experimental groups were: control group (LG without DHEA), LG with DHEA, HG without DHEA, and HG with DHEA. Reactive oxygen species (ROS) production, apoptosis, and messenger RNA (mRNA) expression of NADPH oxidase (NOX) 1 and 4, and interleukin-6 (IL-6) were determined. In the in vivo study, diabetic rats were divided into a control group and a DHEA-injected group (DHEA group). NOX1 and NOX4 protein expression and mRNA expression of NOX1, NOX4, IL-6, matrix metalloproteinase (MMP)-2, tissue inhibitors of matrix metalloproteinase (TIMP)-2, and type I and III collagens in the Achilles tendon were determined. Results In rat tenocytes, DHEA decreased the expression of NOX1 and IL-6, ROS accumulation, and apoptotic cells. In the diabetic rat Achilles tendon, NOX1 protein expression and mRNA expression of NOX1, IL-6, MMP-2, TIMP-2, and type III collagen were significantly lower, while type I collagen expression was significantly lower in the DHEA group.Conclusions DHEA showed antioxidant and anti-inflammatory effects both in vitro and in vivo. Moreover, DHEA improved tendon matrix synthesis and turnover which are affected by hyperglycemic conditions. DHEA could be a preventive drug for the diabetic tendinopathy.

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Pomegranate juice and punicalagin attenuate oxidative stress and apoptosis in human placenta and in human placental trophoblasts

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00003.2012 ◽

2012 ◽

Vol 302 (9) ◽

pp. E1142-E1152 ◽

Cited By ~ 58

Author(s):

Baosheng Chen ◽

Methodius G. Tuuli ◽

Mark S. Longtine ◽

Joong Sik Shin ◽

Russell Lawrence ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Death ◽

Human Placenta ◽

Apple Juice ◽

Kinase Inhibitor ◽

Pomegranate Juice ◽

Control Group ◽

Induced Apoptosis

The human placenta is key to pregnancy outcome, and the elevated oxidative stress present in many complicated pregnancies contributes to placental dysfunction and suboptimal pregnancy outcomes. We tested the hypothesis that pomegranate juice, which is rich in polyphenolic antioxidants, limits placental trophoblast injury in vivo and in vitro. Pregnant women with singleton pregnancies were randomized at 35∼38 wk gestation to 8 oz/day of pomegranate juice or apple juice (placebo) until the time of delivery. Placental tissues from 12 patients (4 in the pomegranate group and 8 in the control group) were collected for analysis of oxidative stress. The preliminary in vivo results were extended to oxidative stress and cell death assays in vitro. Placental explants and cultured primary human trophoblasts were exposed to pomegranate juice or glucose (control) under defined oxygen tensions and chemical stimuli. We found decreased oxidative stress in term human placentas from women who labored after prenatal ingestion of pomegranate juice compared with apple juice as control. Moreover, pomegranate juice reduced in vitro oxidative stress, apoptosis, and global cell death in term villous explants and primary trophoblast cultures exposed to hypoxia, the hypoxia mimetic cobalt chloride, and the kinase inhibitor staurosporine. Punicalagin, but not ellagic acid, both prominent polyphenols in pomegranate juice, reduced oxidative stress and stimulus-induced apoptosis in cultured syncytiotrophoblasts. We conclude that pomegranate juice reduces placental oxidative stress in vivo and in vitro while limiting stimulus-induced death of human trophoblasts in culture. The polyphenol punicalagin mimics this protective effect. We speculate that antenatal intake of pomegranate may limit placental injury and thereby may confer protection to the exposed fetus.

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Erythrocyte Fraction in Thrombi Is Increased with Serum Iron by Influencing Fibrin Networks via Oxidative Stress

Oxidative Medicine and Cellular Longevity ◽

10.1155/2021/3673313 ◽

2021 ◽

Vol 2021 ◽

pp. 1-13

Author(s):

Mingli Liu ◽

Minghui Chen ◽

Zhongfei Hao ◽

Qingbin Li ◽

Yan Feng ◽

...

Keyword(s):

Oxidative Stress ◽

Serum Iron ◽

Iron Concentration ◽

Clinical Samples ◽

Control Group ◽

Serum Iron Concentration ◽

Fibrin Networks ◽

Stroke Center

Objective. This study investigated whether the erythrocyte fraction in thrombi would be increased with serum iron via oxidative stress. Methods. This study retrospectively enrolled patients with acute ischemic stroke treated using endovascular treatment in a single stroke center from October to December 2019. We examined the relationship between serum iron and erythrocyte-rich thrombi and the correlation of serum iron and the erythrocyte fraction in thrombi using clinical samples. Experiments in vivo and in vitro were performed to investigate the influence of oxidative stress on the correlation between serum iron concentration and erythrocyte fraction in thrombi. Results. We found from the clinical samples that serum iron concentration was related to erythrocyte-rich thrombi and positively associated with the erythrocyte fraction in thrombi in vivo. Further, the tightness of the fibrin networks regulating the erythrocyte fraction in thrombi was increased with serum iron concentration in vivo. Additionally, the oxidative stress level was increased with serum iron concentration in vivo. Moreover, we found that the tightness of the fibrin networks increased with higher oxidative stress levels in vitro. Lastly, experiments in vivo with inhibiting oxidative stress showed that the erythrocyte fraction in thrombi and the tightness of fibrin networks significantly increased in the iron group than those in the iron with oxidative stress inhibitor group and control group. Conclusions. Oxidative stress played a role in the process that the erythrocyte fraction in thrombi was increased with serum iron by influencing fibrin networks.

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Radiocontrast-induced nephropathy is attenuated by autophagy through regulation of apoptosis and inflammation

Human & Experimental Toxicology ◽

10.1177/0960327115604198 ◽

2015 ◽

Vol 35 (7) ◽

pp. 724-736 ◽

Cited By ~ 19

Author(s):

Gang Jee Ko ◽

So Yeon Bae ◽

Yu-Ah Hong ◽

Heui Jung Pyo ◽

Young Joo Kwon

Keyword(s):

Oxidative Stress ◽

Cellular Damage ◽

Control Group ◽

Tubular Injury ◽

Number Of Patients ◽

Apoptosis And Inflammation ◽

Autophagy Inhibition

Radiocontrast-induced nephropathy (RCN) is the third most common cause of acute renal failure among inpatients. Although the number of patients undergoing exams using radiocontrast is increasing, little progress has been made for RCN treatment. The pathophysiology of RCN is known as tubular injury due to oxidative stress. As autophagy regulates cellular damage under stressful conditions, we investigated the role of autophagy in RCN. RCN was induced in male C57BL/6 J mice by intraperitoneal injection of iohexol, and 3-methyladenine (3-MA) was used as an autophagy inhibitor. Tubular injury caused by iohexol was also examined in vitro using rat tubular cells (NRK-52E). Increased autophagy after iohexol administration was demonstrated by the increase of light chain 3-II in the damaged kidney tubules both in vivo and in vitro. Serum creatinine and tubular injury were significantly increased at 24 h after iohexol treatment, as compared to control group. Further they worsened with autophagy inhibition by 3-MA. In vitro studies also demonstrated that decreased cell viability by iohexol was aggravated with 3-MA pretreatment. Malondialdehyde measured for oxidative stress was increased by iohexol, and it was accentuated by autophagy inhibition, which resulted in increase of cytochrome c. Apoptosis, increased by iohexol treatment, was augmented with autophagy inhibition. Macrophage infiltration and increase of monocyte chemotactic protein-1 in kidneys were induced by iohexol, and it was aggravated with autophagy inhibition. This study showed that autophagy was involved with the pathophysiology of RCN, and the role of autophagy in modulation of apoptosis, oxidative stress, and inflammatory cell infiltration was supposed as mechanisms mitigating RCN.

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