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 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 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).

Taxane associated with trastuzumab-induced early ventricular impairment: Correlation with biologic markers of chronic inflammation and oxidative stress.

2014 ◽  
Vol 32 (15_suppl) ◽  
pp. e11566-e11566
Author(s):  
Clelia Madeddu ◽  
Mariele Dessi' ◽  
Christian Cadeddu ◽  
Alessandra Piras ◽  
Giorgia Antoni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Inflammation ◽  
Biologic Markers ◽  
And Oxidative Stress

scholarly journals New Insights in the Pathogenesis of HPV Infection and the Associated Carcinogenic Processes: The Role of Chronic Inflammation and Oxidative Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Simona Roxana Georgescu ◽  
Cristina Iulia Mitran ◽  
Madalina Irina Mitran ◽  
Constantin Caruntu ◽  
Maria Isabela Sarbu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Inflammation ◽  
Cell Damage ◽  
Redox Homeostasis ◽  
Harmful Effect ◽  
Hpv Infection ◽  
Host Cells ◽  
E6 And E7 ◽  
And Oxidative Stress

Human papillomavirus (HPV) is a small double-stranded DNA virus with tropism for epithelial cells. To this date, over 150 genotypes are known and are classified into two major groups, low-risk and high-risk strains, depending on the ability of the virus to induce malignant transformation. The host’s immunity plays a central role in the course of the infection; therefore, it may not be clinically manifest or may produce various benign or malignant lesions. The pathogenic mechanisms are complex and incompletely elucidated. Recent research suggests the role of chronic inflammation and oxidative stress (OS) in the pathogenesis of HPV infection and the associated carcinogenic processes. Chronic inflammation induces OS, which in turn promotes the perpetuation of the inflammatory process resulting in the release of numerous molecules which cause cell damage. Reactive oxygen species exert a harmful effect on proteins, lipids, and nucleic acids. Viral oncogenes E5, E6, and E7 are involved in the development of chronic inflammation through various mechanisms. In addition, HPV may interfere with redox homeostasis of host cells, inducing OS which may be involved in the persistence of the infection and play a certain role in viral integration and promotion of carcinogenesis. Knowledge regarding the interplay between chronic inflammation and OS in the pathogenesis of HPV infection and HPV-induced carcinogenesis has important consequences on the development of new therapeutic strategies.

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