• Journal of Life Science
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• v.9 no.5
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• pp.548-555
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• 1999

Long-term effects of Ganoderma lucidum (GL) on memory and oxidative stress of senescence-accelerated mice (SAM) were investigated. Senescence-resistant (R1) and prone (P8) strains of SAM were fed GL diets, premixed with low (20 mg/kg/day, T1) or high (200 mg/kg/day, T2) levels of GL powder for 9 months starting from young (3 months of age) or for 5 months starting from old (7 months of age). After the final feeding at 12 months of age, all animals were subjected to passive avoidance test for the evaluation of memory function. In addition, the changes in hepatic thiobarbituric acid-reactive substance (TBARS) and glutathione were analyzed. SAMP8 fed GL diets from old age (7 months) exhibited the improvement of memory, although GL rather inhibited the memory function of both SAMR1 and SAMP8 mice fed diets from young (3 months of age). Hepatic TBARS contents were decreased in SAMP8 fed high GL diet for 9 months and in SAMR1 fed low GL diet for 5 months. Hepatic glutathione content was also remarkably increased in SAMR1 following both feeding periods, and less extent in SAMP8 fed diet for 5 months of age. Taken together, it is proposed that GL extracts may play an anti-aging role through antioxidant action, and thereby may improve the senescence-related memory dysfunction.

• Plant Biotechnology Reports
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• v.3 no.4
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• pp.285-292
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• 2009

Zoysiagrass (Zoysia japonica) is one of the important turfgrass species. Extending green period of zoysiagrass via delaying leaf senescence will make this species have more potential in the turfgrass industry. In this study, we found that zoysiagrass seedlings treated with $GA_3$ could delay the leaf senescence induced by darkness. To study expression of genes responsive to staying green in zoysiagrass, suppression subtractive hybridization (SSH) was used to identify differentially expressed genes between non-$non-GA_3-treated$ and $GA_3-treated$ seedlings subjected to darkness. A total of 307 ESTs were generated, of which 226 ESTs clustered into 54 contigs and 81 were singlets. Differentially expressed genes selected by subtractions were classified into six categories according to their putative functions generated by BLAST analysis. Expression of five selected genes, Met, SAM, V-ATPase, Cry (Cryptochrome gene), and An (diphthine synthase gene) were examined by RT-PCR and Real-time PCR. Both RT-PCR and Real-time PCR results demonstrated that the differential expressions of these genes were attributable to delaying senescence by exogenously applied gibberellic acid. This is the first genome-wide study of senescence in a species of turfgrass.

• Journal of the Korean Society of Tobacco Science
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• v.18 no.2
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• pp.138-144
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• 1996

This experiment was conducted to obtain the basic information on the morphological and physiological changes in tobacco leaf during the growth period by measuring the changes of chlorophyll, sugar, lipid and mineral contents in tobacco plant. Leaf length and width have been fully developed at 25 days after leaf emergence. Dry weight was rapidly increased between 10 and 15 days after leaf emergence and reached the highest at 30 days. Crude lipid content, palmitic acid, and the major saturated fatty acid were increased with progressing senescence, while unsaturated fatty acid including linolenic acid was decreased as the senescence was advanced. The total nitrogen content showed the highest value at IS days after leaf emergence. On the other hand, the total sugar content showed the highest value at 45 days after leaf emergence and glucose, fructose and sucrose were decreased with leaf development and increased at the end of senescence. The content of chlorophyll showed the highest value at 15 days after leaf emergence and began to decrease at 30 days after leaf emergence. The contents of p, Cu, Zn, and Fe in tobacco leaves were decreased by the end of senescence after leaf emergence but those of Ca, Mg, and Mn in leaves were increased. Key words : Nicotiana tabacum chlorophyll, fatty acid, senescence.

• Korean Journal of Plant Resources
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• v.27 no.6
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• pp.601-609
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• 2014

In this study, the effect of plant extract on the senescence action and cell survival rate in two types of cells, in which aging was derived by adriamycin, was analyzed to find the materials for suppressing cell senescence from natural resources. The results are as follows. For human umbilical vein endothelial cells (HUVECs), the fruit of Physalis angulata L. and the aerial part of Synurus deltoides (Aiton) Nakai showed excellent cell-senescence inhibition activities in a treatment concentration-dependent manner, demonstrating the high possibility for utilization as a material for prevention and treatment for vascular diseases. The water extract from the root of Polygonatum odoratum var. pluriflorum for variegatum Y. N. Lee showed potent cell-senescence inhibitory effect for human dermal fibroblasts (HDFs). Thus it is considered that the additional study on the plant needs for elucidating the possible utilization as material for skin health improvement.

• Molecules and Cells
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• v.42 no.3
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• pp.210-217
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• 2019

The maintenance of mitochondrial function is closely linked to the control of senescence. In our previous study, we uncovered a novel mechanism in which senescence amelioration in normal aging cells is mediated by the recovered mitochondrial function upon Ataxia telangiectasia mutated (ATM) inhibition. However, it remains elusive whether this mechanism is also applicable to senescence amelioration in accelerated aging cells. In this study, we examined the role of ATM inhibition on mitochondrial function in Hutchinson-Gilford progeria syndrome (HGPS) and Werner syndrome (WS) cells. We found that ATM inhibition induced mitochondrial functional recovery accompanied by metabolic reprogramming, which has been known to be a prerequisite for senescence alleviation in normal aging cells. Indeed, the induced mitochondrial metabolic reprogramming was coupled with senescence amelioration in accelerated aging cells. Furthermore, the therapeutic effect via ATM inhibition was observed in HGPS as evidenced by reduced progerin accumulation with concomitant decrease of abnormal nuclear morphology. Taken together, our data indicate that the mitochondrial functional recovery by ATM inhibition might represent a promising strategy to ameliorate the accelerated aging phenotypes and to treat age-related disease.

• Proceedings of the Korean Society of Crop Science Conference
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• 2017.06a
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• pp.201-201
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• 2017

Delayed stem senescence of soybean is a phenomenon of retarded leaf and stem yellowing, where plants maintain a high stem water content and remain chlorophyll in leaf and stem at maturity stage. This phenomenon was one of the most important physiological disease in Japanese soybean cultivation. The occurrence of delayed stem senescence was affected by sowing time. And the most of Japanese field, soybean seeds were sowed in June. June is the rainy season in Japan, and the soil water content of field become higher in this season. In this study, the effects of late sowing (July sowing) on the yield and the occurrence of delayed stem senescence in soybean cultivars Enrei, Tachinagaha and Ayakogane were examined from 2013 to 2015, in the experimental farm at Nihon University (Fujisawa-city, Kanagawa, Japan). The seeds of all cultivars were sowed in June (June-normal density plot) or July (July-normal density plot, July-high density plot and July-super high density plot) in field experiment. The pot experiments were carried out in 2014. In all cultivars, the yield of July-high density plot and July-super high density were higher than that of June normal density plot. And the yield of June-normal density plot was the same as that of July-normal density plot. In all cultivars, the occurrence of delayed stem senescence was increased by seeding in June sowing. And in July sowing plots, no significance difference in the occurrence of delayed stem senescence was observed among density plots. One of reason about the increasing the occurrence of delayed stem senescence in June-normal plot was the increasing of the damaged seeds by bean bugs. Add one of reason about the decreasing of the occurrence of delayed stem senescence of July plots was the decreasing of the amount of cytokinin supplied from root to top and water stress after the flowering time was improved compared with the June plot. In conclusion, the yield of Enrei, Tachinagaha and Ayakogane were not changed by changing the sowing time from June to July. In all cultivars, the occurrence of delayed stem senescence were decreasing by seeding in July.

• Journal of Ginseng Research
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• v.45 no.2
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• pp.344-353
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• 2021

Background: Korean Red ginseng extract (KRGE) has beneficial effects on the cardiovascular system by improving endothelial cell function. However, its pharmacological effect on endothelial cell senescence has not been clearly elucidated. Therefore, we examined the effect and molecular mechanism of KRGE on the senescence of human umbilical vein endothelial cells (HUVECs). Methods: HUVECs were grown in normal or KRGE-supplemented medium. Furthermore, they were transfected with heme oxygenase-1 (HO-1) gene or treated with its inhibitor, a NF-κB inhibitor, and a miR-155-5p mimic or inhibitor. Senescence-associated characteristics of endothelial cells were determined by biochemical and immunohistochemical analyses. Results: Treatment of HUVECs with KRGE resulted in delayed onset and progression of senescence-associated characteristics, such as increased lysosomal acidic β-galactosidase and decreased telomerase activity, angiogenic dysfunction, and abnormal cell morphology. KRGE preserved the levels of anti-senescent factors, such as eNOS-derived NO, MnSOD, and cyclins D and A: however, it decreased the levels of senescence-promoting factors, such as ROS, activated NF-κB, endothelial cell inflammation, and p21 expression. The beneficial effects of KRGE were due to the induction of HO-1 and the inhibition of NF-κB-dependent biogenesis of miR-155-5p that led to the downregulation of eNOS. Moreover, treatment with inhibitors of HO-1, NF-κB, and miR-155-5p abolished the anti-senescence effects of KRGE. Conclusion: KRGE delayed or prevented HUVEC senescence through a signaling cascade involving the induction of HO-1, the inhibition of NF-κB-dependent miR-155-5p biogenesis, and the maintenance of the eNOS/NO axis activity, suggesting that it may protect against vascular diseases associated with endothelial senescence.

• BMB Reports
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• v.47 no.10
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• pp.575-580
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• 2014

In this study, we investigate whether arsenite-induced DNA damage leads to p53-dependent premature senescence using human glioblastoma cells with p53-wild type (U87MG-neo) and p53 deficient (U87MG-E6). A dose dependent relationship between arsenite and reduced cell growth is demonstrated, as well as induced ${\gamma}H2AX$ foci formation in both U87MG-neo and U87MG-E6 cells at low concentrations of arsenite. Senescence was induced by arsenite with senescence-associated ${\beta}$-galactosidase staining. Dimethyl- and trimethyl-lysine 9 of histone H3 (H3DMK9 and H3TMK9) foci formation was accompanied by p21 accumulation only in U87MG-neo but not in U87MG-E6 cells. This suggests that arsenite induces premature senescence as a result of DNA damage with heterochromatin forming through a p53/p21 dependent pathway. p21 and p53 siRNA consistently decreased H3TMK9 foci formation in U87M G-neo but not in U87MG-E6 cells after arsenite treatment. Taken together, arsenite reduces cell growth independently of p53 and induces premature senescence via p53/p21-dependent pathway following DNA damage.

• BMB Reports
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• v.50 no.10
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• pp.528-533
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• 2017

Peroxiredoxin I (Prx I) plays an important role as a reactive oxygen species (ROS) scavenger in protecting and maintaining cellular homeostasis; however, the underlying mechanisms are not well understood. Here, we identified a critical role of Prx I in protecting cells against ROS-mediated cellular senescence by suppression of $p16^{INK4a}$ expression. Compared to wild-type mouse embryonic fibroblasts (WT-MEFs), Prx $I^{-/-}$ MEFs exhibited senescence-associated phenotypes. Moreover, the aged Prx $I^{-/-}$ mice showed an increased number of cells with senescence associated-${\beta}$-galactosidase (SA-${\beta}$-gal) activity in a variety of tissues. Increased ROS levels and SA-${\beta}$-gal activity, and reduction of chemical antioxidant in Prx $I^{-/-}$ MEF further supported an essential role of Prx I peroxidase activity in cellular senescence that is mediated by oxidative stress. The up-regulation of $p16^{INK4a}$ expression in Prx $I^{-/-}$ and suppression by overexpression of Prx I indicate that Prx I possibly modulate cellular senescence through $ROS/p16^{INK4a}$ pathway.

• Molecules and Cells
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• v.37 no.8
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• pp.620-627
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• 2014

We have previously shown that microRNAs (miRNAs) miR-760, miR-186, miR-337-3p, and miR-216b stimulate premature senescence through protein kinase CK2 (CK2) downregulation in human colon cancer cells. Here, we examined whether these four miRNAs are involved in the replicative senescence of human lung fibroblast IMR-90 cells. miR-760 and miR-186 were significantly upregulated in replicatively senescent IMR-90 cells, and their joint action with both miR-337-3p and miR-216b was necessary for efficient downregulation of the ${\alpha}$ subunit of CK2 ($CK2{\alpha}$) in IMR-90 cells. A mutation in any of the four miRNA-binding sequences within the $CK2{\alpha}3^{\prime}$-untranslated region (UTR) indicated that all four miRNAs should simultaneously bind to the target sites for $CK2{\alpha}$ downregulation. The four miRNAs increased senescence-associated ${\beta}$-galactosidase (SA-${\beta}$-gal) staining, p53 and $p21^{Cip1/WAF1}$ expression, and reactive oxygen species (ROS) production in proliferating IMR-90 cells. $CK2{\alpha}$ overexpression almost abolished this event. Taken together, the present results suggest that the upregulation of miR-760 and miR-186 is associated with replicative senescence in human lung fibroblast cells, and their cooperative action with miR-337-3p and miR-216b may induce replicative senescence through $CK2{\alpha}$ downregulation-dependent ROS generation.