scholarly journals Anti-Aging Activity of Xylocarpus Granatum Phytoextracts and Xyloccensins K Compound

2021 ◽  
pp. 365-375
Author(s):  
Syarif Maulana Yusuf ◽  
Rika Indri Astuti ◽  
Irmanida Batubara ◽  
Warinthorn Chavasiri
Keyword(s):  
Oxidative Stress ◽  
Cellular Level ◽  
Cellular Aging ◽  
Mitochondrial Activity ◽  
Response Gene ◽  
Xylocarpus Granatum ◽  
Aging Properties ◽  
Ros Scavenger ◽  
Stem Leaf ◽  
Stress Response Gene

Cellular aging is promoted by the deleterious effect of free radicals. This can be lowered by antioxidant treatments. Xylocarpus granatum and its compound, Xyloccensins K have been reported to have antioxidant activity but there have been no reports of antioxidant and anti-aging activities at the cellular level. Thus, the aim of this study to investigate the antioxidant and anti-aging properties of X. granatum-derived extract and Xyloccensins K at a cellular level in yeast Schizosaccharomyces pombe. Four vegetative and three generative parts of X. granatum organs including root, stem, leaf, twig, seed, flesh of fruit, and peel of fruit were extracted using 70% ethanol by the maceration method. Whereas, Xyloccensins K was obtained from seed of X. granatum.  The samples tested, other than peel of fruit, prolonged cell longevity in lower concentration as compared to that without phytoextracts treatment. Also, our data indicate that all samples could promote oxidative stress tolerance phenotype, as yeast was capable of dealing with H2O2-induced oxidative stress treatment at 1, 2, and 3 mM H2O2 with the best phenotypes by the administration of twig extracts. Most of the phytoextracts showed an increase in mitochondrial activity, except that of seed extract. The result showed the administration of Xyloccensins K compound did not increase the expression of transcriptional factors of oxidative stress response gene cluster, sty1 and pap1. We suggest that the Xyloccensins K compound acts as direct Reactive Oxygen Species (ROS) scavenger. Thus further study in elucidating the phenomenon of longevity-induced X. granatum extract is required.

scholarly journals Rapamycin increases oxidative stress response gene expression in adult stem cells

Aging ◽  
2012 ◽  
Vol 4 (4) ◽  
pp. 279-289 ◽  
Author(s):  
Amber E. Kofman ◽  
Margeaux R. McGraw ◽  
Christopher J. Payne
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Stem Cells ◽  
Stress Response ◽  
Adult Stem Cells ◽  
Oxidative Stress Response ◽  
Response Gene ◽  
Stress Response Gene

scholarly journals OKL38 is an oxidative stress response gene stimulated by oxidized phospholipids

2006 ◽  
Vol 48 (3) ◽  
pp. 709-715 ◽  
Author(s):  
Rongsong Li ◽  
Wendy Chen ◽  
Rolando Yanes ◽  
Sangderk Lee ◽  
Judith A. Berliner
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Oxidized Phospholipids ◽  
Response Gene ◽  
Stress Response Gene

Expression Levels of the Oxidative Stress Response Gene ALDH3A2 in Granulosa-Lutein Cells Are Related to Female Age and Infertility Diagnosis

2015 ◽  
Vol 23 (5) ◽  
pp. 604-609 ◽  
Author(s):  
Rebeca González-Fernández ◽  
Jairo Hernández ◽  
Pablo Martín-Vasallo ◽  
Maria Puopolo ◽  
Angela Palumbo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Oxidative Stress Response ◽  
Response Gene ◽  
Female Age ◽  
Expression Levels ◽  
Stress Response Gene

scholarly journals Deletion of the Stress Response Gene DDR48 from Histoplasma capsulatum Increases Sensitivity to Oxidative Stress, Increases Susceptibility to Antifungals, and Decreases Fitness in Macrophages

2021 ◽  
Vol 7 (11) ◽  
pp. 981
Author(s):  
Logan T. Blancett ◽  
Kauri A. Runge ◽  
Gabriella M. Reyes ◽  
Lauren A. Kennedy ◽  
Sydney C. Jackson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Response ◽  
Histoplasma Capsulatum ◽  
Cellular Stress ◽  
Cellular Stress Response ◽  
Antifungal Compounds ◽  
Negative Effects ◽  
Response Gene ◽  
Preferential Expression ◽  
Stress Response Gene

The stress response gene DDR48 has been characterized in Saccharomyces cerevisiae and Candida albicans to be involved in combating various cellular stressors, from oxidative agents to antifungal compounds. Surprisingly, the biological function of DDR48 has yet to be identified, though it is likely an important part of the stress response. To gain insight into its function, we characterized DDR48 in the dimorphic fungal pathogen Histoplasma capsulatum. Transcriptional analyses showed preferential expression of DDR48 in the mycelial phase. Induction of DDR48 in Histoplasma yeasts developed after treatment with various cellular stress compounds. We generated a ddr48∆ deletion mutant to further characterize DDR48 function. Loss of DDR48 alters the transcriptional profile of the oxidative stress response and membrane synthesis pathways. Treatment with ROS or antifungal compounds reduced survival of ddr48∆ yeasts compared to controls, consistent with an aberrant cellular stress response. In addition, we infected RAW 264.7 macrophages with DDR48-expressing and ddr48∆ yeasts and observed a 50% decrease in recovery of ddr48∆ yeasts compared to wild-type yeasts. Loss of DDR48 function results in numerous negative effects in Histoplasma yeasts, highlighting its role as a key player in the global sensing and response to cellular stress by fungi.

scholarly journals Oxidative stress: Its role in regulating aging and longevity

2015 ◽  
Vol 37 (4) ◽  
pp. 16-19
Author(s):  
Catherine E. Aiken ◽  
Jane L. Tarry-Adkins ◽  
Susan E. Ozanne
Keyword(s):  
Oxidative Stress ◽  
Oxidative Damage ◽  
Aging Process ◽  
Cellular Level ◽  
Cellular Aging ◽  
Free Radical Damage ◽  
Early Life Environment ◽  
Cellular Components ◽  
Radical Damage

Although aging is ubiquitous across organisms, the rate at which it occurs varies considerably between species and individuals. The initial links between oxidative stress and rates of cellular aging were postulated over 50 years ago by Harman, who published a theory connecting free radical damage with the aging process in 19561. Since then a wide body of literature has accumulated demonstrating the links between oxidative damage to various cellular components and cellular senescence2. Oxidative stress is known to contribute to the aetiology of a wide variety of pathological processes including metabolic, cardiovascular and neoplastic diseases, all of which can shorten lifespan. Macromolecules such as proteins, lipids and particularly DNA can be irreversibly damaged by oxidative stress, leading to a decline in cellular function and apoptosis. This leads to aging, initially at a cellular level, then of the tissues and organs, culminating in whole organism pathology and eventually death. This article explores the various processes by which cells accrue oxidative damage and how such long-term damage leads to senescence. In particular, we focus on how the early-life environment influences the accumulation of oxidative stress over the entire life-course of an individual and how this may accelerate the normal aging process.

Exploiting Anti-Inflammation Effects of Flavonoids in Chronic Inflammatory Diseases

2020 ◽  
Vol 26 (22) ◽  
pp. 2610-2619 ◽  
Author(s):  
Tarique Hussain ◽  
Ghulam Murtaza ◽  
Huansheng Yang ◽  
Muhammad S. Kalhoro ◽  
Dildar H. Kalhoro
Keyword(s):  
Oxidative Stress ◽  
Chronic Diseases ◽  
Inflammatory Diseases ◽  
Therapeutic Option ◽  
Cellular Level ◽  
Antiinflammatory Drugs ◽  
Suitable Alternative ◽  
Chronic Inflammatory Diseases

Background: Inflammation is a complex response of the host defense system to different internal and external stimuli. It is believed that persistent inflammation may lead to chronic inflammatory diseases such as, inflammatory bowel disease, neurological and cardiovascular diseases. Oxidative stress is the main factor responsible for the augmentation of inflammation via various molecular pathways. Therefore, alleviating oxidative stress is effective a therapeutic option against chronic inflammatory diseases. Methods: This review article extends the knowledge of the regulatory mechanisms of flavonoids targeting inflammatory pathways in chronic diseases, which would be the best approach for the development of suitable therapeutic agents against chronic diseases. Results: Since the inflammatory response is initiated by numerous signaling molecules like NF-κB, MAPK, and Arachidonic acid pathways, their encountering function can be evaluated with the activation of Nrf2 pathway, a promising approach to inhibit/prevent chronic inflammatory diseases by flavonoids. Over the last few decades, flavonoids drew much attention as a potent alternative therapeutic agent. Recent clinical evidence has shown significant impacts of flavonoids on chronic diseases in different in-vivo and in-vitro models. Conclusion: Flavonoid compounds can interact with chronic inflammatory diseases at the cellular level and modulate the response of protein pathways. A promising approach is needed to overlook suitable alternative compounds providing more therapeutic efficacy and exerting fewer side effects than commercially available antiinflammatory drugs.

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