scholarly journals Protective Effects of Taurine Chloramine on Experimentally Induced Colitis: NFκB, STAT3, and Nrf2 as Potential Targets

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 479
Author(s):  
Seong Hoon Kim ◽  
Hye-Won Yum ◽  
Seung Hyeon Kim ◽  
Wonki Kim ◽  
Su-Jung Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Parent Compound ◽  
Oxidative Stress Marker ◽  
Heme Oxygenase 1 ◽  
Trinitrobenzene Sulfonic Acid ◽  
Protective Effects ◽  
Taurine Chloramine ◽  
Proinflammatory Mediators ◽  
Experimentally Induced

Taurine chloramine (TauCl) is an endogenous anti-inflammatory substance which is derived from taurine, a semi-essential sulfur-containing β-amino acid found in some foods including meat, fish, eggs and milk. In general, TauCl as well as its parent compound taurine downregulates production of tissue-damaging proinflammatory mediators, such as chemokines and cytokines in many different types of cells. In the present study, we investigated the protective effects of TauCl on experimentally induced colon inflammation. Oral administration of TauCl protected against mouse colitis caused by 2,4,6-trinitrobenzene sulfonic acid (TNBS). TauCl administration attenuated apoptosis in the colonic mucosa of TNBS-treated mice. This was accompanied by reduced expression of an oxidative stress marker, 4-hydroxy-2-nonenal and proinflammatory molecules including tumor necrosis factor-α, interleukin-6 and cyclooxygenase-2 in mouse colon. TauCl also inhibited activation of NFκB and STAT3, two key transcription factors mediating proinflammatory signaling. Notably, the protective effect of TauCl on oxidative stress and inflammation in the colon of TNBS-treated mice was associated with elevated activation of Nrf2 and upregulation of its target genes encoding heme oxygenase-1, NAD(P)H:quinone oxidoreductase, glutamate cysteine ligase catalytic subunit, and glutathione S-transferase. Taken together, these results suggest that TauCl exerts the protective effect against colitis through upregulation of Nrf2-dependent cytoprotective gene expression while blocking the proinflammatory signaling mediated by NFκB and STAT3.

scholarly journals Oral Administration of Gintonin Protects the Brains of Mice against Aβ-Induced Alzheimer Disease Pathology: Antioxidant and Anti-Inflammatory Effects

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Muhammad Ikram ◽  
Min Gi Jo ◽  
Tae Ju Park ◽  
Min Woo Kim ◽  
Ibrahim Khan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mouse Model ◽  
Amyloid Β ◽  
Microglial Cells ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Protective Effects ◽  
Biochemical Tests ◽  
Proinflammatory Mediators ◽  
Ad Mouse Model

The study was aimed at analyzing the protective effects of gintonin in an amyloid beta- (Aβ-) induced Alzheimer’s disease (AD) mouse model. For the development of the Aβ-induced AD mouse model, the amyloid-β (Aβ1-42) peptide was stereotaxically injected into the brains of mice. Subsequently, gintonin was administered at a dose of 100 mg/kg/day/per oral (p.o) for four weeks daily, and its effects were evaluated by using western blotting, fluorescence analysis of brain sections, biochemical tests, and memory-related behavioral evaluations. To elucidate the effects of gintonin at the mechanistic level, the activation of endogenous antioxidant mechanisms, as well as the activation of astrocytes, microglia, and proinflammatory mediators such as nuclear factor erythroid 2-related factor 2 (NRF-2) and heme oxygenase-1 (HO-1), was evaluated. In addition, microglial cells (BV-2 cells) were used to analyze the effects of gintonin on microglial activation and signaling mechanisms. Collectively, the results suggested that gintonin reduced elevated oxidative stress by improving the expression of NRF-2 and HO-1 and thereby reducing the generation of reactive oxygen species (ROS) and lipid peroxidation (LPO). Moreover, gintonin significantly suppressed activated microglial cells and inflammatory mediators in the brains of Aβ-injected mice. Our findings also indicated improved synaptic and memory functions in the brains of Aβ-injected mice after treatment with gintonin. These results suggest that gintonin may be effective for relieving AD symptoms by regulating oxidative stress and inflammatory processes in a mouse model of AD. Collectively, the findings of this preclinical study highlight and endorse the potential, multitargeted protective effects of gintonin against AD-associated oxidative damage, neuroinflammation, cognitive impairment, and neurodegeneration.

scholarly journals Epoetin Delta Reduces Oxidative Stress in Primary Human Renal Tubular Cells

2010 ◽  
Vol 2010 ◽  
pp. 1-9 ◽  
Author(s):  
Annelies De Beuf ◽  
Xiang-hua Hou ◽  
Patrick C. D'Haese ◽  
Anja Verhulst
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Stress Reduction ◽  
Renal Tissue ◽  
Heme Oxygenase 1 ◽  
Protective Effects ◽  
Renal Tubular Cells ◽  
Species Formation ◽  
Dependent Inhibition ◽  
Renal Tubular

Erythropoietin (EPO) exerts (renal) tissue protective effects. Since it is unclear whether this is a direct effect of EPO on the kidney or not, we investigated whether EPO is able to protect human renal tubular epithelial cells (hTECs) from oxidative stress and if so which pathways are involved. EPO (epoetin delta) could protect hTECs against oxidative stress by a dose-dependent inhibition of reactive oxygen species formation. This protective effect is possibly related to the membranous expression of the EPO receptor (EPOR) since our data point to the membranous EPOR expression as a prerequisite for this protective effect. Oxidative stress reduction went along with the upregulation of renoprotective genes. Whilst three of these, heme oxygenase-1 (HO-1), aquaporin-1 (AQP-1), and B-cell CLL/lymphoma 2 (Bcl-2) have already been associated with EPO-induced renoprotection, this study for the first time suggests carboxypeptidase M (CPM), dipeptidyl peptidase IV (DPPIV), and cytoglobin (Cygb) to play a role in this process.

scholarly journals Neurological Alterations and Testicular Damages in Aging Induced by D-Galactose and Neuro and Testicular Protective Effects of Combinations of Chitosan Nanoparticles, Resveratrol and Quercetin in Male Mice

Coatings ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 435
Author(s):  
Reham Z. Hamza ◽  
Mohammad S. Al-Harbi ◽  
Munirah A. Al-Hazaa
Keyword(s):  
Oxidative Stress ◽  
Chitosan Nanoparticles ◽  
Oxidative Stress Marker ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Enzymatic Antioxidants ◽  
Protective Effects ◽  
Biochemical Alterations ◽  
Wide Range ◽  
Neurological Alterations

Aging is a neurological disease that is afforded by incidence of oxidative stress. Chitosan has received global interests due to its wide medical uses. Quercetin (Q) is a bioflavonoid and widely distributed in vegetables and fruits. Resveratrol is considered as a potent antioxidant and is a component of a wide range of foods. The using of either chitosan nanopartciles (CH-NPs), querectin (Q), and resveratrol (RV) to reduce the oxidative stress and biochemical alterations on brain and testicular tissues induced by D-galactose (DG) (100 mg/Kg) were the aim of the present study. This study investigated the probable protective effects of CH-NPs in two doses (140,280 mg/Kg), Q (20 mg/Kg) and RV (20 mg/Kg), against DG induced aging and neurological alterations. Brain antioxidant capacity as malonaldehyde (MDA), catalase (CAT), and glutathione reductase (GRx), as well as histopathological damages of the brain and testicular tissues were measured. The DG treated group had significantly elevated the oxidative stress markers by 96% and 91.4% in brain and testicular tissues respectively and lower significantly the antioxidant enzyme activities of both brain and testicular tissues than those of the control group by 86.95%, 69.27%, 83.07%, and 69.43%. Groups of DG that treated with a combination of CH-NPs in two doses, Q and RV, the levels of oxidative stress marker declined significantly by 68.70%, 76.64% in brain tissues and by 74.07% and 76.61% in testicular tissues, and the enzymatic antioxidants increased significantly by 75.55%, 79.24%, 62.32%, and 61.97% as compared to the DG group. The present results indicate that CH-NPs, Q, and RV have protective effects against DG-induced brain and testis tissue damage at the biochemical and histopathological levels. Mechanisms of this protective effect of used compounds against neurological and testicular toxicity may be due to the enhanced brain and testis antioxidant capacities.

P1572EFFECTIVENESS OF COENZYME Q10-MICELLE COMPARED WITH COENZYME Q10 ON TACROLIMUS-INDUCED RENAL INJURY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Sheng Cui ◽  
Kang Luo ◽  
Yi Quan ◽  
Sun Woo Lim ◽  
Chul-Woo Yang
Keyword(s):  
Oxidative Stress ◽  
Coenzyme Q10 ◽  
Renal Injury ◽  
Apoptotic Cell ◽  
Oxidative Stress Marker ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Male Adult ◽  
Sprague Dawley Rats ◽  
Pathologic Lesions

Abstract Background and Aims We and others have recently demonstrated that Coenzyme Q10 (CoQ10) has protective effects against diabetes mellitus and various types of renal injury. This study investigated whether CoQ10-micelle treatment would affords superior renoprotection compared with CoQ10 in the governing tacrolimus (Tacrolimus)-induced renal injury in the rats. Method Male adult Sprague-dawley Rats were treated daily with Tacrolimus (1.5mg/kg/day, subcutaneous), CoQ10 (20mg/kg/day, oral), and CoQ10-micelle (20 mg/kg/day, oral) for 4 weeks. The effects of CoQ10 orCoQ10-micelle on Tac-induced renal injury were assessed in terms of renal function, histopathology, oxidative stress and apoptotic cell death. Results After 4 weeks of Tacrolimus treatment to rats caused renal dysfunction, typical pathologic lesions, and oxidative stress marker. The serum creatinine was reduced by Tac co-treatment with CoQ10 or CoQ10-micelle groups compared with the Tac and VH group (0.31 ± 0.03 in the VH group vs. 0.43 ± 0.041 in the Tac group vs.0.37 ± 0.031 in the Tac+CoQ10 group 0.30 ± 0.02123 in the Tac+CoQ10-micellegroup; 1P<0.05 vs. VH. 2P<0.05 vs. TAC. . 3P<0.05 vs. TAC+C.) The administration of CoQ10-micelle improved renal immunoreactivity, which was accompanied by reductions in oxidative stress and apoptosis. Assessment of the mitochondrial ultrastructure by electron microscopy revealed that tacrolimus co-treatment with CoQ10-micelle increased the size and number of mitochondria more than co-treatment with CoQ10, compared with that induced by TAC treatment alone. Conclusion These findings suggest that both CoQ10 and CoQ10-micelle effectively attenuates Tac-induced renal injury, and CoQ10-micelle provides more benefits than that of CoQ10.

scholarly journals The Protective Effect of Hispidin against Hydrogen Peroxide-Induced Oxidative Stress in ARPE-19 Cells via Nrf2 Signaling Pathway

Biomolecules ◽  
2019 ◽  
Vol 9 (8) ◽  
pp. 380 ◽  
Author(s):  
Huang ◽  
Chang ◽  
Chau ◽  
Chiu
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Protective Effect ◽  
Retinal Pigment ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Dependent Manner ◽  
Glutamate Cysteine Ligase ◽  
Jnk Pathway ◽  
Nrf2 Signaling Pathway

Hispidin, a polyphenol compound isolated from Phellinus linteus, has been reported to possess antioxidant activities. In this study, we aimed to investigate the mechanisms underlying the protective effect of hispidin against hydrogen peroxide (H2O2)-induced oxidative stress on Adult Retinal Pigment Epithelial cell line-19 (ARPE-19) cells. Hispidin was not cytotoxic to ARPE-19 cells at concentrations of less than 50 μM. The levels of intracellular reactive oxygen species (ROS) were analyzed by dichlorofluorescin diacetate (DCFDA) staining. Hispidin significantly restored H2O2-induced cell death and reduced the levels of intracellular ROS. The expression levels of antioxidant enzymes, such as NAD(P)H:Quinine oxidoreductase-1 (NQO-1), heme oxygenase-1 (HO-1), glutamate-cysteine ligase catalytic subunit (GCLC), and glutamate-cysteine ligase modifier subunit (GCLM) were examined using real-time PCR and Western blotting. Our results showed that hispidin markedly enhanced the expression of nuclear factor erythroid 2-related factor 2 (Nrf2), HO-1, NQO-1, GCLM, and GCLC in a dose-dependent manner. Furthermore, knockdown experiments revealed that transfection with Nrf2 siRNA successfully suppresses the hispidin activated Nrf2 signaling in ARPE-19 cells. Moreover, activation of the c-Jun N-terminal kinase (JNK) pathway is involved in mediating the protective effects of hispidin on the ARPE-19 cells. Thus, the present study demonstrated that hispidin provides protection against H2O2-induced damage in ARPE-19 cells via activation of Nrf2 signaling and up-regulation of its downstream targets, including Phase II enzymes, which might be associated with the activation of the JNK pathway.

scholarly journals Gypenosides Prevent H2O2-Induced Retinal Ganglion Cell Apoptosis by Concurrently Suppressing the Neuronal Oxidative Stress and Inflammatory Response

2020 ◽  
Vol 70 (4) ◽  
pp. 618-630 ◽  
Author(s):  
Hong-Kan Zhang ◽  
Yuan Ye ◽  
Kai-Jun Li ◽  
Zhen-ni Zhao ◽  
Jian-Feng He
Keyword(s):  
Oxidative Stress ◽  
Optic Neuritis ◽  
Ganglion Cells ◽  
Nerve Fibers ◽  
Inflammatory Factors ◽  
Heme Oxygenase 1 ◽  
Protective Effects ◽  
Retinal Ganglion ◽  
Apoptotic Pathway ◽  
Neuroprotective Effects

AbstractOur previous study demonstrated that gypenosides (Gp) exert protective effects on retinal nerve fibers and axons in a mouse model of experimental autoimmune optic neuritis. However, the therapeutic mechanisms remain unclear. Thus, in this study, a model of oxidative damage in retinal ganglion cells (RGCs) was established to investigate the protective effect of Gp, and its possible influence on oxidative stress in RGCs. Treatment of cells with H2O2 induced RGC injury owing to the generation of intracellular reactive oxygen species (ROS). In addition, the activities of antioxidative enzymes decreased and the expression of inflammatory factors increased, resulting in an increase in cellular apoptosis. Gp helped RGCs to become resistant to oxidation damage by directly reducing the amount of ROS in cells and exerting protective effects against H2O2-induced apoptosis. Treatment with Gp also reduced the generation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and increased nuclear respiratory factor 2 (Nrf-2) levels so as to increase the levels of heme oxygenase-1 (HO-1) and glutathione peroxidase 1/2 (Gpx1/2), which can enhance antioxidation in RGCs. In conclusion, our data indicate that neuroprotection by Gp involves its antioxidation and anti-inflammation effects. Gp prevents apoptosis through a mitochondrial apoptotic pathway. This finding might provide novel insights into understanding the mechanism of the neuroprotective effects of gypenosides in the treatment of optic neuritis.

scholarly journals Antioxidant Effects and Cytoprotective Potentials of Herbal Tea against H2O2-Induced Oxidative Damage by Activating Heme Oxygenase1 Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Ke-Xin Zhang ◽  
Jian-Bin Tan ◽  
Cheng-Liang Xie ◽  
Rong-Bo Zheng ◽  
Xiao-Dan Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Activity ◽  
Protective Effect ◽  
Functional Foods ◽  
Cell Damage ◽  
Damage Model ◽  
Enrichment Analysis ◽  
Protective Effects ◽  
Herbal Tea ◽  
Antioxidant Effects

Herbal tea with antioxidant ingredients has gained increasing attention in the field of functional foods due to their amelioration potential in aging-related diseases. Wanglaoji herbal tea (WHT) is a kind of traditional beverage made from herbal materials. This study was performed to investigate its antioxidant activity and identify its protective effect on a H2O2-induced cell damage model. In this study, we identified six kinds of phenolic acids with antioxidant activity in WHT, among which rosmarinic acid had the highest content and the highest contribution ratio to the antioxidant activity of WHT. Moreover, compared with the H2O2-induced damage group, the WHT treatment group can significantly increase the viability of cells and decrease the ratio of senescence-associated β-galactosidase-positive cells, intracellular malondialdehyde levels, and the percentage of G1 phase. Furthermore, enrichment analysis of differentially expressed genes revealed that heme oxygenase1 (HMOX1) was a key gene for protective effect of WHT on oxidative stress-induced cell damage. Thus, WHT exerted protective effects not only by scavenging reactive oxygen species but also by inducing the expression of cytoprotective genes by activating the HMOX1 pathway, which showed that WHT had a potential of promoting health by reducing oxidative stress-induced cell damage.

scholarly journals Involvement of Heme Oxygenase-1 Induction in the Cytoprotective and Immunomodulatory Activities ofViola patriniiin Murine Hippocampal and Microglia Cells

2012 ◽  
Vol 2012 ◽  
pp. 1-12 ◽  
Author(s):  
Bin Li ◽  
Dong-Sung Lee ◽  
Hyun-Gyu Choi ◽  
Kyoung-Su Kim ◽  
Gil-Saeng Jeong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heme Oxygenase ◽  
Therapeutic Potential ◽  
Reactive Oxygen Species Generation ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Ht22 Cells ◽  
Proinflammatory Mediators ◽  
Bv2 Cells ◽  
Anti Inflammatory

A number of diseases that lead to injury of the central nervous system are caused by oxidative stress and inflammation in the brain. In this study, NNMBS275, consisting of the ethanol extract ofViola patrinii, showed potent antioxidative and anti-inflammatory activity in murine hippocampal HT22 cells and BV2 microglia. NNMBS275 increased cellular resistance to oxidative injury caused by glutamate-induced neurotoxicity and reactive oxygen species generation in HT22 cells. In addition, the anti-inflammatory effects of NNMBS275 were demonstrated by the suppression of proinflammatory mediators, including proinflammatory enzymes (inducible nitric oxide synthase and cyclooxygenase-2) and cytokines (tumor necrosis factor-αand interleukin-1β). Furthermore, we found that the neuroprotective and anti-inflammatory effects of NNMBS275 were linked to the upregulation of nuclear transcription factor-E2-related factor 2-dependent expression of heme oxygenase-1 in HT22 and BV2 cells. These results suggest that NNMBS275 possesses therapeutic potential against neurodegenerative diseases that are induced by oxidative stress and neuroinflammation.

scholarly journals Protective Effect of Ginsenoside Against Acute Renal Failure via Reduction of Renal Oxidative Stress and Enhanced Expression of ChAT in the Proximal Convoluted Tubule and ERK1/2 in the Paraventricular Nuclei

2014 ◽  
pp. 597-604 ◽  
Author(s):  
J. ZHOU ◽  
H. A. ZHANG ◽  
Y. LIN ◽  
H. M. LIU ◽  
Y. M. CUI ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Protective Effect ◽  
Protective Effects ◽  
Paraventricular Nuclei ◽  
Mitogen Activated Protein ◽  
Enhanced Expression ◽  
Mapk Signal Pathway ◽  
Hypothalamic Paraventricular Nuclei

Generation of reactive oxygen species significantly contributes to the pathogenesis of acute renal failure (ARF) induced by myoglobin release. Ginsenosides (GS), the principal active ingredients of ginseng, is considered as an extremely good antioxidative composition of Chinese traditional and herbal drugs. The purpose of the present study was to investigate the protective effect of ginsenoside in rats with ARF on the changes of cholinergic nervous system in the kidney as well as on the involvement of mitogen-activated protein kinases (MAPK) in the hypothalamic paraventricular nuclei (PVN). In our assay, glycerol-induced acute renal failure in rats was employed to study the protective effects of ginsenoside. Our results indicated that the treatment of ARF rats with ginsenosides for 48 h significantly reduced lipid peroxidation, restored the superoxide dismutase (SOD) level. Meanwhile, the obvious increase of choline acetyltransferase-immunoreactivity (ChAT-IR) in the proximal convoluted tubular cells (PCT) was observed by immunohistochemistry in ARF+GS group. The same effect was also observed in the changes of p-ERK1/2-IR in the hypothalamic paraventricular nuclei. Our results suggest that ginsenoside administered orally may have a strong renal protective effect against glycerol-induced ARF, reduce the renal oxidative stress, and ginsenoside can also activate the cholinergic system in PCT, simultaneously MAPK signal pathway in the PVN was also activated.

scholarly journals GLP-1(9-36), a GLP-1 cleavage product, protects against oxidative stress and apoptosis through PI3K/Akt/NOS pathway in H9c2 cardiomyoblasts

2021 ◽  
Author(s):  
Narawat Nuamnaichati ◽  
Warisara Parichatikanond ◽  
Supachoke Mangmool
Keyword(s):  
Oxidative Stress ◽  
Active Form ◽  
Heme Oxygenase 1 ◽  
No Production ◽  
Protective Effects ◽  
Dipeptidyl Peptidase 4 ◽  
Akt Phosphorylation ◽  
H9c2 Cardiomyoblasts ◽  
Underlying Mechanisms ◽  
Induced Apoptosis

Abstract GLP-1(7–36), a major active form of GLP-1 hormone, is rapidly cleaved by dipeptidyl peptidase-4 to generate a truncated metabolite, GLP-1(9–36) which has a low affinity for GLP-1 receptor (GLP-1R). GLP-1(7–36) has been shown to have protective effects on cardiovascular system through GLP-1R-dependent way. Nevertheless, the cardioprotective effects of GLP-1(9–36) have not fully understood. The present study investigated the effects of GLP-1(9–36), including its underlying mechanisms against oxidative stress and apoptosis in H9c2 cardiomyoblasts. Here, we reported that GLP-1(9–36) protects H9c2 cardiomyoblasts from hydrogen peroxide (H2O2)-induced oxidative stress by promoting the synthesis of antioxidant enzymes, glutathione peroxidase-1, catalase, and heme oxygenase-1. In addition, treatment with GLP-1(9–36) suppressed H2O2-induced apoptosis by attenuating caspase-3 activity and upregulating proapoptotic proteins, Bcl-2 and Bcl-xL. These protective effects of GLP-1(9–36) are attenuated by blockade of PI3K-mediated Akt phosphorylation and prevention of nitric oxide synthase (NOS)-induced NO production. Collectively, GLP-1(9–36) represents the potential therapeutic target for prevention of oxidative stress and apoptosis in the heart.

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