Cyamopsis tetragonoloba annexin-1 gene (AnnCt1) is up-regulated under oxidative stress, and its protein has calcium-binding and an antioxidant property in-vitro

2022 ◽  
Author(s):  
Manjeshree Shail ◽  
Ramasare Prasad
Keyword(s):  
Oxidative Stress ◽  
Calcium Binding ◽  
Antioxidant Property ◽  
Cyamopsis Tetragonoloba ◽  
Annexin 1

scholarly journals Caffeine Modulates Cadmium-Induced Oxidative Stress, Neuroinflammation, and Cognitive Impairments by Regulating Nrf-2/HO-1 In Vivo and In Vitro

2019 ◽  
Vol 8 (5) ◽  
pp. 680 ◽  
Author(s):  
Amjad Khan ◽  
Muhammad Ikram ◽  
Tahir Muhammad ◽  
Junsung Park ◽  
Myeong Ok Kim
Keyword(s):  
Oxidative Stress ◽  
Cell Lines ◽  
Cognitive Deficits ◽  
Calcium Binding ◽  
Neuronal Loss ◽  
Treated Group ◽  
Nuclear Factor ◽  
Acute And Chronic Exposure

Cadmium (Cd), a nonbiodegradable heavy metal and one of the most neurotoxic environmental and industrial pollutants, promotes disturbances in major organs and tissues following both acute and chronic exposure. In this study, we assessed the neuroprotective potential of caffeine (30 mg/kg) against Cd (5 mg/kg)-induced oxidative stress-mediated neuroinflammation, neuronal apoptosis, and cognitive deficits in male C57BL/6N mice in vivo and in HT-22 and BV-2 cell lines in vitro. Interestingly, our findings indicate that caffeine markedly reduced reactive oxygen species (ROS) and lipid peroxidation (LPO) levels and enhanced the expression of nuclear factor-2 erythroid-2 (Nrf-2) and hemeoxygenase-1 (HO-1), which act as endogenous antioxidant regulators. Also, 8-dihydro-8-oxoguanine (8-OXO-G) expression was considerably reduced in the caffeine-treated group as compared to the Cd-treated group. Similarly, caffeine ameliorated Cd-mediated glial activation by reducing the expression of glial fibrillary acidic protein (GFAP), ionized calcium-binding adapter molecule 1 (Iba-1), and other inflammatory mediators in the cortical and hippocampal regions of the mouse brain. Moreover, caffeine markedly attenuated Cd-induced neuronal loss, synaptic dysfunction, and learning and cognitive deficits. Of note, nuclear factor-2 erythroid-2 (Nrf-2) gene silencing and nuclear factor-κB (NF-κB) inhibition studies revealed that caffeine exerted neuroprotection via regulation of Nrf-2- and NF-κB-dependent mechanisms in the HT-22 and BV-2 cell lines, respectively. On the whole, these findings reveal that caffeine rescues Cd-induced oxidative stress-mediated neuroinflammation, neurodegeneration, and memory impairment. The present study suggests that caffeine might be a potential antioxidant and neuroprotective agent against Cd-induced neurodegeneration.

scholarly journals Evaluation of anti-oxidant status in-vitro and in-vivo in hydro-alcoholic extract of Eugenia caryophyllus

2016 ◽  
Vol 4 (1) ◽  
pp. 19
Author(s):  
Roma Ghai ◽  
Kandasamy Nagarajan ◽  
Jitendra Singh ◽  
Shiwam Swarup ◽  
Minu Keshari
Keyword(s):  
Oxidative Stress ◽  
High Fat Diet ◽  
Antioxidant Property ◽  
Total Phenolic ◽  
Alcoholic Extract ◽  
Flavonoid Content ◽  
Anti Oxidant ◽  
Oxidant Status

<p>Free radicals mediated oxidative stress is the major risk factor for many chronic diseases like atherosclerosis, diabetes mellitus, arthritis, cancer, ageing and neurodegenerative diseases. Therapy with anti-oxidants is gradually gaining lot of importance for treatment of such diseases. Hydro-alcoholic extract of <em>Eugenia caryophyllus</em> was studied for its <em>in-vivo</em> antioxidant activity using two different animal models viz. Triton induced hyperlipidemia and High fat diet induced hyperlipidemia. Total phenolic content and total flavonoid content, DPPH assay was also carried out for <em>in vitro</em> anti-oxidant efficacy. Total protein, lipid peroxidation (MDA), reduced glutathione, superoxide dismutase and catalase were evaluated in the liver tissue in Triton induced hyperlipidemia and diet induced hyperlipidemia models. The study findings indicated significant <em>in-vivo</em> and <em>in-vitro</em> antioxidant property that may be related to the amount of polyphenols and flavonoids present in the extract. These results clearly indicate that <em>Eugenia caryophyllus</em> is effective against free radical mediated oxidative stress.</p>

HPLC phenolic fingerprinting, antioxidant and anti-phosphodiesterase-5 properties of Rauwolfia vomitoria extract

2019 ◽  
Vol 30 (5) ◽  
Author(s):  
Ganiyu Oboh ◽  
Adeniyi A. Adebayo ◽  
Ayokunle O. Ademosun
Keyword(s):  
Oxidative Stress ◽  
Vascular Dysfunction ◽  
Radical Scavenging ◽  
Antioxidant Property ◽  
Dependent Manner ◽  
Antioxidant Power ◽  
Phosphodiesterase 5 ◽  
Rauwolfia Vomitoria ◽  
And Oxidative Stress

Abstract Background In Nigerian traditional medicine, Rauwolfia vomitoria has been reported to be useful in the management of various human diseases, but there is no relevant information to substantiate its involvement in managing diseases arising from vascular dysfunction and oxidative stress. However, this study sought to investigate the antioxidant property of R. vomitoria and its effect on phophodiesterase-5 activity in vitro. Methods The antioxidant property was assessed through ferric-reducing antioxidant power (FRAP), copper chelation, and ABTS radical-scavenging activity. In addition, the effect of R. vomitoria on phosphodiesterase-5 (PDE-5) activity was assessed in vitro. Furthermore, analysis of phenolic compounds present in R. vomitoria was carried out using high-performance liquid chromatography (HPLC). Results The findings in this study revealed that R. vomitoria inhibited PDE-5 in a dose-dependent manner (IC50 = 252.42 μg/mL). Furthermore, the antioxidant activity of R. vomitoria was established through FRAP (19.68 mg AAE/g), ABTS radical-scavenging ability (74.25 mmol TEAC/g), and Cu2+-chelating ability (IC50 = 0.13 mg/mL). Conclusions The antioxidant property of R. vomitoria and its inhibitory effect on PDE-5 could be useful in the management of diseases arising from vascular dysfunction and oxidative stress.

scholarly journals Glaucocalyxin B Alleviates Lipopolysaccharide-Induced Parkinson’s Disease by Inhibiting TLR/NF-κB and Activating Nrf2/HO-1 Pathway

2017 ◽  
Vol 44 (6) ◽  
pp. 2091-2104 ◽  
Author(s):  
Wei Xu ◽  
Deyu Zheng ◽  
Yuanyuan Liu ◽  
Ji Li ◽  
Li Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Calcium Binding ◽  
Microglial Cells ◽  
Related Factor ◽  
Nuclear Factor ◽  
Related Factors ◽  
Stress Injury

Background/Aims: Parkinson’s disease (PD) is a common neurodegenerative disease in the old population, characterized by dopaminergic neuron loss, inflammation and oxidative stress injury in the substantia nigra. Glaucocalyxin B (GLB), an ent-kauranoid diterpenoid isolated from Rabdosia japonica, has anti-inflammation and anti-tumor effects. However, its effects on PD remain unclear. Methods: PD was introduced in rats via injection of lipopolysaccharide (LPS) into cerebral corpus striatum, and GLB was given intracerebroventricularly to these rats. Their walking, climbing and sensory states were detected by Stepping, Whisker and Cylinder Tests. The expression of tyrosine hydroxylase (TH), glial fibrillary acidic protein (GFAP), CD11b and ionized calcium binding adaptor molecule (IBA)-1 were detected by immunohischemical staining. The levels of a series of inflammatory factors, oxidative stress-related factors and apoptosis-related factors were measured by real-time PCR, immunoblotting and ELISA. In addition, Toll-like receptor (TLR)/nuclear factor kappa B (NF-κB) and nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase (HO)-1 pathways were investigated to illustrate the underlying mechanism. In vitro, microglial cells exposed to LPS were treated with GLB. Results: The injection of LPS caused walking, climbing and sensory disturbances in rats, induced inflammation, oxidative stress response and apoptosis, and activated TLR/NF-κB and Nrf2/ HO-1 pathways in the cerebral tissue. GLB administration attenuated LPS-induced alterations. The TLR/NF-κB pathway was deactivated and Nrf2/HO-1 was activated after application of GLB. In vitro, cytotoxic effects induced by the conditioned medium derived from microglial cells exposed to LPS in PC12 cells were attenuated by GLB. Conclusion: GLB suppresses LPS-induced PD symptoms by modification of TLR/NF-κB and Nrf2/HO-1 pathways in vivo and in vitro.

scholarly journals The Long Noncoding RNA Hotair Regulates Oxidative Stress and Cardiac Myocyte Apoptosis during Ischemia-Reperfusion Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-19 ◽  
Author(s):  
Kai Meng ◽  
Jiao Jiao ◽  
Rui-Rui Zhu ◽  
Bo-Yuan Wang ◽  
Xiao-Bo Mao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Calcium Binding ◽  
Cardiac Myocyte ◽  
Heart Diseases ◽  
Ischemia Reperfusion ◽  
Negative Regulator ◽  
Dependent Manner ◽  
Myocyte Apoptosis ◽  
Cardiac Myocyte Apoptosis

Oxidative stress and subsequent cardiac myocyte apoptosis play central roles in the initiation and progression of myocardial ischemia-reperfusion (I/R) injury. Homeobox transcript antisense intergenic RNA (Hotair) was previously implicated in various heart diseases, yet its role in myocardial I/R injury has not been clearly demonstrated. Mice with cardiac-restricted knockdown or overexpression of Hotair were exposed to I/R surgery. H9c2 cells were cultured and subjected to hypoxia/reoxygenation (H/R) stimulation to further verify the role and underlying mechanisms of Hotair in vitro. Histological examination, molecular detection, and functional parameters were determined in vivo and in vitro. In response to I/R or H/R treatment, Hotair expression was increased in a bromodomain-containing protein 4-dependent manner. Cardiac-restricted knockdown of Hotair exacerbated, whereas Hotair overexpression prevented I/R-induced oxidative stress, cardiac myocyte apoptosis, and cardiac dysfunction. Mechanistically, we observed that Hotair exerted its beneficial effects via activating AMP-activated protein kinase alpha (AMPKα). Further detection revealed that Hotair activated AMPKα through regulating the enhancer of zeste homolog 2/microRNA-451/calcium-binding protein 39 (EZH2/miR-451/Cab39) axis. We provide the evidence that endogenous lncRNA Hotair is an essential negative regulator for oxidative stress and cardiac myocyte apoptosis in myocardial I/R injury, which is dependent on AMPKα activation via the EZH2/miR-451/Cab39 axis.

scholarly journals miR-451 Silencing Inhibited Doxorubicin Exposure-Induced Cardiotoxicity in Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Jun Li ◽  
Weiguo Wan ◽  
Tao Chen ◽  
Suiyang Tong ◽  
Xuejun Jiang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Calcium Binding ◽  
Cell Injury ◽  
Contractile Function ◽  
Cardiac Injury ◽  
Specific Inhibitor ◽  
Whole Body ◽  
Ampk Signaling

Oxidative stress and cardiomyocytes apoptosis were closely involved in the pathological process of doxorubicin- (Dox-) induced cardiac injury. MicroRNA-451 (miR-451) was mainly expressed in cardiomyocytes. However, the role of miR-451 in Dox-induced cardiac injury remained unclear. Our study aimed to investigate the effect of miR-451 on Dox-induced cardiotoxicity in mice. We established a Dox-induced cardiotoxicity model in the mice and manipulated miR-451 expression in the heart using a miR-451 inhibitor, which was injected every other day beginning at one day before Dox injection. Oxidative stress and apoptosis in the hearts were evaluated. miR-451 levels were significantly increased in Dox-treated mice or cardiomyocytes. miR-451 inhibition attenuated Dox-induced whole-body wasting and heart atrophy, reduced cardiac injury, restored cardiac function, and improved cardiomyocyte contractile function. Moreover, miR-451 inhibition reduced oxidative stress and cardiomyocytes apoptosis in vivo and in vitro. miR-451 inhibition increased the expression of calcium binding protein 39 (Cab39) and activated adenosine monophosphate activated protein kinase (AMPK) signaling pathway. A specific inhibitor of AMPK abolished the protection provided by miR-451 inhibition against cell injury in vitro. In conclusion, miR-451 inhibition protected against Dox-induced cardiotoxicity via activation of AMPK signaling pathway.

Interactions Between Dental Composite Resins and Saliva A comparative biochemical in vitro study

2019 ◽  
Vol 56 (3) ◽  
pp. 529-533
Author(s):  
Mihaela Pantea ◽  
Diana Andreea Ighigeanu ◽  
Alexandra Totan ◽  
Maria Greabu ◽  
Daniela Miricescu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
In Vitro Study ◽  
Composite Resins ◽  
Vitro Study ◽  
Dental Composite ◽  
Gamma Glutamyl Transferase ◽  
Specific Protocol ◽  
Dental Composite Resins ◽  
Glutamyl Transferase

This in vitro study analyses the biochemical interaction between saliva and three types of dental composite resins (a direct resin, an indirect resin and a dual-cure resin used for cementation of indirect dental restorations). The resin samples were obtained following a specific protocol and in line with the producers� recommendations; the resin samples were incubated with saliva samples collected from 19 healthy volunteers. The obtained results showed that the tested composite resins did not produce significant changes in oxidative stress parameters that were analysed (albumin, uric acid, GGT / gamma glutamyl transferase, OXSR-1 / oxidative stress responsive kinase 1) and do not influence the inflammatory salivary status reflected by the levels of IL-6 - an inflammatory marker.

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