scholarly journals Therapeutic Influence on Important Targets Associated with Chronic Inflammation and Oxidative Stress in Cancer Treatment

Cancers ◽  
2021 ◽  
Vol 13 (23) ◽  
pp. 6062
Author(s):  
Margarita Neganova ◽  
Junqi Liu ◽  
Yulia Aleksandrova ◽  
Sergey Klochkov ◽  
Ruitai Fan
Keyword(s):  
Oxidative Stress ◽  
Chronic Inflammation ◽  
Defense Mechanisms ◽  
Cell Transformation ◽  
Oncogenic Signaling ◽  
Predisposing Factor ◽  
Tumor Spread ◽  
Chronic Inflammatory Response ◽  
Cell Defense ◽  
And Oxidative Stress

Chronic inflammation and oxidative stress are the interconnected pathological processes, which lead to cancer initiation and progression. The growing level of oxidative and inflammatory damage was shown to increase cancer severity and contribute to tumor spread. The overproduction of reactive oxygen species (ROS), which is associated with the reduced capacity of the endogenous cell defense mechanisms and/or metabolic imbalance, is the main contributor to oxidative stress. An abnormal level of ROS was defined as a predisposing factor for the cell transformation that could trigger pro-oncogenic signaling pathways, induce changes in gene expression, and facilitate accumulation of mutations, DNA damage, and genomic instability. Additionally, the activation of transcription factors caused by a prolonged oxidative stress, including NF-κB, p53, HIF1α, etc., leads to the expression of several genes responsible for inflammation. The resulting hyperactivation of inflammatory mediators, including TNFα, TGF-β, interleukins, and prostaglandins can contribute to the development of neoplasia. Pro-inflammatory cytokines were shown to trigger adaptive reactions and the acquisition of resistance by tumor cells to apoptosis, while promoting proliferation, invasion, and angiogenesis. Moreover, the chronic inflammatory response leads to the excessive production of free radicals, which further aggravate the initiated reactions. This review summarizes the recent data and progress in the discovery of mechanisms that associate oxidative stress and chronic inflammation with cancer onset and metastasis. In addition, the review provides insights for the development of therapeutic approaches and the discovery of natural substances that will be able to simultaneously inhibit several key oncological and inflammation-related targets.

scholarly journals Hyperbaric Oxygen Treatment: Effects on Mitochondrial Function and Oxidative Stress

Biomolecules ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 1827
Author(s):  
Nofar Schottlender ◽  
Irit Gottfried ◽  
Uri Ashery
Keyword(s):  
Oxidative Stress ◽  
Hyperbaric Oxygen ◽  
Mitochondrial Function ◽  
Defense Mechanisms ◽  
Term Treatment ◽  
Mitochondrial Activity ◽  
Hyperbaric Oxygen Treatment ◽  
Oxygen Treatment ◽  
Long Term Treatment ◽  
And Oxidative Stress

Hyperbaric oxygen treatment (HBOT)—the administration of 100% oxygen at atmospheric pressure (ATA) greater than 1 ATA—increases the proportion of dissolved oxygen in the blood five- to twenty-fold. This increase in accessible oxygen places the mitochondrion—the organelle that consumes most of the oxygen that we breathe—at the epicenter of HBOT’s effects. As the mitochondrion is also a major site for the production of reactive oxygen species (ROS), it is possible that HBOT will increase also oxidative stress. Depending on the conditions of the HBO treatment (duration, pressure, umber of treatments), short-term treatments have been shown to have deleterious effects on both mitochondrial activity and production of ROS. Long-term treatment, on the other hand, improves mitochondrial activity and leads to a decrease in ROS levels, partially due to the effects of HBOT, which increases antioxidant defense mechanisms. Many diseases and conditions are characterized by mitochondrial dysfunction and imbalance between ROS and antioxidant scavengers, suggesting potential therapeutic intervention for HBOT. In the present review, we will present current views on the effects of HBOT on mitochondrial function and oxidative stress, the interplay between them and the implications for several diseases.

scholarly journals Rag1 immunodeficiency‐induced early aging and senescence in zebrafish are dependent on chronic inflammation and oxidative stress

Aging Cell ◽  
2019 ◽  
Vol 18 (5) ◽  
Author(s):  
Beatriz Novoa ◽  
Patricia Pereiro ◽  
Azucena López‐Muñoz ◽  
Mónica Varela ◽  
Gabriel Forn‐Cuní ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Inflammation ◽  
Early Aging ◽  
And Oxidative Stress

scholarly journals Reduced uterine perfusion pressure T-helper 17 cells cause pathophysiology associated with preeclampsia during pregnancy

2016 ◽  
Vol 311 (6) ◽  
pp. R1192-R1199 ◽  
Author(s):  
Denise C. Cornelius ◽  
Lorena M. Amaral ◽  
Kedra Wallace ◽  
Nathan Campbell ◽  
Alexia J. Thomas ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Inflammation ◽  
Intrauterine Growth Restriction ◽  
Perfusion Pressure ◽  
Type I ◽  
T Helper ◽  
T Helper 17 ◽  
Uterine Perfusion ◽  
Agonistic Autoantibodies ◽  
And Oxidative Stress

Preeclampsia is associated with chronic inflammation and an imbalance among T-helper cell subtypes with an increase in T-helper 17 (TH17) cells. The objective of this study was to determine a role for TH17s, from the reduced uterine perfusion pressure (RUPP) rat model of preeclampsia, in the etiology of hypertension and chronic inflammation during pregnancy. CD4+/CD25− T cells were isolated from rat spleens, cultured in TH17 media, and were verified as TH17s via flow cytometry. On day 12 of gestation, 1×106 TH17 cells from RUPP rats were adoptively transferred into NP rats, carotid catheters were inserted on day 18, and on day 19, mean arterial pressure (MAP) was recorded, serum and plasma were collected, and oxidative stress and production of agonistic autoantibodies to the ANG II type I receptor (AT1-AA) were analyzed. MAP increased from 100.3 ± 1.7 mmHg in normal pregnant (NP; n = 17) to 124.8 ± 2.1 mmHg in RUPP ( n = 22; P < 0.0001) and to 110.8 ± 2.8 mmHg in NP+RUPP TH17 ( n = 11). Pup weights in NP+RUPP TH17s were decreased to 1.92 ± 0.09 g from 2.39 ± 0.14 in NP rats ( P < 0.01). AT1-AA significantly increased from 0.1 ± 0.2 beats/min in NP to 15.6 ± 0.7 beats/min in NP+RUPP TH17s. IL-6 was 22.3 ± 5.7 pg/ml in NP and increased to 60.45 ± 13.8 pg/ml in RUPP ( P < 0.05) and 75.9 ± 6.8 pg/ml in NP+RUPP TH17 rats ( P < 0.01). Placental and renal oxidative stress were 238 ± 27.5 and 411 ± 129.9 relative light units·min−1·mg−1 in NP and 339 ± 104.6 and 833 ± 331.1 relative light units·min−1·mg−1 in NP+RUPP TH17, respectively. In conclusion, RUPP TH17 cells induced intrauterine growth restriction and increased blood pressure, AT1-AA, IL-6, and tissue oxidative stress when transferred to NP rats, indicating a role for autoimmune associated TH17 cells, to cause much of the pathophysiology associated with preeclampsia.

scholarly journals Cardioprotective Effect of Quercetin in 5/6-Nephrectomized Rats: Focus on Myocardial fibrosis and Oxidative Stress

2017 ◽  
Vol 2 (3) ◽  
pp. 87-95
Author(s):  
Tri Yuliani ◽  
Melva Louisa ◽  
Wawaimuli Arozal ◽  
Vivian Soetikno ◽  
Nafrialdi Nafrialdi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Myocardial Fibrosis ◽  
Defense Mechanisms ◽  
Chronic Administration ◽  
Cardioprotective Effect ◽  
Sprague Dawley ◽  
Antioxidant Mechanism ◽  
Uremic Cardiomyopathy ◽  
And Oxidative Stress ◽  
Gpx Activity

Uremic cardiomyopathy is the leading cause of death in patients with chronic kidney disease. Fluid overload and oxidative stress play important roles in its pathogenesis. This study aims to determine the effect of quercetin on uremic cardiomyopathy in 5/6-nephrectomized rats. To our knowledge, its cardioprotective effect on uremic cardiomyopathy induced in rats by 5/6 nephrectomy has not been investigated yet. Uremia was induced surgically in male Sprague-Dawley rats via 5/6 nephrectomy. Quercetin was administered per orally at a dose of 100 mg/kg/day for 8 weeks prior to sacrifice. Meanwhile, captopril was administered at a dose of 10 mg/kg/day. Lipid peroxidation was assessed using TBARS reaction, while GPX activity was determined to explore the endogen antioxidant mechanism. Myocardial fibrosis was analyzed using Massons’ Trichrome staining and the level of NT-proBNP in plasma was measured as a marker of cardiac dysfunction. Nephrectomy 5/6 had no effects on plasma NT– proBNP levels, cardiac and plasma MDA levels, but induced mild myocardial fibrosis and significant increase in cardiac GPX activity in comparison with normal rat (p<0.05). However, administration of quercetin or captopril did not ameleriote those mild myocardial fibrosis and increased GPX activity. Uremic cardiomyopathy induced by 5/6 nephrectomy demonstrated mild myocardial fibrosis but preservation of cardiac function demonstrated by NT-proBNP levels. Increased of GPX activity in the nephrectomized-rats compared to the control rats (p<0.05) suggests induction of antioxidant defense mechanisms that might not be exhausted yet. This condition highlighted a compensatory phase which was unchanged following chronic administration of either quercetin or captopril.

scholarly journals Cannabinoids Terpenes and Inflammation

2021 ◽  
Vol 7 (2) ◽  
pp. 1-6
Author(s):  
Erhan Yarar ◽  
Keyword(s):  
Oxidative Stress ◽  
Chronic Inflammation ◽  
Autoimmune Disorders ◽  
And Oxidative Stress

Inflammation and oxidative stress are involved in many diseases. Chronic inflammation may be caused by autoimmune disorders, untreated infections, or illnesses, and often plays a role in conditions such as asthma, cancer, and diabetes.

scholarly journals Review of polymorphisms, associated with cardiovascular diseases

2021 ◽  
pp. 333-338
Author(s):  
A. A. Akopyan ◽  
I. D. Strazhesko ◽  
O. N. Tkacheva ◽  
A. P. Yesakova ◽  
I. A. Orlova
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Cardiovascular Diseases ◽  
Chronic Inflammation ◽  
Gene Polymorphisms ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
System Activation ◽  
And Oxidative Stress

In this research we examined studies of gene polymorphisms, associated with cardiovascular diseases through renin-angiotensin-aldosterone system activation (AGT с.521С>Т, AСE Ins>Del), nitric oxide decline (NOS3 с.894G>T), chronic inflammation (TNF -238G>A, MMP9 -1562С>T) and oxidative stress (CYBA c.214Т>С).

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