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

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.

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

The American Journal of Sports Medicine ◽

10.1177/03635465211059821 ◽

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.

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

BioMed Research International ◽

10.1155/2014/406960 ◽

2014 ◽

Vol 2014 ◽

pp. 1-11 ◽

Cited By ~ 189

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.

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Modulation of Antipsychotic-induced Oxidative Stress by Selective and Non Selective COX2 Nonsteroidal Anti-inflammatory Drugs

Pharmacologia ◽

10.5567/pharmacologia.2012.622.626 ◽

2012 ◽

Vol 3 (11) ◽

pp. 622-626 ◽

Cited By ~ 1

Author(s):

Sally A. El-Awdan ◽

Omar M. Abdel-Sala

Keyword(s):

Oxidative Stress ◽

Inflammatory Drugs ◽

Anti Inflammatory

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

European Journal of Preventive Cardiology ◽

10.1177/2047487319870344 ◽

2019 ◽

Vol 27 (5) ◽

pp. 494-510 ◽

Cited By ~ 11

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.

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