Improve Stress Resistance Research Articles

Multiple Ways of Nitric Oxide Production in Plants and Its Functional Activity under Abiotic Stress Conditions.

Nitric oxide (NO) is an endogenous signaling molecule that plays an important role in plant ontogenesis and responses to different stresses. The most widespread abiotic stress factors limiting significantly plant growth and crop yield are drought, salinity, hypo-, hyperthermia, and an excess of heavy metal (HM) ions. Data on the accumulation of endogenous NO under stress factors and on the alleviation of their negative effects under exogenous NO treatments indicate the perspectives of its practical application to improve stress resistance and plant productivity. This requires fundamental knowledge of the NO metabolism and the mechanisms of its biological action in plants. NO generation occurs in plants by two main alternative mechanisms: oxidative or reductive, in spontaneous or enzymatic reactions. NO participates in plant development by controlling the processes of seed germination, vegetative growth, morphogenesis, flower transition, fruit ripening, and senescence. Under stressful conditions, NO contributes to antioxidant protection, osmotic adjustment, normalization of water balance, regulation of cellular ion homeostasis, maintenance of photosynthetic reactions, and growth processes of plants. NO can exert regulative action by inducing posttranslational modifications (PTMs) of proteins changing the activity of different enzymes or transcriptional factors, modulating the expression of huge amounts of genes, including those related to stress tolerance. This review summarizes the current data concerning molecular mechanisms of NO production and its activity in plants during regulation of their life cycle and adaptation to drought, salinity, temperature stress, and HM ions.

Reprogramming of the transcriptome after heat stress mediates heat hormesis in Caenorhabditis elegans

Transient stress experiences not only trigger acute stress responses, but can also have long-lasting effects on cellular functions. In Caenorhabditis elegans, a brief exposure to heat shock during early adulthood extends lifespan and improves stress resistance, a phenomenon known as heat hormesis. Here, we investigated the prolonged effect of hormetic heat stress on the transcriptome of worms and found that the canonical heat shock response is followed by a profound transcriptional reprogramming in the post-stress period. This reprogramming relies on the endoribonuclease ENDU-2 but not the heat shock factor 1. ENDU-2 co-localizes with chromatin and interacts with RNA polymerase II, enabling specific regulation of transcription after the stress period. Failure to activate the post-stress response does not affect the resistance of animals to heat shock but eliminates the beneficial effects of hormetic heat stress. In summary, our work discovers that the RNA-binding protein ENDU-2 mediates the long-term impacts of transient heat stress via reprogramming transcriptome after stress exposure.

Transcriptome-Wide Identification of the GRAS Transcription Factor Family in Pinus massoniana and Its Role in Regulating Development and Stress Response.

Pinus massoniana is a species used in afforestation and has high economic, ecological, and therapeutic significance. P. massoniana experiences a variety of biotic and abiotic stresses, and thus presents a suitable model for studying how woody plants respond to such stress. Numerous families of transcription factors are involved in the research of stress resistance, with the GRAS family playing a significant role in plant development and stress response. Though GRASs have been well explored in various plant species, much research remains to be undertaken on the GRAS family in P. massoniana. In this study, 21 PmGRASs were identified in the P. massoniana transcriptome. P. massoniana and Arabidopsis thaliana phylogenetic analyses revealed that the PmGRAS family can be separated into nine subfamilies. The results of qRT-PCR and transcriptome analyses under various stress and hormone treatments reveal that PmGRASs, particularly PmGRAS9, PmGRAS10 and PmGRAS17, may be crucial for stress resistance. The majority of PmGRASs were significantly expressed in needles and may function at multiple locales and developmental stages, according to tissue-specific expression analyses. Furthermore, the DELLA subfamily members PmGRAS9 and PmGRAS17 were nuclear localization proteins, while PmGRAS9 demonstrated transcriptional activation activity in yeast. The results of this study will help explore the relevant factors regulating the development of P. massoniana, improve stress resistance and lay the foundation for further identification of the biological functions of PmGRASs.

Homeodomain-interacting protein kinase maintains neuronal homeostasis during normal Caenorhabditis elegans aging and systemically regulates longevity from serotonergic and GABAergic neurons.

Aging and the age-associated decline of the proteome is determined in part through neuronal control of evolutionarily conserved transcriptional effectors, which safeguard homeostasis under fluctuating metabolic and stress conditions by regulating an expansive proteostatic network. We have discovered the Caenorhabditis elegans homeodomain-interacting protein kinase (HPK-1) acts as a key transcriptional effector to preserve neuronal integrity, function, and proteostasis during aging. Loss of hpk-1 results in drastic dysregulation in expression of neuronal genes, including genes associated with neuronal aging. During normal aging hpk-1 expression increases throughout the nervous system more broadly than any other kinase. Within the aging nervous system, hpk-1 induction overlaps with key longevity transcription factors, which suggests hpk-1 expression mitigates natural age-associated physiological decline. Consistently, pan-neuronal overexpression of hpk-1 extends longevity, preserves proteostasis both within and outside of the nervous system, and improves stress resistance. Neuronal HPK-1 improves proteostasis through kinase activity. HPK-1 functions cell non-autonomously within serotonergic and GABAergic neurons to improve proteostasis in distal tissues by specifically regulating distinct components of the proteostatic network. Increased serotonergic HPK-1 enhances the heat shock response and survival to acute stress. In contrast, GABAergic HPK-1 induces basal autophagy and extends longevity, which requires mxl-2 (MLX), hlh-30 (TFEB), and daf-16 (FOXO). Our work establishes hpk-1 as a key neuronal transcriptional regulator critical for preservation of neuronal function during aging. Further, these data provide novel insight as to how the nervous system partitions acute and chronic adaptive response pathways to delay aging by maintaining organismal homeostasis.

Genome-wide analysis and expression profiling of glyoxalase gene families in oat (Avena sativa) indicate their responses to abiotic stress during seed germination.

Abiotic stresses have deleterious effects on seed germination and seedling establishment, leading to significant crop yield losses. Adverse environmental conditions can cause the accumulation of methylglyoxal (MG) within plant cells, which can negatively impact plant growth and development. The glyoxalase system, which consists of the glutathione (GSH)-dependent enzymes glyoxalase I (GLX1) and glyoxalase II (GLX2), as well as the GSH-independent glyoxalase III (GLX3 or DJ-1), plays a crucial role in detoxifying MG. However, genome-wide analysis of glyoxalase genes has not been performed for one of the agricultural important species, oat (Avena sativa). This study identified a total of 26 AsGLX1 genes, including 8 genes encoding Ni2+-dependent GLX1s and 2 genes encoding Zn2+-dependent GLX1s. Additionally, 14 AsGLX2 genes were identified, of which 3 genes encoded proteins with both lactamase B and hydroxyacylglutathione hydrolase C-terminal domains and potential catalytic activity, and 15 AsGLX3 genes encoding proteins containing double DJ-1 domains. The domain architecture of the three gene families strongly correlates with the clades observed in the phylogenetic trees. The AsGLX1, AsGLX2, and AsGLX3 genes were evenly distributed in the A, C, and D subgenomes, and gene duplication of AsGLX1 and AsGLX3 genes resulted from tandem duplications. Besides the core cis-elements, hormone responsive elements dominated the promoter regions of the glyoxalase genes, and stress responsive elements were also frequently observed. The subcellular localization of glyoxalases was predicted to be primarily in the cytoplasm, chloroplasts, and mitochondria, with a few presents in the nucleus, which is consistent with their tissue-specific expression. The highest expression levels were observed in leaves and seeds, indicating that these genes may play important roles in maintaining leaf function and ensuring seed vigor. Moreover, based on in silico predication and expression pattern analysis, AsGLX1-7A, AsGLX2-5D, AsDJ-1-5D, AsGLX1-3D2, and AsGLX1-2A were suggested as promising candidate genes for improving stress resistance or seed vigor in oat. Overall, the identification and analysis of the glyoxalase gene families in this study can provide new strategies for improving oat stress resistance and seed vigor.

Oxidized quercetin has stronger anti-amyloid activity and anti-aging effect than native form

Quercetin (QUE) is one of the most widely distributed and used flavonoid. It has many biological activities and pharmacological effect. As a polyhydroxy phenol, QUE is easily oxidized. However, it is unclear how its biology efficacy changes after oxidation. In this study, we prepared QUE oxidation product (QUE-ox) through enzymatic oxidation of QUE. We found the oxidation reduced the antioxidant activity of QUE but increased its anti-amyloid activity in vitro. In C. elegans, oxidation increased the anti-aging effects of QUE. Further experiments showed that both QUE and QUE-ox delayed aging by improving stress resistance, but they have different molecular mechanisms. QUE mainly increased the transcriptional activities of DAF-16 and SKN-1, resulting in the enhancement of expression of oxidative stress resistance genes, and further increased the oxidative resistance in C. elegans. QUE-ox increased the transcriptional activities of DAF-16 and HSF-1 transcription factors to enhance the heat stress resistance. In summary, our study indicated oxidized QUE has stronger anti-amyloid activity and anti-aging effect than native form. This study provides a theoretical basis for the safe and rational application of QUE, especially for its antioxidant, anti-amyloid and anti-aging effects.

AccsHSP21.7 enhances the antioxidant capacity of Apis cerana cerana.

The widespread use of glyphosate has many adverse effects on Apis cerana cerana. Due to the incomplete understanding of the molecular mechanisms of glyphosate toxicity, there are no available methods for mitigating the threat of glyphosate to Apis cerana cerana. Small heat shock proteins (sHSPs) play an important role in resisting oxidative stress, but their mechanism of action in Apis cerana cerana remains unclear. In this experiment, we cloned and identified AccsHSP21.7. Studies have shown that AccsHSP21.7 contains binding motifs for various transcription factors related to oxidative stress. Abiotic stresses induced the expression of AccsHSP21.7. Bacteriostatic testing of a recombinant AccsHSP21.7 protein proved that Escherichia coli overexpressing AccsHSP21.7 showed increased resistance to oxidative stress. Knocking down the AccsHSP21.7 gene caused significant damage to midgut cells, which seriously disrupted the antioxidant system in Apis cerana cerana and greatly increased mortality under glyphosate stress. This study investigated the relationship between antioxidant regulation and the AccsHSP21.7 gene at the molecular level, and the results have guiding significance for the improvement of stress resistance in Apis cerana cerana. © 2023 Society of Chemical Industry.

Improving Saccharomyces cerevisiae acid and oxidative stress resistance using a prokaryotic gene identified by functional metagenomics

Innovations in obtaining products from lignocellulosic biomass have been largely based on the improvement of microorganisms and enzymes capable of degrading these materials. To complete the whole process, microorganisms must be able to ferment the resulting sugars and tolerate high concentrations of product, osmotic pressure, ion toxicity, temperature, toxic compounds from lignocellulose pretreatment, low pH, and oxidative stress. In this work, we engineered laboratory and industrial Saccharomyces cerevisiae strains by combining a gene (hu) recovered from a metagenomic approach with different native and synthetic promoters to obtain improved acid and oxidative stress resistance. Laboratorial strains harboring hu gene under the control of the synthetic stress responsive PCCW14v5 showed increased survival rates after 2 h exposure to pH 1.5. The hu gene was also able to significantly enhance the tolerance of the industrial strain to high concentrations of H2O2 when combined with PTEF1, PYGP1 or PYGP1v7 after 3 h exposure.

Vanillic Acid Improves Stress Resistance and Substantially Extends Life Span in Caenorhabditis elegans.

Aging is the root cause of several pathologies like neurological and cardiovascular diseases. Identifying compounds that improve health span and extend life span, called geroprotectors, could be crucial to preventing or at least delaying the onset of age-related diseases. In this regard, the nematode Caenorhabditis elegans (C.elegans) is emerging as an easy, efficient, low-cost model system to screen natural products and identify novel geroprotectors. Phenolic acids can be found in a wide range of natural products that are part of the human diet. Vanillic acid (VA) is a phenolic acid that has previously been attributed with antioxidant, anti-inflammatory, and neuroprotective features. To determine whether these beneficial health effects amount to an extension of health span and life span, in this work, we thoroughly explore the effect of VA on C.elegans stress resistance and life span. We found that VA increases thermotolerance (19.4%), reduces protein aggregation (between 30% and 40%), improves motility, and extends life span by almost 50%, an extent hardly ever achieved with a natural compound. The increased thermotolerance induced by VA is independent of the insulin/insulin-like growth factor-1 signaling pathway but requires heat shock factor-1 and is associated with increased heat shock protein-4 (HSP-4) and hsp-16.2 expression. These results provide new insight into understanding the therapeutical properties of VA and warrant further investigation of VA as a novel geroprotector.

The Emerging Role of Autophagy as a Target of Environmental Pollutants: An Update on Mechanisms.

Autophagy is an evolutionarily conserved cellular system crucial for cellular homeostasis that protects cells from a broad range of internal and extracellular stresses. Autophagy decreases metabolic load and toxicity by removing damaged cellular components. Environmental contaminants, particularly industrial substances, can influence autophagic flux by enhancing it as a protective response, preventing it, or converting its protective function into a pro-cell death mechanism. Environmental toxic materials are also notorious for their tendency to bioaccumulate and induce pathophysiological vulnerability. Many environmental pollutants have been found to influence stress which increases autophagy. Increasing autophagy was recently shown to improve stress resistance and reduce genetic damage. Moreover, suppressing autophagy or depleting its resources either increases or decreases toxicity, depending on the circumstances. The essential process of selective autophagy is utilized by mammalian cells in order to eliminate particulate matter, nanoparticles, toxic metals, and smoke exposure without inflicting damage on cytosolic components. Moreover, cigarette smoke and aging are the chief causes of chronic obstructive pulmonary disease (COPD)-emphysema; however, the disease's molecular mechanism is poorly known. Therefore, understanding the impacts of environmental exposure via autophagy offers new approaches for risk assessment, protection, and preventative actions which will counter the harmful effects of environmental contaminants on human and animal health.

Cruciferin improves stress resistance and simulated gastrointestinal survival of probiotic Limosilactobacillus reuteri in the model encapsulation system

Encapsulation is a viable strategy to improve the stability and survival of probiotics during processing, storage, and consumption. Cruciferin, a major canola protein with high denaturation temperature and resistance to gastric degradation, has potential for encapsulation and protection of probiotics against harsh conditions in processing and gastrointestinal tract. Cruciferin/alginate capsules were fabricated to encapsulate probiotics, and were characterized using confocal and scanning electron microscopy (SEM). The bacterial viability was studied during storage, processing, and gastro-intestinal transit. Limosilactobacillus reuteri TMW 1.656 was encapsulated in spherical cruciferin/alginate capsules (2.2 ± 0.1 mm) prepared using an extrusion method. SEM images of the capsules showed that the bacteria were entrapped within the porous structure which was formed by the complexation of cruciferin and alginate. The confocal microscopy images confirmed that cruciferin and alginate were homogeneously distributed throughout the capsules. The shelf life of the bacteria in the presence of cruciferin and alginate increased up to 8 weeks at 4 °C, while unencapsulated (free) bacteria lost their viability after 2 weeks storage. The heat resistance of encapsulated bacteria exposed to 65 °C and 70 °C was improved by up to ∼ 4 and 2 log cycles, respectively, compared to unencapsulated bacteria. Encapsulation also protected L. reuteri against gastric low pH and enzymes; the viability was 3 logs higher when compared to unencapsulated bacteria. The capsules were degraded in simulated intestinal fluid, leading to the release of the encapsulated bacteria, whereas the wall materials increased the resistance of released bacteria to bile salts. Comparison between the viability of unencapsulated bacteria in presence of cruciferin/alginate mixtures and bacteria encapsulated in the capsules revealed that capsule formation provided physical barriers to the harsh conditions and played a key role in the protection of bacteria. This study showed that cruciferin/alginate capsules are capable to improve stability and shelf life of Limosilactobacillus reuteri.

A new AMPK isoform mediates glucose-restriction induced longevity non-cell autonomously by promoting membrane fluidity

Dietary restriction (DR) delays aging and the onset of age-associated diseases. However, it is yet to be determined whether and how restriction of specific nutrients promote longevity. Previous genome-wide screens isolated several Escherichia coli mutants that extended lifespan of Caenorhabditis elegans. Here, using 1H-NMR metabolite analyses and inter-species genetics, we demonstrate that E. coli mutants depleted of intracellular glucose extend C. elegans lifespans, serving as bona fide glucose-restricted (GR) diets. Unlike general DR, GR diets don’t reduce the fecundity of animals, while still improving stress resistance and ameliorating neuro-degenerative pathologies of Aβ42. Interestingly, AAK-2a, a new AMPK isoform, is necessary and sufficient for GR-induced longevity. AAK-2a functions exclusively in neurons to modulate GR-mediated longevity via neuropeptide signaling. Last, we find that GR/AAK-2a prolongs longevity through PAQR-2/NHR-49/Δ9 desaturases by promoting membrane fluidity in peripheral tissues. Together, our studies identify the molecular mechanisms underlying prolonged longevity by glucose specific restriction in the context of whole animals.

Genome-wide identification, characterization and gene expression of BES1 transcription factor family in grapevine (Vitis vinifera L.)

BES1, as the most important transcription factor responsible for brassinolide (BR) signaling, has been confirmed to play a significant role in regulating plant growth and the improvement of stress resistance. The transcriptional regulatory mechanism of BES1 has been well elucidated in several plants, such as Arabidopsis thaliana (A. thaliana), Triticum aestivum L. (T. aestivum), and Oryza sativa L. (O. sativa). Nevertheless, the genome-wide analysis of the BES1 family in Vitis vinifera L. (V. vinifera). has not been comprehensively carried out. Thus, we have conducted a detailed analysis and identification of the BES1 transcription factors family in V. vinifera; a total of eight VvBES1 genes was predicted, and the phylogenetic relationships, gene structures, and Cis-acting element in their promoters were also analyzed. BES1 genes have been divided into three groups (I, II and III) based on phylogenetic relationship analysis, and most of VvBES1 genes were in group III. Also, we found that VvBES1 genes was located at seven of the total nineteen chromosomes, whereas VvBES1-2 (Vitvi04g01234) and VvBES1-5 (Vitvi18g00924) had a collinearity relationship, and their three copies are well preserved. In addition, the intron–exon model of VvBES1 genes were mostly conserved, and there existed several Cis-acting elements related to stress resistance responsive and phytohormones responsive in BES1s genes promoter. Moreover, the BES1 expressions were different in different V. vinifera organs, and BES1 expressions were different in different V. vinifera varieties under saline-alkali stress and heat stress, the expression of VvBES1 also changed with the prolongation of saline-alkali stress treatment time. The above findings could not only lay a primary foundation for the further validation of VvBES1 function, but could also provide a reference for molecular breeding in V. vinifera.

Appropriate cold stimulation changes energy distribution to improve stress resistance in broilers.

Appropriate cold stimulation can improve stress resistance in broilers and alleviate the adverse impacts of a cold environment. To investigate the effects of intermittent mild cold stimulation (IMCS) on energy distribution in the livers of broilers, 96 healthy 1-d-old Ross-308 male broilers were randomly divided into the control group (CC) and the cold stimulation group (H5). The CC group was raised at a normal thermal temperature, i.e., 35 °C until 3 d, after which the temperature was dropped gradually by 0.5 °C/d until 20 °C at 33 d. This temperature was maintained until 49 d. The H5 group was raised at the same temperature as the CC group until 14 d (35 to 29.5 °C) and at 3 °C below the temperature of the CC group starting at 0930 hours for 5 h every other day from 15 to 35 d (26 to 17°C). The temperature was returned to 20 °C at 36 d and maintained until 49 d. At 50 d, all broilers were subjected to acute cold stress (ACS) at 10 °C for 6 and 12 h. We found that IMCS had positive effects on production performance. Using transcriptome sequencing of the broiler livers, 327 differentially expressed genes (DEG) were identified, and highly enriched in fatty acid biosynthesis, fatty acid degradation, and the pyruvate metabolism pathway. When compared to the CC group, the mRNA levels of ACAA1, ACAT2, ACSL1, CPT1A, LDHB, and PCK1 in the H5 group were increased at 22 d (P < 0.05). The LDHB mRNA level was upregulated in the H5 group at 29 d compared to the CC group (P < 0.05). After 21 d of IMCS (at 36 d), the mRNA expression levels of ACAT2 and PCK1 were found to be significantly increased in the H5 group compared to the CC group (P < 0.05). Seven days after the IMCS had ended (at 43 d), the mRNA levels of ACAA1, ACAT2, and LDHB in the H5 group were higher than in the CC group (P < 0.05). The mRNA levels of heat shock protein (HSP) 70, HSP90, and HSP110 in the H5 group were higher than in the CC group after 6 h of ACS (P < 0.05). The protein levels of HSP70 and HSP90 in the H5 group were downregulated after 12 h of ACS, compared to the CC group (P < 0.05). These results indicated that IMCS at 3 °C lower than the normal temperature could improve energy metabolism and stress resistance in the livers of broilers, alleviate the damage of short-term ACS on broilers, help broilers adapt to the low temperature, and maintain stable of energy metabolism in the body.

A novel peptide derived from Haematococcus pluvialis residue exhibits anti-aging activity in Caenorhabditis elegans via the insulin/IGF-1 signaling pathway.

To explore the value of Haematococcus pluvialis (H. pluvialis) residue remaining after astaxanthin extraction and being discarded uneconomically, in our previous study, we discovered a novel peptide (HPp) as a potential bioactive component. However, the possible anti-aging activity in vivo was not illuminated. In this study, the capacity of extending the lifespan and the mechanism based on Caenorhabditis elegans (C. elegans) were determined. The results showed that 100 μM HPp not only enhanced the lifespan of C. elegans in normal environments by 20.96% but also strengthened the lifespan in oxidative and thermal conditions effectively. Moreover, HPp succeeded in lessening the decline in physiological functions of aging worms. In terms of antioxidant efficacy, SOD and CAT enzyme activity were promoted, but the level of MDA was diminished significantly after HPp treatment. Subsequent analysis directly reflected the relationship between higher stress resistance and up-regulation of skn-1 and hsp-16.2, and between greater antioxidant ability and up-regulation of sod-3 and ctl-2. Further studies illustrated that HPp up-graded the mRNA transcription of the genes associated with the insulin/insulin-like growth factor signaling (IIS) pathway and some co-factors, including daf-16, daf-2, ins-18, and sir-2.1. Particularly, the activation of the IIS pathway required the regulation of subcellular localization of DAF-16/FOXO. Taken together, HPp could promote longevity with improved stress resistance and antioxidant properties in vivo through the IIS pathway. These data suggested that HPp might serve as a good source of anti-aging actives, and in particular, laid a foundation for the high value-added application of marine microalgae.

MicroRNA biogenesis pathway alterations in aging

Aging is characterized by genomic instability and dysregulation of gene expression. MicroRNAs (miRNAs) are small non-coding RNAs that play a crucial role in post-transcriptional gene regulation. This work explores the impact of dysregulated miRNA biogenesis on the aging process. During aging, alterations in the transcription of primary miRNAs (pri-miRNAs) occur due to genomic changes, DNA damage, and epigenetic modifications. The microprocessor complex, comprising DGCR8 and Drosha proteins, is vital for pri-miRNA processing. Age-related changes in this complex affect miRNA biogenesis and miRNA expression profiles, linking these alterations with age-related conditions. Conversely, interventions like caloric restriction and mTOR inhibition enhance microprocessor activity, suggesting a connection between microprocessor function, aging-related pathways, and lifespan extension. Exportin-5 mediates the transport of pre-miRNAs from the nucleus to the cytoplasm. Although the role of miRNA export in aging is not well understood, accelerated export of pre-miRNAs is observed in response to DNA damage, and nucleocytoplasmic transport has been linked to cellular senescence. Dicer is responsible for processing pre-miRNAs into mature miRNAs. Reduced Dicer expression during aging is reported in various organisms and tissues and is associated with premature aging phenotypes. Conversely, the upregulation of Dicer improves stress resistance and metabolic adaptations induced by caloric restriction and exercise training. Understanding the role of miRNA biogenesis disruption in aging provides insights into the molecular mechanisms of aging and age-related diseases. Targeting this pathway may hold promise for therapeutic strategies and contribute to healthy aging.

Cremastra appendiculata polysaccharides improve stress resistance and prolong the lifespan of Caenorhabditis elegans via daf-16 in the insulin signaling pathway

Cremastra appendiculata polysaccharide (CAP) exhibits potential anti-aging and stress resistance effects. In this study, we investigated the structure, antioxidant properties, and mechanism of action of CAP in Caenorhabditis elegans. The results showed that CAP primarily comprises mannose and glucose and exerts antioxidant activity in vitro. In vivo, CAP prolonged the lifespan of C. elegans in a concentration-dependent manner, with 2.0 mg/mL CAP prolonging the lifespan by 39.97 %. Compared with the control, the activities of superoxide dismutase (SOD) and catalase (CAT) antioxidant enzymes increased by 46 % and 57 %, respectively. However, the reactive oxygen species (ROS) and malondialdehyde (MDA) contents decreased by 38 % and 19.92 %, respectively, at the same CAP concentration, oxidative and heat stress resistance increased. The target genes of the insulin/insulin-like growth factor (IGF) signaling pathway, daf-16, sod-3, ctl-1, and hsp-16.2, were activated by CAP; their mRNA expression levels were upregulated by 7.23 %, 69.78 %, 43.62 %, and 58.62 %, respectively. A transgenic worm assay indicated that CAP regulates the lifespan of C. elegans through daf-16. These results suggest that CAP improves stress resistance and prolongs the lifespan of C. elegans through daf-16 in the insulin/IGF signaling pathway.

INITIAL EFFICACY OF AN APP-BASED MINDFULNESS MEDITATION FOR BEREAVED KOREAN OLDER ADULTS DURING THE PANDEMIC

Abstract Given the onset of COVID-19, older adults who recently lost their significant others feel more stressed. There yet exist a study utilizing smartphones for web-based delivery of mindfulness intervention among bereaved older adults. Therefore, this study aimed to test the initial efficacy of an app-based mindfulness-meditation (AMM) to alleviate stress and depressive symptoms and improve stress resistance, social support, and self-esteem in Korean older adults experiencing bereavement. Participants included 22 Korean older adults who had been bereaved within the preceding year. AMM involved sound therapy, breathing exercises, and narrated meditation sessions, and the program was conducted over eight weeks. The linear regression results showed that stress level among participants was significantly lower after the intervention, with decreased scores from the baseline. By confirming that AMM is an effective way of reducing stress, more active usage of devices like smartphones should be promoted to develop mental health interventions for older adults.

A FAT-PROMOTING BOTANICAL EXTRACT ARTEMISIA SCOPARIA EXERTS GEROPROTECTION IN C. ELEGANS

Abstract Like other biological processes, aging is not random but subject to molecular control. Natural products that modify core metabolic parameters, including fat content, may provide entry points to extend animal lifespan and promote healthy aging. Here, we show that a botanical extract from Artemisia scoparia (SCO), which promotes fat storage and metabolic resiliency in mice, extends the lifespan of the nematode Caenorhabditis elegans by up to 40%. Notably, this lifespan extension depends significantly on SCO’s effects on fat; SCO-treated worms exhibit heightened levels of unsaturated fat, and inhibiting Δ9 desaturases, which oversee biosynthesis of monounsaturated fatty acids, prevents SCO-dependent fat accumulation and lifespan extension. At an upstream signaling level, SCO prompts changes to C. elegans fat regulation by stimulating nuclear translocation of transcription factor DAF-16/FOXO, an event that requires AMP-activated protein kinase under this condition. Importantly, animals treated with SCO are not only long lived but also show improved stress resistance in late adulthood, suggesting that this fat-promoting intervention may enhance some aspects of physiological health in older age. These findings identify SCO as a natural product that can modify fat regulation for longevity benefit and add to growing evidence indicating that elevated fat can be pro-longevity in some circumstances.

A FAT-PROMOTING BOTANICAL EXTRACT ARTEMISIA SCOPARIA EXERTS GEROPROTECTION IN C. ELEGANS

Abstract Like other biological processes, aging is not random but subject to molecular control. Natural products that modify core metabolic parameters, including fat content, may provide entry points to extend animal lifespan and promote healthy aging. Here, we show that a botanical extract from Artemisia scoparia (SCO), which promotes fat storage and metabolic resiliency in mice, extends the lifespan of the nematode Caenorhabditis elegans by up to 40%. Notably, this lifespan extension depends significantly on SCO’s effects on fat; SCO-treated worms exhibit heightened levels of unsaturated fat, and inhibiting Δ9 desaturases, which oversee biosynthesis of monounsaturated fatty acids, prevents SCO-dependent fat accumulation and lifespan extension. At an upstream signaling level, SCO prompts changes to C. elegans fat regulation by stimulating nuclear translocation of transcription factor DAF-16/FOXO, an event that requires AMP-activated protein kinase under this condition. Importantly, animals treated with SCO are not only long lived but also show improved stress resistance in late adulthood, suggesting that this fat-promoting intervention may enhance some aspects of physiological health in older age. These findings identify SCO as a natural product that can modify fat regulation for longevity benefit and add to growing evidence indicating that elevated fat can be pro-longevity in some circumstances.