scholarly journals Ehretiquinone from Onosma bracteatum Wall Exhibits Antiaging Effect on Yeasts and Mammals through Antioxidative Stress and Autophagy Induction

2021 ◽  
Vol 2021 ◽  
pp. 1-15
Author(s):  
Yanjun Pan ◽  
Yanan Liu ◽  
Rui Fujii ◽  
Umer Farooq ◽  
Lihong Cheng ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Lifespan Extension ◽  
Oxygen Species ◽  
Replicative Lifespan ◽  
Significant Evidence ◽  
Chronological Lifespan ◽  
Healthcare Product ◽  
Autophagy Induction ◽  
Type Molecule ◽  
Antioxidative Stress

The antiaging benzoquinone-type molecule ehretiquinone was isolated in a previous study as a leading compound from the herbal medicine Onosma bracteatum wall. This paper reports the antiaging effect and mechanism of ehretiquinone by using yeasts, mammal cells, and mice. Ehretiquinone extends not only the replicative lifespan but also the chronological lifespan of yeast and the yeast-like chronological lifespan of mammal cells. Moreover, ehretiquinone increases glutathione peroxidase, catalase, and superoxide dismutase activity and reduces reactive oxygen species and malondialdehyde (MDA) levels, contributing to the lifespan extension of the yeasts. Furthermore, ehretiquinone does not extend the replicative lifespan of Δsod1, Δsod2, Δuth1, Δskn7, Δgpx, Δcat, Δatg2, and Δatg32 mutants of yeast. Crucially, ehretiquinone induces autophagy in yeasts and mice, thereby providing significant evidence on the antiaging effects of the molecule in the mammalian level. Concomitantly, the silent information regulator 2 gene, which is known for its contributions in prolonging replicative lifespan, was confirmed to be involved in the chronological lifespan of yeasts and participates in the antiaging activity of ehretiquinone. These findings suggest that ehretiquinone shows an antiaging effect through antioxidative stress, autophagy, and histone deacetylase Sir2 regulation. Therefore, ehretiquinone is a promising molecule that could be developed as an antiaging drug or healthcare product.

Corrigendum to “Autophagy induction by the 30–100 kDa fraction of areca nut in both normal and malignant cells through reactive oxygen species”

Oral Oncology ◽  
2011 ◽  
Vol 47 (3) ◽  
pp. 228
Author(s):  
Mei-Huei Lin ◽  
Wan-Fang Hsieh ◽  
Wei-Fan Chiang ◽  
Wen-Zhai Hong ◽  
Yu-Rung Hsu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Areca Nut ◽  
Oxygen Species ◽  
Malignant Cells ◽  
Autophagy Induction

scholarly journals A New Geniposidic Acid Derivative Exerts Antiaging Effects through Antioxidative Stress and Autophagy Induction

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 987
Author(s):  
Ying Wang ◽  
Yanjun Pan ◽  
Yanan Liu ◽  
Dejene Disasa ◽  
Matsuura Akira ◽  
...  
Keyword(s):  
Fluorescent Protein ◽  
Replicative Lifespan ◽  
Gardenia Jasminoides ◽  
Autophagy Induction ◽  
Antioxidative Stress ◽  
Green Fluorescent ◽  
Yeast Mutants ◽  
Acid Compound ◽  
Gene Expression Levels ◽  
Geniposidic Acid

Two compounds that can prolong the replicative lifespan of yeast, geniposidic acid (Compound 1) and geniposide (Compound 2), were isolated from Gardenia jasminoides Ellis. Compared with Compound 1, Compound 2 was different at C11 and showed better bioactivity. On this basis, seven new geniposidic derivatives (3–9) were synthesized. Geniposidic 4-isoamyl ester (8, GENI), which remarkably prolonged the replicative and chronological lifespans of K6001 yeast at 1 µM, was used as the lead compound. Autophagy and antioxidative stress were examined to clarify the antiaging mechanism of GENI. GENI increased the enzymes activities and gene expression levels of superoxide dismutase (SOD) and reduced the contents of reactive oxygen species (ROS) and malondialdehyde (MDA) to improve the survival rate of yeast under oxidative stress. In addition, GENI did not extend the replicative lifespan of ∆sod1, ∆sod2, ∆uth1, ∆skn7, ∆cat, and ∆gpx mutants with K6001 background. The free green fluorescent protein (GFP) signal from the cleavage of GFP-Atg8 was increased by GENI. The protein level of free GFP showed a considerable increase and was time-dependent. Furthermore, GENI failed to extend the replicative lifespans of ∆atg32 and ∆atg2 yeast mutants. These results indicated that antioxidative stress and autophagy induction were involved in the antiaging effect of GENI.

scholarly journals Major Components of Energy Drinks (Caffeine, Taurine, and Guarana) Exert Cytotoxic Effects on Human Neuronal SH-SY5Y Cells by Decreasing Reactive Oxygen Species Production

2013 ◽  
Vol 2013 ◽  
pp. 1-22 ◽  
Author(s):  
Fares Zeidán-Chuliá ◽  
Daniel Pens Gelain ◽  
Eduardo Antônio Kolling ◽  
José Luiz Rybarczyk-Filho ◽  
Priscilla Ambrosi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Flow Cytometric Analysis ◽  
Reactive Oxygen ◽  
Energy Drinks ◽  
Oxygen Species ◽  
Flow Cytometric ◽  
Antioxidative Stress ◽  
Species Production ◽  
Neurite Degeneration

Scope. To elucidate the morphological and biochemicalin vitroeffects exerted by caffeine, taurine, and guarana, alone or in combination, since they are major components in energy drinks (EDs).Methods and Results. On human neuronal SH-SY5Y cells, caffeine (0.125–2 mg/mL), taurine (1–16 mg/mL), and guarana (3.125–50 mg/mL) showed concentration-dependent nonenzymatic antioxidant potential, decreased the basal levels of free radical generation, and reduced both superoxide dismutase (SOD) and catalase (CAT) activities, especially when combined together. However, guarana-treated cells developed signs of neurite degeneration in the form of swellings at various segments in a beaded or pearl chain-like appearance and fragmentation of such neurites at concentrations ranging from 12.5 to 50 mg/mL. Swellings, but not neuritic fragmentation, were detected when cells were treated with 0.5 mg/mL (or higher doses) of caffeine, concentrations that are present in EDs. Cells treated with guarana also showed qualitative signs of apoptosis, including membrane blebbing, cell shrinkage, and cleaved caspase-3 positivity. Flow cytometric analysis confirmed that cells treated with 12.5–50 mg/mL of guarana and its combinations with caffeine and/or taurine underwent apoptosis.Conclusion. Excessive removal of intracellular reactive oxygen species, to nonphysiological levels (or “antioxidative stress”), could be a cause ofin vitrotoxicity induced by these drugs.

Hyperandrogenism and insulin resistance induce gravid uterine defects in association with mitochondrial dysfunction and aberrant reactive oxygen species production

2019 ◽  
Vol 316 (5) ◽  
pp. E794-E809 ◽  
Author(s):  
Min Hu ◽  
Yuehui Zhang ◽  
Xiaozhu Guo ◽  
Wenyan Jia ◽  
Guoqi Liu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Stress Responses ◽  
Reactive Oxygen ◽  
Daily Injection ◽  
Gravid Uterus ◽  
Oxygen Species ◽  
Pregnant Rats ◽  
Expression Of Genes ◽  
Antioxidative Stress

Women with polycystic ovary syndrome (PCOS) are at increased risk of miscarriage, which often accompanies the hyperandrogenism and insulin resistance seen in these patients. However, neither the combinatorial interaction between these two PCOS-related etiological factors nor the mechanisms of their actions in the uterus during pregnancy are well understood. We hypothesized that hyperandrogensim and insulin resistance exert a causative role in miscarriage by inducing defects in uterine function that are accompanied by mitochondrial-mediated oxidative stress, inflammation, and perturbed gene expression. Here, we tested this hypothesis by studying the metabolic, endocrine, and uterine abnormalities in pregnant rats after exposure to daily injection of 5α-dihydrotestosterone (DHT; 1.66 mg·kg body wt−1·day−1) and/or insulin (6.0 IU/day) from gestational day 7.5 to 13.5. We showed that whereas DHT-exposed and insulin-exposed pregnant rats presented impaired insulin sensitivity, DHT + insulin-exposed pregnant rats exhibited hyperandrogenism and peripheral insulin resistance, which mirrors pregnant PCOS patients. Compared with controls, hyperandrogenism and insulin resistance in the dam were associated with alterations in uterine morphology and aberrant expression of genes responsible for decidualization ( Prl8a2, Fxyd2, and Mt1g), placentation ( Fcgr3 and Tpbpa), angiogenesis ( Flt1, Angpt1, Angpt2, Ho1, Ccl2, Ccl5, Cxcl9, and Cxcl10) and insulin signaling (Akt, Gsk3, and Gluts). Moreover, we observed changes in uterine mitochondrial function and homeostasis (i.e., mitochondrial DNA copy number and the expression of genes responsible for mitochondrial fusion, fission, biogenesis, and mitophagy) and suppression of both oxidative and antioxidative defenses (i.e., reactive oxygen species, Nrf2 signaling, and interactive networks of antioxidative stress responses) in response to the hyperandrogenism and insulin resistance. These findings demonstrate that hyperandrogenism and insulin resistance induce mitochondria-mediated damage and a resulting imbalance between oxidative and antioxidative stress responses in the gravid uterus.

Autophagy induction by the 30–100kDa fraction of areca nut in both normal and malignant cells through reactive oxygen species

Oral Oncology ◽  
2010 ◽  
Vol 46 (11) ◽  
pp. 822-828 ◽  
Author(s):  
Mei-Huei Lin ◽  
Wan-Fang Hsieh ◽  
Wei-Fan Chiang ◽  
Wen-Zhai Hong ◽  
Yu-Rung Hsu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Areca Nut ◽  
Oxygen Species ◽  
Malignant Cells ◽  
Autophagy Induction

scholarly journals Reactive Oxygen Species as a Link between Antioxidant Pathways and Autophagy

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Dan Li ◽  
Zongxian Ding ◽  
Kaili Du ◽  
Xiangshi Ye ◽  
Shixue Cheng
Keyword(s):  
Reactive Oxygen Species ◽  
Oxidative Damage ◽  
Reactive Oxygen ◽  
Dual Function ◽  
Oxygen Species ◽  
Physiological Conditions ◽  
Pathological Conditions ◽  
Autophagy Induction ◽  
Cellular Machinery ◽  
Survival Mechanisms

Reactive oxygen species (ROS) are highly reactive molecules that can oxidize proteins, lipids, and DNA. Under physiological conditions, ROS are mainly generated in the mitochondria during aerobic metabolism. Under pathological conditions, excessive ROS disrupt cellular homeostasis. High levels of ROS result in severe oxidative damage to the cellular machinery. However, a low/mild level of ROS could serve as a signal to trigger cell survival mechanisms. To prevent and cope with oxidative damage to biomolecules, cells have developed various antioxidant and detoxifying mechanisms. Meanwhile, ROS can initiate autophagy, a process of self-clearance, which helps to reduce oxidative damage by engulfing and degrading oxidized substance. This review summarizes the interactions among ROS, autophagy, and antioxidant pathways. The effects of natural phytochemicals on autophagy induction, antioxidation, and dual-function are also discussed.

Sign in / Sign up

Export Citation Format

Share Document