scholarly journals Ginsenoside Rg1 attenuates arsenic-induced mice nephrotoxicity via the activated HO-1/mTOR-associated apoptosis or autophagy signaling

2021 ◽  
Author(s):  
yuan yang
Keyword(s):  
Oxidative Stress ◽  
Sodium Arsenite ◽  
Animal Experiments ◽  
Arsenic Exposure ◽  
Pharmacological Effects ◽  
Ginsenoside Rg1 ◽  
Sequestosome 1 ◽  
Bioactive Product ◽  
Apoptotic Effects ◽  
And Oxidative Stress

Nephrotoxicity attributed to environmental arsenic exposure, has been recognized by animal experiments and populational survey over 30 years in China, given a significance of public health by preventing from the disorder of renal function and hispathological abnormality. Here, Ginsenoside Rg1 (Rg1) as the commercial bioactive product of ginseng, play a beneficial role via antioxidant, anti-inflammatory and anti-apoptotic effects, which is poorly understood in arsenic-induced nephrotoxicity. The present study applied animal experiments to explore the pharmacological effects of Rg1 on sodium arsenite (SA)-induced nephrotoxicity in mice. Results showed that SA exposure led to renal pathological damage, and induced renal oxidative stress and the elevated levels of apoptosis or autophagy-associated indices in kidney. Further, western-blotting results confirmed the upregulations of pro-apoptotic Bax or autophagic unc-51-like kinase-1 (ULK1) or LC3-B signal, and the downregulations of HO-1 or mTOR signal and autophagy substrate sequestosome 1 (p62/SQSTM1) in kidney. Significantly, the intervention with Rg1 alleviated arsenic-induced renal pathological damage and oxidative stress, and upregulated the levels of HO-1, mTOR and p62, while the levels of Bax, ULK1 or LC3-B downregulated in kidney. In conclusion, the intervention with Rg1 relieves arsenic-induced mice nephrotoxicity maybe involved in the regulation of HO-1/mTOR-related apoptotic or autophagic signaling.

scholarly journals Tamoxifen and oxidative stress: an overlooked connection

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Nermin S. Ahmed ◽  
Marek Samec ◽  
Alena Liskova ◽  
Peter Kubatka ◽  
Luciano Saso
Keyword(s):  
Breast Cancer ◽  
Oxidative Stress ◽  
Gold Standard ◽  
Pharmacological Activities ◽  
Standard Drug ◽  
Menopausal Women ◽  
Wide Range ◽  
Post Menopausal ◽  
Apoptotic Effects ◽  
And Oxidative Stress

AbstractTamoxifen is the gold standard drug for the treatment of breast cancer in pre and post-menopausal women. Its journey from a failing contraceptive to a blockbuster is an example of pharmaceutical innovation challenges. Tamoxifen has a wide range of pharmacological activities; a drug that was initially thought to work via a simple Estrogen receptor (ER) mechanism was proven to mediate its activity through several non-ER mechanisms. Here in we review the previous literature describing ER and non-ER targets of tamoxifen, we highlighted the overlooked connection between tamoxifen, tamoxifen apoptotic effects and oxidative stress.

scholarly journals Roles of Thyroid Hormone-Associated microRNAs Affecting Oxidative Stress in Human Hepatocellular Carcinoma

2019 ◽  
Vol 20 (20) ◽  
pp. 5220 ◽  
Author(s):  
Po-Shuan Huang ◽  
Chia-Siu Wang ◽  
Chau-Ting Yeh ◽  
Kwang-Huei Lin
Keyword(s):  
Oxidative Stress ◽  
Thyroid Hormone ◽  
Liver Cancer ◽  
Negative Impact ◽  
Animal Experiments ◽  
Supporting Evidence ◽  
Antioxidant Genes ◽  
Physiological Processes ◽  
Cellular Components ◽  
And Oxidative Stress

Oxidative stress occurs as a result of imbalance between the generation of reactive oxygen species (ROS) and antioxidant genes in cells, causing damage to lipids, proteins, and DNA. Accumulating damage of cellular components can trigger various diseases, including metabolic syndrome and cancer. Over the past few years, the physiological significance of microRNAs (miRNA) in cancer has been a focus of comprehensive research. In view of the extensive level of miRNA interference in biological processes, the roles of miRNAs in oxidative stress and their relevance in physiological processes have recently become a subject of interest. In-depth research is underway to specifically address the direct or indirect relationships of oxidative stress-induced miRNAs in liver cancer and the potential involvement of the thyroid hormone in these processes. While studies on thyroid hormone in liver cancer are abundantly documented, no conclusive information on the potential relationships among thyroid hormone, specific miRNAs, and oxidative stress in liver cancer is available. In this review, we discuss the effects of thyroid hormone on oxidative stress-related miRNAs that potentially have a positive or negative impact on liver cancer. Additionally, supporting evidence from clinical and animal experiments is provided.

Alteration of the protein synthesis pattern in Neurospora crassa cells by hyperthermal and oxidative stress

1987 ◽  
Vol 33 (2) ◽  
pp. 162-168 ◽  
Author(s):  
M. Kapoor ◽  
J. Lewis
Keyword(s):  
Oxidative Stress ◽  
Heat Shock ◽  
Heat Shock Proteins ◽  
Neurospora Crassa ◽  
Sodium Arsenite ◽  
Dna Binding Protein ◽  
Specific Protein ◽  
One Dimensional ◽  
Shock Proteins ◽  
And Oxidative Stress

Neurospora crassa cells, grown at 28 °C for 14 h and heat shocked at 48 °C for 45 min, showed the synthesis of 11 heat-shock proteins (nHSPs) in one-dimensional electrophoretic profiles. Treatment with sodium arsenite induced the synthesis of two heat-shock proteins, nHSP70 and nHSP80, and a third, arsenite-specific protein, not induced by hyperthermia. Exposure to 0.5 or 1.0 mM H2O2 led to the induction of two of the heat-inducible nHSP70 family polypeptides. Sodium selenite, used in concert with H2O2, and arsenite were observed to modulate that heat-shock response. In addition, H2O2, menadione, and the glutathione depleters diamide and diethyl maleate promoted the synthesis of another protein, designated oxidative stress-responsive protein (OSP). A DNA-binding protein, specific for Neurospora DNA, was also demonstrated in extracts of heat-shocked cells.

scholarly journals Buprenorphine Alters Inflammatory and Oxidative Stress Molecular Markers in Arthritis

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Mahadevappa Hemshekhar ◽  
Vidyanand Anaparti ◽  
Carol Hitchon ◽  
Neeloffer Mookherjee
Keyword(s):  
Oxidative Stress ◽  
Molecular Markers ◽  
Murine Model ◽  
Animal Experiments ◽  
Response To Therapy ◽  
Prediction Of Response ◽  
Stress Markers ◽  
Oxidative Markers ◽  
Pain Scores ◽  
And Oxidative Stress

Buprenorphine is recommended for use as an analgesic in animal models including in murine models of collagen-induced arthritis (CIA). However, the effect of buprenorphine on the expression of disease-associated biomarkers is not well defined. We examined the effect of buprenorphine administration on disease progression and the expression of inflammatory and oxidative stress markers, in a murine model of CIA. Buprenorphine administration altered the expression of cytokines, IFN-γ, IL-6, and MMP-3, and oxidative markers, for example, iNOS, superoxide dismutase (SOD1), and catalase (CAT), in the CIA mice. As buprenorphine is an analgesic, we further monitored the association of expression of these biomarkers with pain scores in a human cohort of early rheumatoid arthritis (RA). Serum MMP-3 levels and blood mRNA expression of antioxidants sod1 and cat correlated with pain scores in the RA cohort. We have demonstrated that administration of buprenorphine alters the expression of inflammatory and oxidative stress-related molecular markers in a murine model of CIA. This caveat needs to be considered in animal experiments using buprenorphine as an analgesic, as it can be a confounding factor in murine studies used for prediction of response to therapy. Furthermore, the antioxidant enzymes that showed an association with pain scores in the human cohort may be explored as biomarkers for pain in future studies.

Modulatory role ofAcaciahoney from north-west Nigeria on sodium arsenite-induced clastogenicity and oxidative stress in male Wistar rats

2014 ◽  
Vol 29 (4) ◽  
pp. 321-326 ◽  
Author(s):  
Aliyu Muhammad ◽  
Oyeronke A. Odunola ◽  
Michael A. Gbadegesin ◽  
Ayodeji M. Adegoke ◽  
J. Olorunjuwon Olugbami ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Wistar Rats ◽  
Sodium Arsenite ◽  
North West ◽  
Male Wistar Rats ◽  
And Oxidative Stress

scholarly journals Inflammatory Response and Oxidative Stress as Mechanism of Reducing Hyperuricemia of Gardenia jasminoides-Poria cocos with Network Pharmacology

2021 ◽  
Vol 2021 ◽  
pp. 1-18
Author(s):  
Lijun Liu ◽  
Shengjun Jiang ◽  
Xuqiang Liu ◽  
Qi Tang ◽  
Yan Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Inflammatory Response ◽  
Inflammatory Responses ◽  
Animal Experiments ◽  
Kidney Injury ◽  
Network Pharmacology ◽  
Poria Cocos ◽  
Gardenia Jasminoides ◽  
And Oxidative Stress

Hyperuricemia (HUA) is a metabolic disease, closely related to oxidative stress and inflammatory responses, caused by reduced excretion or increased production of uric acid. However, the existing therapeutic drugs have many side effects. It is imperative to find a drug or an alternative medicine to effectively control HUA. It was reported that Gardenia jasminoides and Poria cocos could reduce the level of uric acid in hyperuricemic rats through the inhibition of xanthine oxidase (XOD) activity. But there were few studies on its mechanism. Therefore, the effective ingredients in G. jasminoides and P. cocoa extracts (GPE), the active target sites, and the further potential mechanisms were studied by LC-/MS/MS, molecular docking, and network pharmacology, combined with the validation of animal experiments. These results proved that GPE could significantly improve HUA induced by potassium oxazine with the characteristics of multicomponent, multitarget, and multichannel overall regulation. In general, GPE could reduce the level of uric acid and alleviate liver and kidney injury caused by inflammatory response and oxidative stress. The mechanism might be related to the TNF-α and IL-7 signaling pathway.

Luteolin Attenuates Diabetic Nephropathy through Suppressing Inflammatory Response and Oxidative Stress by Inhibiting STAT3 Pathway

2020 ◽  
Author(s):  
Miaoyuan Zhang ◽  
Liyu He ◽  
Jingsong Liu ◽  
Lin Zhou
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Inflammatory Response ◽  
Animal Experiments ◽  
Pathological Feature ◽  
Tubular Injury ◽  
Oral Gavage ◽  
Stat3 Pathway ◽  
Kidney Protection ◽  
And Oxidative Stress

Abstract Background Diabetic nephropathy (DN) is the leading cause of end-stage renal disease (ESRD). DN has many pathological changes, but tubular injury is considered to be a crucial pathological feature and plays a key role in the progression of DN. Accumulating studies have confirmed that Luteolin (3,4,5,7-tetrahydroxyflavone, Lut) possesses anti-inflammatory and antioxidant activities, which may play a role in kidney protection in DN. Objectives This paper described the effects of Lut on appropriated tubular injury in the kidneys of db/db mice and searched the possible mechanisms underlying the kidney protection effect in DN. Methods Twelve-week-old male C57BL/6 J db/db and C57BL/6 J db/m mice were used for the animal experiments. They were organized into the following five groups for the animal experiments: a db/m group (control, n=6); a db/db group(n=8) ; a db/db group receiving Lut (10 mg/kg/day, n=8)treatment by oral gavage; a db/db group receiving stattic (a selective STAT3 inhibitor,50 mg/Kg/day, n=8) treatment by oral gavage and a db/db group receiving both stattic and Lut treatment by oral gavage. Results In this study, we found that Lut might ameliorate glomerular sclerosis and interstitial fibrosis in DN mouse models through inhibiting the inflammatory response and oxidative stress. And it might play its biological function mainly through repressing the STAT3 activation. Conclusions Lut attenuates DN mainly via suppression of inflammatory response and oxidative response. STAT3 pathway is the potential target, which ultimately reduces renal fibrosis and delays the progress of DN.

L-Ascorbate protects rat hepatocytes against sodium arsenite—induced cytotoxicity and oxidative damage

2009 ◽  
Vol 29 (2) ◽  
pp. 103-111 ◽  
Author(s):  
Asit Kumar Bera ◽  
Tanmoy Rana ◽  
Subhashree Das ◽  
Subhasish Bandyopadhyay ◽  
Debasis Bhattacharya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Proliferation ◽  
Sodium Arsenite ◽  
In Vitro Study ◽  
Rat Hepatocytes ◽  
Proliferation Index ◽  
No Production ◽  
Cell Proliferation Index ◽  
And Oxidative Stress

Sodium arsenite—exposed hepatocytes of rat showed higher production of nitric oxide (NO) and increased lipid peroxidation (LPO) level vis-a-vis activity of superoxide dismutase (SOD) and catalase (CAT) were significantly lowered. Subsequently, the cell proliferation index (CPI) and cell viability were also reduced. Treatment with L-ascorbate was found effective in normalizing the arsenic-induced alteration of SOD and CAT activity and LPO level in rat hepatocytes. These observations indicated that L-ascorbate also has potent cytoprotective role as it could reduce the NO production and normalize the cell proliferation and viability of hepatocytes. Therefore, the in vitro study suggested that ascorbic acid is helpful to ameliorate the arsenic-induced cytotoxicity and oxidative stress of rat hepatocytes.

Nanocurcumin Prevents Oxidative Stress Induced following Arsenic and Fluoride Co-exposure in Rats

2016 ◽  
Vol 1 (1) ◽  
pp. 69 ◽  
Author(s):  
Abhishek Yadav ◽  
S.J.S. Flora ◽  
Pramod Kushwaha
Keyword(s):  
Oxidative Stress ◽  
Sodium Arsenite ◽  
Aminolevulinic Acid ◽  
Promising Result ◽  
Chitosan Nanoparticles ◽  
Arsenic Exposure ◽  
Oxygen Species ◽  
Curcumin Nanoparticles ◽  
Preventive Efficacy ◽  
Male Wistar Rats

<p>The present study is in continuation of our previous efforts to investigate the preventive efficacy of encapsulated curcumin nanoparticles (nanocurcumin) in mitigating effects of arsenic and/or fluoride. Curcumin was encapsulated in chitosan nanoparticles having a size distribution in the range of 50 nm. Sodium arsenite (2 mg/kg, orally) and Fluoride (50 ppm in drinking water) either alone or in combination were administered to male Wistar rats for four weeks to evaluate the efficacy of nanocurcumin (15 mg/kg) in rats. The preventive efficacy of nanocurcumin was evaluated against various altered biochemical variables suggestive of oxidative stress in liver and kidneys, and concentration of As and F in blood. Nanocurcumin co-administration with arsenic and fluoride resulted in lowering of reactive oxygen species and restoration of blood glutathione level which were found to be altered in arsenic and fluoride intoxicated groups. Nanocurcumin were also found to be effective in reversing δ-aminolevulinic acid dehydratase (ALAD) inhibition caused by arsenic exposure. The most promising result from our study shows that nanocurcumin removes not only arsenic but also fluoride from blood which may be due to the enhanced bioavailability and moderate chelating potential of nanocurcumin.</p>

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