Irreversible inhibition of glucose-6-phosphate dehydrogenase by the coenzyme A conjugate of ketoprofen: A key to oxidative stress induced by non-steroidal anti-inflammatory drugs?

2007 ◽  
Vol 73 (3) ◽  
pp. 405-416 ◽  
Author(s):  
Carine Asensio ◽  
Nicolas Levoin ◽  
Cécile Guillaume ◽  
Marie-Justine Guerquin ◽  
Koukeb Rouguieg ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coenzyme A ◽  
Irreversible Inhibition ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Glucose 6 Phosphate Dehydrogenase

Differential effects of non-steroidal anti-inflammatory drugs on mitochondrial dysfunction during oxidative stress

2009 ◽  
Vol 490 (1) ◽  
pp. 1-8 ◽  
Author(s):  
Nirupama Lal ◽  
Jitendra Kumar ◽  
Warren E. Erdahl ◽  
Douglas R. Pfeiffer ◽  
Martha. E. Gadd ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Differential Effects ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

scholarly journals A Review on the Effects of Melatonin on Fetal Protection during Pregnancy with Intrauterine Inflammation

2020 ◽  
Vol 24 (4) ◽  
pp. 196-203
Author(s):  
Jang Mee Kim ◽  
Ji Yeon Lee
Keyword(s):  
Oxidative Stress ◽  
Pregnant Women ◽  
Animal Studies ◽  
Protective Effects ◽  
Fetal Protection ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
The Brain ◽  
Fetal Inflammatory Response

Intrauterine inflammation is defined as the inflammation of the chorion, amnion, and placenta. Untreated inflammation increases the risk of fetal inflammatory response syndrome, which may result in multiorgan diseases involving the brain, cardiovascular system, lung, eye, and intestine. Therefore, controlling inflammation is critical in pregnant women to reduce the risk of diseases. However, there are no safe and effective anti-inflammatory drugs for administration during pregnancy. Although the primary function of melatonin is to control circadian rhythms, it has protective effects against cellular insults occurring from hypoxia, oxidative stress, and inflammation. While animal studies support the effective and safe role of melatonin in improving pregnancy-related morbidities, it leaves plenty of opportunities for clinical studies investigating its anti-inflammatory, antioxidant, and protective effects against insults induced by intrauterine inflammation. Therefore, it will be worthwhile to investigate antenatal supplementation of melatonin in pregnant women with intrauterine inflammation to reduce the incidence of associated comorbidities.

Evaluation of Therapeutic Effects of Quercetin Against Achilles Tendinopathy in Rats via Oxidative Stress, Inflammation, Apoptosis, Autophagy, and Metalloproteinases

2021 ◽  
pp. 036354652110598
Author(s):  
Halil Sezgin Semis ◽  
Cihan Gur ◽  
Mustafa Ileriturk ◽  
Fatih Mehmet Kandemir ◽  
Ozgur Kaynar
Keyword(s):  
Oxidative Stress ◽  
Achilles Tendinopathy ◽  
Therapeutic Effects ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Alternative Treatment Option ◽  
Markers Of Oxidative Stress ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
The One

Background: Achilles tendinopathy, seen in athletes and manual labor workers, is an inflammatory condition characterized by chronic tendon pain. Owing to the toxicity that develops in various organs attributed to the use of anti–inflammatory drugs, there is a need for new therapeutic agents. Purpose: In the present study, the effects of quercetin (Que), the one that attracted the most attention of researchers studying this group of flavonoids, were investigated against collagenase–induced tendinopathy. Study Design: Controlled laboratory study. Methods: A total of 35 Sprague-Dawley rats were used in the study. Tendinopathy was created by injecting a single dose of collagenase (10 μL; 10 mg/mL) into the tendons of rats. Thirty minutes after the injection, Que was administered at doses of 25 or 50 mg/kg. Que administration was carried out for 7 days. Animals underwent a motility test at the end of the study. In addition, markers of oxidative stress, inflammation, apoptosis, and autophagy, as well as the expression levels of matrix metalloproteinases (MMPs 2, 3, 9, and 13), ICAM-1, and STAT3, were measured in tendon tissues with biochemical, molecular, and Western blot techniques. Results: The results showed that oxidative stress, inflammation, apoptosis, and autophagy were triggered by the injection of collagenase. In addition, MMPs, ICAM-1, and STAT3 were activated to participate in the development of tendinopathy. Que was found to reduce ICAM-1 levels in tendon tissue. Moreover, Que showed antioxidant, anti–inflammatory, antiapoptotic, and antiautophagic effects on tendons against tendinopathy. More important, Que suppressed the expression of MMPs in the tendon tissues. Conclusion: Que has protective properties against collagenase–induced tendon damage in rats. Clinical Relevance: We believe that with further study, Que may be shown to be an alternative treatment option for athletes or others who experience tendon injuries.

scholarly journals Roles of Inflammation, Oxidative Stress, and Vascular Dysfunction in Hypertension

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Quynh N. Dinh ◽  
Grant R. Drummond ◽  
Christopher G. Sobey ◽  
Sophocles Chrissobolis
Keyword(s):  
Oxidative Stress ◽  
Endothelial Dysfunction ◽  
Potential Benefit ◽  
Animal Studies ◽  
Vascular Dysfunction ◽  
Inflammatory Cascade ◽  
Inflammatory Drugs ◽  
Sympathetic Nervous ◽  
Anti Inflammatory ◽  
Key Steps

Hypertension is a complex condition and is the most common cardiovascular risk factor, contributing to widespread morbidity and mortality. Approximately 90% of hypertension cases are classified as essential hypertension, where the precise cause is unknown. Hypertension is associated with inflammation; however, whether inflammation is a cause or effect of hypertension is not well understood. The purpose of this review is to describe evidence from human and animal studies that inflammation leads to the development of hypertension, as well as the evidence for involvement of oxidative stress and endothelial dysfunction—both thought to be key steps in the development of hypertension. Other potential proinflammatory conditions that contribute to hypertension—such as activation of the sympathetic nervous system, aging, and elevated aldosterone—are also discussed. Finally, we consider the potential benefit of anti-inflammatory drugs and statins for antihypertensive therapy. The evidence reviewed suggests that inflammation can lead to the development of hypertension and that oxidative stress and endothelial dysfunction are involved in the inflammatory cascade. Aging and aldosterone may also both be involved in inflammation and hypertension. Hence, in the absence of serious side effects, anti-inflammatory drugs could potentially be used to treat hypertension in the future.

Oxidative stress and inflammation in the evolution of heart failure: From pathophysiology to therapeutic strategies

2019 ◽  
Vol 27 (5) ◽  
pp. 494-510 ◽  
Author(s):  
Alberto Aimo ◽  
Vincenzo Castiglione ◽  
Chiara Borrelli ◽  
Luigi F Saccaro ◽  
Maria Franzini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Chronic Heart Failure ◽  
Current Knowledge ◽  
Interleukin 1 ◽  
Prognostic Significance ◽  
Deep Understanding ◽  
Future Research ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Both oxidative stress and inflammation are enhanced in chronic heart failure. Dysfunction of cardiac mitochondria is a hallmark of heart failure and a leading cause of oxidative stress, which in turn exerts detrimental effects on cellular components, including mitochondria themselves, thus generating a vicious circle. Oxidative stress also causes myocardial tissue damage and inflammation, contributing to heart failure progression. Furthermore, a subclinical inflammatory state may be caused by heart failure comorbidities such as obesity, diabetes mellitus or sleep apnoeas. Some markers of both oxidative stress and inflammation are enhanced in chronic heart failure and hold prognostic significance. For all these reasons, antioxidants or anti-inflammatory drugs may represent interesting additional therapies for subjects either at high risk or with established heart failure. Nonetheless, only a few clinical trials on antioxidants have been carried out so far, with several disappointing results except for vitamin C, elamipretide and coenzyme Q10. With regard to anti-inflammatory drugs, only preliminary data on the interleukin-1 antagonist anakinra are currently available. Therefore, a comprehensive, deep understanding of our current knowledge on oxidative stress and inflammation in chronic heart failure is key to providing some suggestions for future research on this topic.

scholarly journals Conservative Nonhormonal Options for the Treatment of Male Infertility: Antibiotics, Anti-Inflammatory Drugs, and Antioxidants

2017 ◽  
Vol 2017 ◽  
pp. 1-17 ◽  
Author(s):  
Aldo E. Calogero ◽  
Rosita A. Condorelli ◽  
Giorgio Ivan Russo ◽  
Sandro La Vignera
Keyword(s):  
Oxidative Stress ◽  
Male Infertility ◽  
Medical Treatment ◽  
Sperm Quality ◽  
Specific Treatment ◽  
Vitamin Supplementation ◽  
Antioxidant Compounds ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Infertile Patients

The nonhormonal medical treatment can be divided into empirical, when the cause has not been identified, and nonempirical, if the pathogenic mechanism causing male infertility can be solved or ameliorated. The empirical nonhormonal medical treatment has been proposed for patients with idiopathic or noncurable oligoasthenoteratozoospermia and for normozoospermic infertile patients. Anti-inflammatory, fibrinolytic, and antioxidant compounds, oligo elements, and vitamin supplementation may be prescribed. Infection, inflammation, and/or increased oxidative stress often require a specific treatment with antibiotics, anti-inflammatory drugs, and/or antioxidants. Combined therapies can contribute to improve sperm quality.

scholarly journals Oxidative Stress and Inflammation: What Polyphenols Can Do for Us?

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Tarique Hussain ◽  
Bie Tan ◽  
Yulong Yin ◽  
Francois Blachier ◽  
Myrlene C. B. Tossou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Oxygen Species ◽  
Molecular Signaling ◽  
Protective Mechanisms ◽  
Inflammatory Drugs ◽  
Chronic Disorders ◽  
Anti Inflammatory ◽  
Anti Inflammation ◽  
Inflammatory Effect

Oxidative stress is viewed as an imbalance between the production of reactive oxygen species (ROS) and their elimination by protective mechanisms, which can lead to chronic inflammation. Oxidative stress can activate a variety of transcription factors, which lead to the differential expression of some genes involved in inflammatory pathways. The inflammation triggered by oxidative stress is the cause of many chronic diseases. Polyphenols have been proposed to be useful as adjuvant therapy for their potential anti-inflammatory effect, associated with antioxidant activity, and inhibition of enzymes involved in the production of eicosanoids. This review aims at exploring the properties of polyphenols in anti-inflammation and oxidation and the mechanisms of polyphenols inhibiting molecular signaling pathways which are activated by oxidative stress, as well as the possible roles of polyphenols in inflammation-mediated chronic disorders. Such data can be helpful for the development of future antioxidant therapeutics and new anti-inflammatory drugs.

scholarly journals Targeting the Canonical WNT/β-Catenin Pathway in Cancer Treatment Using Non-Steroidal Anti-Inflammatory Drugs

Cells ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 726 ◽  
Author(s):  
Alexandre Vallée ◽  
Yves Lecarpentier ◽  
Jean-Noël Vallée
Keyword(s):  
Oxidative Stress ◽  
Tumor Growth ◽  
Cancer Treatment ◽  
Chronic Inflammation ◽  
Tumor Therapy ◽  
Pparγ Agonists ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Canonical Wnt ◽  
And Oxidative Stress

Chronic inflammation and oxidative stress are common and co-substantial pathological processes accompanying and contributing to cancers. Numerous epidemiological studies have indicated that non-steroidal anti-inflammatory drugs (NSAIDs) could have a positive effect on both the prevention of cancer and tumor therapy. Numerous hypotheses have postulated that NSAIDs could slow tumor growth by acting on both chronic inflammation and oxidative stress. This review takes a closer look at these hypotheses. In the cancer process, one of the major signaling pathways involved is the WNT/β-catenin pathway, which appears to be upregulated. This pathway is closely associated with both chronic inflammation and oxidative stress in cancers. The administration of NSAIDs has been observed to help in the downregulation of the WNT/β-catenin pathway and thus in the control of tumor growth. NSAIDs act as PPARγ agonists. The WNT/β-catenin pathway and PPARγ act in opposing manners. PPARγ agonists can promote cell cycle arrest, cell differentiation, and apoptosis, and can reduce inflammation, oxidative stress, proliferation, invasion, and cell migration. In parallel, the dysregulation of circadian rhythms (CRs) contributes to cancer development through the upregulation of the canonical WNT/β-catenin pathway. By stimulating PPARγ expression, NSAIDs can control CRs through the regulation of many key circadian genes. The administration of NSAIDs in cancer treatment would thus appear to be an interesting therapeutic strategy, which acts through their role in regulating WNT/β-catenin pathway and PPARγ activity levels.

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