scholarly journals Oolonghomobisflavans from Camellia sinensis increase Caenorhabditis elegans lifespan and healthspan

GeroScience ◽  
2021 ◽  
Author(s):  
Chatrawee Duangjan ◽  
Sean P. Curran
Keyword(s):  
Caenorhabditis Elegans ◽  
Camellia Sinensis ◽  
Healthy Aging ◽  
Health Benefits ◽  
Normal Diet ◽  
Bioactive Molecules ◽  
Protective Effects ◽  
Oolong Tea ◽  
Age Related ◽  
Antioxidant Agents

AbstractTea polyphenols are widely considered as excellent antioxidant agents which can contribute to human health and longevity. However, the identification of the active biomolecules in complex tea extracts that promote health and longevity are not fully known. Here we used the nematode Caenorhabditis elegans to analyze the health benefits and longevity effects of Camellia sinensis oolong tea extracts (QFT, NFT, and CFT) and oolonghomobisflavan A and oolonghomobisflavan B, which are present in oolong tea extracts. Our results showed that oolong tea extracts and oolonghomobisflavans prolong lifespan and improved healthspan by curtailing the age-related decline in muscle activity and the accumulation of age pigment (lipofuscin). We found that the lifespan and healthspan promoting effects of oolong tea extracts and oolonghomobisflavans were positively correlated with the stress resistance via DAF-16/FOXO transcription factor. Furthermore, oolong tea extracts and oolonghomobisflavans displayed protective effects against Aβ- and polyQ-induced neuro/proteotoxicity. Overall, our study provides new evidence to support the health benefits of oolong tea and importantly identify oolonghomobisflavans as potent bioactive molecules that promote health when supplemented with a normal diet. As such, oolonghomobisflavans represent a valuable new class of compounds that promote healthy aging.

scholarly journals Guarana (Paullinia cupana) Extract Protects Caenorhabditis elegans Models for Alzheimer Disease and Huntington Disease through Activation of Antioxidant and Protein Degradation Pathways

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Patrícia Ferreira Boasquívis ◽  
Giovanna Melo Martins Silva ◽  
Franciny Aparecida Paiva ◽  
Rodrigo Marinho Cavalcanti ◽  
Cecília Verônica Nunez ◽  
...  
Keyword(s):  
Caenorhabditis Elegans ◽  
Protein Misfolding ◽  
Therapeutic Potential ◽  
High Energy ◽  
Protective Effects ◽  
Independent Manner ◽  
Paullinia Cupana ◽  
Age Related ◽  
Polyq Protein ◽  
Underlying Mechanisms

Guarana (Paullinia cupana) is largely consumed in Brazil in high energy drinks and dietary supplements because of its stimulant activity on the central nervous system. Although previous studies have indicated that guarana has some protective effects in Parkinson’s (PD), Alzheimer’s (AD), and Huntington’s (HD) disease models, the underlying mechanisms are unknown. Here, we investigated the protective effects of guarana hydroalcoholic extract (GHE) in Caenorhabditis elegans models of HD and AD. GHE reduced polyglutamine (polyQ) protein aggregation in the muscle and also reduced polyQ-mediated neuronal death in ASH sensory neurons and delayed β-amyloid-induced paralysis in a caffeine-independent manner. Moreover, GHE’s protective effects were not mediated by caloric restriction, antimicrobial effects, or development and reproduction impairment. Inactivation of the transcription factors SKN-1 and DAF-16 by RNAi partially blocked the protective effects of GHE treatment in the AD model. We show that the protective effect of GHE is associated with antioxidant activity and modulation of proteostasis, since it increased the lifespan and proteasome activity, reduced intracellular ROS and the accumulation of autophagosomes, and increased the expression of SOD-3 and HSP-16.2. Our findings suggest that GHE has therapeutic potential in combating age-related diseases associated with protein misfolding and accumulation.

scholarly journals Mesencephalic Astrocyte-Derived Neurotrophic Factor Is Upregulated with Therapeutic Fasting in Humans and Diet Fat Withdrawal in Obese Mice

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Emilia Galli ◽  
Jari Rossi ◽  
Thomas Neumann ◽  
Jaan-Olle Andressoo ◽  
Stefan Drinda ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Metabolic Regulation ◽  
Dietary Intervention ◽  
Human Subjects ◽  
Normal Diet ◽  
Enzyme Linked Immunosorbent Assay ◽  
Protective Effects ◽  
Knock Out ◽  
Positive Effects ◽  
Age Related

Abstract Dietary restriction induces beneficial metabolic changes and prevents age-related deterioration. Mesencephalic astrocyte-derived neurotrophic factor (MANF) shows protective effects on cells in various models of degenerative diseases. Here we studied whether circulating concentrations of MANF are associated with fasting-induced positive effects. We quantified the levels of circulating MANF from 40 human subjects before and after therapeutic fasting. As measured by an enzyme-linked immunosorbent assay (ELISA), the mean concentration of plasma MANF increased after an average fasting of 15 days. Plasma MANF levels correlated inversely with adiponectin, a hormone that regulates metabolism, thus suggesting that MANF levels are related to metabolic homeostasis. To study the effects of dietary intervention on MANF concentrations in mice, we developed an ELISA for mouse MANF and verified its specificity using MANF knock-out (KO) tissue. A switch from high-fat to normal diet increased MANF levels and downregulated the expression of unfolded protein response (UPR) genes in the liver, indicating decreased endoplasmic reticulum (ER) stress. Liver MANF and serum adiponectin concentrations correlated inversely in mice. Our findings demonstrate that MANF expression and secretion increases with dietary intervention. The MANF correlation to adiponectin and its possible involvement in metabolic regulation and overall health warrants further studies.

scholarly journals Changes in ferrous iron and glutathione promote ferroptosis and frailty in aging Caenorhabditis elegans

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Nicole L Jenkins ◽  
Simon A James ◽  
Agus Salim ◽  
Fransisca Sumardy ◽  
Terence P Speed ◽  
...  
Keyword(s):  
Cell Death ◽  
Caenorhabditis Elegans ◽  
Ferrous Iron ◽  
Healthy Aging ◽  
Somatic Tissue ◽  
Glutathione Depletion ◽  
Death Process ◽  
Regulated Cell Death ◽  
Age Related ◽  
Cell Death Process

All eukaryotes require iron. Replication, detoxification, and a cancer-protective form of regulated cell death termed ferroptosis, all depend on iron metabolism. Ferrous iron accumulates over adult lifetime in Caenorhabditis elegans. Here, we show that glutathione depletion is coupled to ferrous iron elevation in these animals, and that both occur in late life to prime cells for ferroptosis. We demonstrate that blocking ferroptosis, either by inhibition of lipid peroxidation or by limiting iron retention, mitigates age-related cell death and markedly increases lifespan and healthspan. Temporal scaling of lifespan is not evident when ferroptosis is inhibited, consistent with this cell death process acting at specific life phases to induce organismal frailty, rather than contributing to a constant aging rate. Because excess age-related iron elevation in somatic tissue, particularly in brain, is thought to contribute to degenerative disease, post-developmental interventions to limit ferroptosis may promote healthy aging.

scholarly journals Neuroprotective Effects of Glochidion zeylanicum Leaf Extract against H2O2/Glutamate-Induced Toxicity in Cultured Neuronal Cells and Aβ-Induced Toxicity in Caenorhabditis elegans

Biology ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 800
Author(s):  
Chatrawee Duangjan ◽  
Panthakarn Rangsinth ◽  
Shaoxiong Zhang ◽  
Xiaojie Gu ◽  
Michael Wink ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caenorhabditis Elegans ◽  
Leaf Extract ◽  
Neuronal Cells ◽  
Antioxidant Properties ◽  
Ros Generation ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Antioxidant Genes ◽  
Age Related

Oxidative stress plays a crucial role in the development of age-related neurodegenerative diseases. Previously, Glochidion zeylanicum methanol (GZM) extract has been reported to have antioxidant and anti-aging properties. However, the effect of GZM on neuroprotection has not been reported yet; furthermore, the mechanism involved in its antioxidant properties remains unresolved. The study is aimed to demonstrate the neuroprotective properties of GZM extract and their underlying mechanisms in cultured neuronal (HT-22 and Neuro-2a) cells and Caenorhabditis elegans models. GZM extract exhibited protective effects against glutamate/H2O2-induced toxicity in cultured neuronal cells by suppressing the intracellular reactive oxygen species (ROS) generation and enhancing the expression of endogenous antioxidant enzymes (SODs, GPx, and GSTs). GZM extract also triggered the expression of SIRT1/Nrf2 proteins and mRNA transcription of antioxidant genes (NQO1, GCLM, and EAAT3) which are the master regulators of cellular defense against oxidative stress. Additionally, GZM extract exhibited protective effects to counteract β-amyloid (Aβ)-induced toxicity in C. elegans and promoted neuritogenesis properties in Neuro-2a cells. Our observations suggest that GZM leaf extract has interesting neuritogenesis and neuroprotective potential and can possibly act as potential contender for the treatment of oxidative stress-induced Alzheimer’s disease (AD) and related neurodegenerative conditions; however, this needs to be studied further in other in vivo systems.

scholarly journals Plant-Derived Bioactives and Oxidative Stress-Related Disorders: A Key Trend towards Healthy Aging and Longevity Promotion

2020 ◽  
Vol 10 (3) ◽  
pp. 947 ◽  
Author(s):  
Bahare Salehi ◽  
Elena Azzini ◽  
Paolo Zucca ◽  
Elena Maria Varoni ◽  
Nanjangud V. Anil Kumar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Healthy Aging ◽  
Biological Effects ◽  
Biologically Active ◽  
Bioactive Molecules ◽  
Human Beings ◽  
Aging Effects ◽  
Treatment And Prevention ◽  
Age Related ◽  
And Oxidative Stress

Plants and their corresponding botanical preparations have been used for centuries due to their remarkable potential in both the treatment and prevention of oxidative stress-related disorders. Aging and aging-related diseases, like cardiovascular disease, cancer, diabetes, and neurodegenerative disorders, which have increased exponentially, are intrinsically related with redox imbalance and oxidative stress. Hundreds of biologically active constituents are present in each whole plant matrix, providing promissory bioactive effects for human beings. Indeed, the worldwide population has devoted increased attention and preference for the use of medicinal plants for healthy aging and longevity promotion. In fact, plant-derived bioactives present a broad spectrum of biological effects, and their antioxidant, anti-inflammatory, and, more recently, anti-aging effects, are considered to be a hot topic among the medical and scientific communities. Nonetheless, despite the numerous biological effects, it should not be forgotten that some bioactive molecules are prone to oxidation and can even exert pro-oxidant effects. In this sense, the objective of the present review is to provide a detailed overview of plant-derived bioactives in age-related disorders. Specifically, the role of phytochemicals as antioxidants and pro-oxidant agents is carefully addressed, as is their therapeutic relevance in longevity, aging-related disorders, and healthy-aging promotion. Finally, an eye-opening look into the overall evidence of plant compounds related to longevity is presented.

scholarly journals Decreasing pdzd8-mediated mitochondrial-ER contacts in neurons improves fitness by increasing mitophagy

2020 ◽  
Author(s):  
Victoria L. Hewitt ◽  
Leonor Miller-Fleming ◽  
Simonetta Andreazza ◽  
Francesca Mattedi ◽  
Julien Prudent ◽  
...  
Keyword(s):  
Quality Control ◽  
Healthy Aging ◽  
Synapse Formation ◽  
Critical Role ◽  
Functional Characterization ◽  
Protective Effects ◽  
Mitochondrial Quality Control ◽  
Age Related ◽  
The Many

AbstractThe complex cellular architecture of neurons combined with their longevity makes maintaining a healthy mitochondrial network particularly important and challenging. One of the many roles of mitochondrial-ER contact sites (MERCs) is to mediate mitochondrial quality control through regulating mitochondrial turn over. Pdzd8 is a newly discovered MERC protein, the organismal functions of which have not yet been explored. Here we identify and provide the first functional characterization of the Drosophila melanogaster ortholog of Pdzd8. We find that reducing pdzd8-mediated MERCs in neurons slows age-associated decline in locomotor activity and increases lifespan in Drosophila. The protective effects of pdzd8 knockdown in neurons correlate with an increase in mitophagy, suggesting that increased mitochondrial turnover may support healthy aging of neurons. In contrast, increasing MERCs by expressing a constitutive, synthetic ER-mitochondria tether disrupts mitochondrial transport and synapse formation, accelerates age-related decline in locomotion and reduces lifespan. We also show that depletion of pdzd8 rescues the locomotor defects characterizing an Alzheimer’s disease (AD) fly model over-expressing Amyloidβ1–42 (Aβ42) and prolongs the survival of flies fed with mitochondrial toxins. Together, our results provide the first in vivo evidence that MERCs mediated by the tethering protein pdzd8 play a critical role in the regulation of mitochondrial quality control and neuronal homeostasis.

The Role of Glyoxalase in Glycation and Carbonyl Stress Induced Metabolic Disorders

2020 ◽  
Vol 21 (9) ◽  
pp. 846-859
Author(s):  
Mohd Saeed ◽  
Mohd Adnan Kausar ◽  
Rajeev Singh ◽  
Arif J. Siddiqui ◽  
Asma Akhter
Keyword(s):  
Protein Misfolding ◽  
Covalent Binding ◽  
Critical Role ◽  
Enzymatic Reaction ◽  
Treatment Strategies ◽  
Bioactive Molecules ◽  
Carbonyl Stress ◽  
Defense System ◽  
Pathological Conditions ◽  
Age Related

Glycation refers to the covalent binding of sugar molecules to macromolecules, such as DNA, proteins, and lipids in a non-enzymatic reaction, resulting in the formation of irreversibly bound products known as advanced glycation end products (AGEs). AGEs are synthesized in high amounts both in pathological conditions, such as diabetes and under physiological conditions resulting in aging. The body’s anti-glycation defense mechanisms play a critical role in removing glycated products. However, if this defense system fails, AGEs start accumulating, which results in pathological conditions. Studies have been shown that increased accumulation of AGEs acts as key mediators in multiple diseases, such as diabetes, obesity, arthritis, cancer, atherosclerosis, decreased skin elasticity, male erectile dysfunction, pulmonary fibrosis, aging, and Alzheimer’s disease. Furthermore, glycation of nucleotides, proteins, and phospholipids by α-oxoaldehyde metabolites, such as glyoxal (GO) and methylglyoxal (MGO), causes potential damage to the genome, proteome, and lipidome. Glyoxalase-1 (GLO-1) acts as a part of the anti-glycation defense system by carrying out detoxification of GO and MGO. It has been demonstrated that GLO-1 protects dicarbonyl modifications of the proteome and lipidome, thereby impeding the cell signaling and affecting age-related diseases. Its relationship with detoxification and anti-glycation defense is well established. Glycation of proteins by MGO and GO results in protein misfolding, thereby affecting their structure and function. These findings provide evidence for the rationale that the functional modulation of the GLO pathway could be used as a potential therapeutic target. In the present review, we summarized the newly emerged literature on the GLO pathway, including enzymes regulating the process. In addition, we described small bioactive molecules with the potential to modulate the GLO pathway, thereby providing a basis for the development of new treatment strategies against age-related complications.

Versatile Health Benefits of Catechin from Green Tea (Camellia sinensis)

2019 ◽  
Vol 15 (1) ◽  
pp. 3-10 ◽  
Author(s):  
Satheesh Babu Natarajan ◽  
Suriyakala Perumal Chandran ◽  
Sahar Husain Khan ◽  
Packiyaraj Natarajan ◽  
Karthiyaraj Rengarajan
Keyword(s):  
Green Tea ◽  
Camellia Sinensis ◽  
Health Benefits ◽  
Epigallocatechin Gallate ◽  
Extraction Methods ◽  
Major Constituent ◽  
Epicatechin Gallate ◽  
Wide Range ◽  
Green Tea Catechin ◽  
Anti Inflammatory

Background: Tea (Camellia sinensis, Theaceae) is the second most consumed beverage in the world. Green tea is the least processed and thus contain rich antioxidant level, and believed to have most of the health benefits. </p><p> Methods: We commenced to search bibliographic collection of peer reviewed research articles and review articles to meet the objective of this study. </p><p> Results: From this study, we found that the tea beverage contains catechins are believed to have a wide range of health benefits which includes neuroprotective, anti-inflammatory, antiulcer, antiviral, antibacterial, and anti-parasitic effects. The four major catechin compounds of green tea are epigallocatechin (EGC), epicatechin (EC), epigallocatechin gallate (EGCG), and epicatechin gallate (ECG), of which EGCG is the major constituent and representing 50-80% of the total catechin content. And also contain xanthine derivatives such as caffeine, theophylline, and theobromine, and the glutamide derivative theanine. It also contains many nutritional components, such as vitamin E, vitamin C, fluoride, and potassium. We sum up the various green tea phytoconstituents, extraction methods, and its medicinal applications. </p><p> Conclusion: In this review article, we have summarized the pharmacological importance of green tea catechin which includes antioxidant potential, anti-inflammatory, antimicrobial, anticancer, antidiabetic and cosmetic application.

Hyperbaric oxygen therapy attenuates D-galactose-induced-age-related cardiac dysfunction through mitigating cardiac mitochondrial dysfunction in pre-diabetic rats

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
C Bo-Htay ◽  
T Shwe ◽  
S Palee ◽  
T Pattarasakulchai ◽  
K Shinlapawittayatorn ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
High Fat Diet ◽  
Diabetic Rats ◽  
Normal Diet ◽  
Lv Function ◽  
High Fat ◽  
Insulin Resistant ◽  
Lv Dysfunction ◽  
Age Related ◽  
Mitochondrial Functions

Abstract Background D-galactose (D-gal) induced ageing has been shown to exacerbate left ventricular (LV) dysfunction via worsening of apoptosis and mitochondrial dysfunction in the heart of obese rats. Hyperbaric oxygen therapy (HBOT) has been demonstrated to exert anti-inflammatory and anti-apoptotic effects in multiple neurological disorders. However, the cardioprotective effect of HBOT on inflammation, apoptosis, LV and mitochondrial functions in D-gal induced ageing rats in the presence of obese-insulin resistant condition has never been investigated. Purpose We sought to determine the effect of HBOT on inflammation, apoptosis, mitochondrial functions and LV function in pre-diabetic rats with D-gal induced ageing. We hypothesized that HBOT attenuates D-gal induced cardiac mitochondrial dysfunctions and reduces inflammation and apoptosis, leading to improved LV function in pre-diabetic rats. Methods Forty-eight male Wistar rats were fed with either normal diet or high-fat diet for 12 weeks. Then, rats were treated with either vehicle groups (0.9% NSS, subcutaneous injection (SC)) or D-gal groups (150 mg/kg/day, SC) for 8 weeks. At week 21, rats in each group were equally divided into 6 sub-groups: normal diet fed rats treated with vehicle (NDV) sham, normal diet fed rats treated with D-gal (NDDg) sham, high fat diet fed rats treated with D-gal (HFDg) sham, high fat diet fed rats treated with vehicle (HFV) + HBOT, NDDg + HBOT and HFDg + HBOT. Sham treated rats were given normal concentration of O2 (flow rate of 80 L/min, 1 ATA for 60 minutes), whereas HBOT treated rats were subjected to 100% O2 (flow rate of 250 L/min, 2 ATA for 60 minutes), given once daily for 2 weeks. Results Under obese-insulin resistant condition, D-gal-induced ageing aggravated LV dysfunction (Fig 1A) and impaired cardiac mitochondrial function, increased cardiac inflammatory and apoptotic markers (Fig 1B). HBOT markedly reduced cardiac TNF-α level and TUNEL positive apoptotic cells, and improved cardiac mitochondrial function as indicated by decreased mitochondrial ROS production, mitochondrial depolarization and mitochondrial swelling, resulting in the restoration of the normal LV function in HFV and NDDg rats, compared to sham NDDg rats. In addition, in HFDg treated rats, HBOT attenuated cardiac TNF-α level, TUNEL positive apoptotic cells and cardiac mitochondrial dysfunction, compared to sham HFDg rats, leading to improved cardiac function as indicated by increased %LV ejection fraction (LVEF) (Figure 1). Conclusion HBOT efficiently alleviates D-gal-induced-age-related LV dysfunction through mitigating inflammation, apoptosis and mitochondrial dysfunction in pre-diabetic rats. Figure 1 Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): 1. The National Science and Technology Development Agency Thailand, 2. Thailand Research Fund Grants

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