• Journal of Korean Biological Nursing Science
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• 제26권2호
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• pp.99-110
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• 2024

Purpose: This study reviewed the pathophysiological mechanisms of cellular aging caused by psychological stress and aimed to establish a biobehavioral theoretical framework for nursing interventions to promote autonomic balance based on these mechanisms. Methods: A comprehensive literature review was conducted. Results: A review of the literature showed that the stress response increases the secretion of catecholamines and glucocorticoids, resulting in a greater allostatic load. This load induces inflammatory reactions and oxidative stress, shortening telomere length and damaging mitochondrial DNA, which can lead to cellular aging. Based on this mechanism, a biobehavioral theoretical framework for nursing interventions was established. This framework focuses on delaying or inhibiting the cellular aging process by acting on the stress response stage and improving autonomic balance. Conclusion: According to the proposed biobehavioral theoretical framework, stress-relieving nursing interventions may act on the mechanism of cellular aging caused by stress responses. We believe that this framework could expand our understanding of the biobehavioral aspects of stress and would facilitate efforts to use biomarkers to evaluate the effectiveness of stress-related nursing interventions at the cellular level.

• 대한화장품학회:학술대회논문집
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• 대한화장품학회 2003년도 IFSCC Conference Proceeding Book II
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• pp.117-138
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• 2003

Reactive oxygen species are capable of damaging biomolecules such as lipids, proteins, and DNA, which can not only lead to various diseases, but also oxidative damage resulting aging. In our previous study, Cercis chinensis (Leguminosae) showed a potent antioxidant activity. Nineteen compounds were isolated through antioxidant activity-guided fractionation. The C. chinensis extract and some of the constituents exhibited a potent antioxidant activity on the free radicals and lipid peroxidation and a notable protective effect on the t-BuOOH induced oxidative damage. In vivo test of skin damage induced by UVB irradiation, the extract of C. chinensis and a constituent, piceatannol, exhibited a significant protective effect. The life-span of the HEK-N/F cells were extended by 1.21-2.12 fold as a result of the continuous administration of 3 $\mu\textrm{g}$/ml of the C. chinensis extract and the active constituents compared to that of the control. These observations were attributed to the inhibitory effect of the C. chinensis extract and its constituents on the age-dependent shortening of the telomere. Thus, C. chinensis was demonstrated to protect the skin cells against oxidative stress and inhibit thereby the cellular aging, followed by expectation as antiaging cosmetic ingredient.

• BMB Reports
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• 제47권2호
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• pp.51-59
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• 2014

Cellular senescence is a physiological process of irreversible cell-cycle arrest that contributes to various physiological and pathological processes of aging. Whereas replicative senescence is associated with telomere attrition after repeated cell division, stress-induced premature senescence occurs in response to aberrant oncogenic signaling, oxidative stress, and DNA damage which is independent of telomere dysfunction. Recent evidence indicates that cellular senescence provides a barrier to tumorigenesis and is a determinant of the outcome of cancer treatment. However, the senescence-associated secretory phenotype, which contributes to multiple facets of senescent cancer cells, may influence both cancer-inhibitory and cancer-promoting mechanisms of neighboring cells. Conventional treatments, such as chemo- and radiotherapies, preferentially induce premature senescence instead of apoptosis in the appropriate cellular context. In addition, treatment-induced premature senescence could compensate for resistance to apoptosis via alternative signaling pathways. Therefore, we believe that an intensive effort to understand cancer cell senescence could facilitate the development of novel therapeutic strategies for improving the efficacy of anticancer therapies. This review summarizes the current understanding of molecular mechanisms, functions, and clinical applications of cellular senescence for anticancer therapy.

• 한국가금학회지
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• 제36권4호
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• pp.293-300
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• 2009

모체 출산 연령이 늦어짐에 따라 태아의 염색체 이상 빈도는 증가하는 것으로 알려져 있는데, 이는 난자의 노화에 따른 염색체의 비분리 현상의 증가 등이 주된 원인이다. 염색체 양 말단에 존재하는 텔로미어는 염색체의 안정성에 관여하고 세포분열이 진행됨으로써 이의 길이가 짧아져 노화의 지표로 활용되고 있다. 따라서 본 연구는 모체의 노화가 생산 배아에 미치는 영향을 알아보기 위하여 닭의 산란 연령별 배아의 염색체 이상 빈도와 이들의 텔로미어 함량을 분석하였다. 시험 분석은 20주령에서부터 70주령까지의 화이트 레그혼 종을 공시하고 10주 간격으로 생산된 수정란의 초기 배아에 대한 핵형 분석과 양적형광보인법(Q-FISH)을 이용한 모계 및 생산 배아의 텔로미어 함량을 분석하였다. 분석 결과, 초기 배아의 염색체 이상 빈도는 산란 연령에 따른 유의적인 차이가 있었는데, 산란 초기에 상대적으로 높은 염색체 이상 빈도를 보이다가 산란 중기에서 안정된 빈도를 유지하고, 후기부터 다시 이상 빈도가 증가하는 양상을 보여 모체의 노화가 태아의 염색체 이상 빈도에 영향을 미치는 것으로 나타났다. 개체의 텔로미어 함량은 연령이 증가함에 따라 점진적 감소 양상을 나타내는 반면, 모계 연령에 따른 생산 배아들의 텔로미어 함량은 연령 간에 차이가 없는 것으로 나타나 모체의 노화가 수정 배아의 텔로미어 함량에는 영향을 미치지 않는 것으로 보여진다. 이는 배란 후 수정이 된 배아는 초기 발생 과정 중 세포들의 reprograming이 일어나 텔로미어가 복구됨을 의미한다.

• Biotechnology and Bioprocess Engineering:BBE
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• 제6권4호
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• pp.231-236
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• 2001

How much do we know about the biology of aging from cell culture studies Most normal somatic cells have a finite potential to divide due to a process termed cellular or replicative senescence. A growing body evidence suggests that senescence evolved to protect higher eu-karyotes, particularly mammals, from developing cancer, We now know that telomere shortening due to the biochemistry of DNA replication, induces replicative senescence in human cells. How-ever in rodent cells, replicative senescence occurs despite very long telomeres. Recent findings suggest that replicative senescence is just the tip of the iceberg of a more general process termed cellular senescence. It appears that cellular senescence is a response to potentially oncogenic in-sults, including oxidative damage. In young orgainsms, growth arrest by cell senescence sup-presses tumor development, but later in life, due to the accumulation of senescent cells which se-cret factors that can disrupt tissues during aging, cellular senescence promotes tumorigenesis. Therefore, antagonistic pleiotropy may explain, if not in whole the apparently paradoxical effects of cellular senescence, though this still remains an open question.

• Journal of Animal Science and Technology
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• 제66권1호
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• pp.178-203
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• 2024

Constipation, which refers to difficulties in defecation and infrequent bowel movement in emptying the gastrointestinal system that ultimately produces hardened fecal matters, is a health concern in livestock and aging animals. The present study aimed to evaluate the potential effects of dairy-isolated lactic acid bacteria (LAB) strains to alleviate constipation as an alternative therapeutic intervention for constipation treatment in the aging model. Rats were aged via daily subcutaneous injection of D-galactose (600 mg/body weight [kg]), prior to induction of constipation via oral administration of loperamide hydrochloride (5 mg/body weight [kg]). LAB strains (L. fermentum USM 4189 or L. plantarum USM 4187) were administered daily via oral gavage (1 × 10 Log CFU/day) while the control group received sterile saline. Aged rats as shown with shorter telomere lengths exhibited increased fecal bulk and soften fecal upon administration of LAB strains amid constipation as observed using the Bristol Stool Chart, accompanied by a higher fecal moisture content as compared to the control (p < 0.05). Fecal water-soluble metabolite profiles showed a reduced concentration of threonine upon administration of LAB strains compared to the control (p < 0.05). Histopathological analysis also showed that the administration of LAB strains contributed to a higher colonic goblet cell count as compared to the control (p < 0.05). The present study illustrates the potential of dairy-sourced LAB strains as probiotics to ameliorate the adverse effect of constipation amid aging, and as a potential dietary intervention strategy for dairy foods including yogurt and cheese.

• BMB Reports
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• 제52권1호
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• pp.24-34
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• 2019

Sirtuin is an essential factor that delays cellular senescence and extends the organismal lifespan through the regulation of diverse cellular processes. Suppression of cellular senescence by Sirtuin is mainly mediated through delaying the age-related telomere attrition, sustaining genome integrity and promotion of DNA damage repair. In addition, Sirtuin modulates the organismal lifespan by interacting with several lifespan regulating signaling pathways including insulin/IGF-1 signaling pathway, AMP-activated protein kinase, and forkhead box O. Although still controversial, it is suggested that the prolongevity effect of Sirtuin is dependent with the level of and with the tissue expression of Sirtuin. Since Sirtuin is also believed to mediate the prolongevity effect of calorie restriction, activators of Sirtuin have attracted the attention of researchers to develop therapeutics for age-related diseases. Resveratrol, a phytochemical rich in the skin of red grapes and wine, has been actively investigated to activate Sirtuin activity with consequent beneficial effects on aging. This article reviews the evidences and controversies regarding the roles of Sirtuin on cellular senescence and lifespan extension, and summarizes the activators of Sirtuin including Sirtuin-activating compounds and compounds that increase the cellular level of nicotinamide dinucleotide.

• Childhood Kidney Diseases
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• 제12권1호
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• pp.1-10
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• 2008

Nucleic scids transfer the genetic information for serving a central biological purpose. The nucleic acids are polymers of nucleotides and they are mainly ribonucleic acid(RNA) and deoxyribonucleic acid(DNA). The nucleotides are stoichiometrically composed of five-carbon sugars, nitrogeneous bases, and phosphoric acids. The chemistry of nucleic acids and characteristics of different genomes are decribed for further study. Most of DNA genomes tend to be circular including bacterial genomes and eukaryotic mitochondrial DNA. Eukaryotic chromosomes in cells, in contrast, are generally linear. The ends of linear chromosomes are called telomeres. The genomes of different species, such as mammals, plants, invertebrates can be compared with the chromosome ends. The telomeric complex allows cells to distinguish the random DNA breaks and natural chromosomal ends. The very ends of chromosomes cannot be replicated by any ordinary mechanisms. The shortening of telomeric DNA templates in semiconservative replication is occurred with each cell division. The short telomere length is critically related to aging, tumors and dieases.

• BMB Reports
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• 제52권1호
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• pp.35-41
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• 2019

Cellular senescence, a permanent state of cell cycle arrest, is believed to have originally evolved to limit the proliferation of old or damaged cells. However, it has been recently shown that cellular senescence is a physiological and pathological program contributing to embryogenesis, immune response, and wound repair, as well as aging and age-related diseases. Unlike replicative senescence associated with telomere attrition, premature senescence rapidly occurs in response to various intrinsic and extrinsic insults. Thus, cellular senescence has also been considered suppressive mechanism of tumorigenesis. Current studies have revealed that therapy-induced senescence (TIS), a type of senescence caused by traditional cancer therapy, could play a critical role in cancer treatment. In this review, we outline the key features and the molecular pathways of cellular senescence. Better understanding of cellular senescence will provide insights into the development of powerful strategies to control cellular senescence for therapeutic benefit. Lastly, we discuss existing strategies for the induction of cancer cell senescence to improve efficacy of anticancer therapy.

• Molecules and Cells
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• 제40권9호
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• pp.607-612
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• 2017

When mammalian cells and animals face a variety of internal or external stresses, they need to make homeostatic changes so as to cope with various stresses. To this end, mammalian cells are equipped with two critical stress responses, autophagy and cellular senescence. Autophagy and cellular senescence share a number of stimuli including telomere shortening, DNA damage, oncogenic stress and oxidative stress, suggesting their intimate relationship. Autophagy is originally thought to suppress cellular senescence by removing damaged macromolecules or organelles, yet recent studies also indicated that autophagy promotes cellular senescence by facilitating the synthesis of senescence-associated secretory proteins. These seemingly opposite roles of autophagy may reflect a complex picture of autophagic regulation on cellular senescence, including different types of autophagy or a unique spatiotemporal activation of autophagy. Thus, a better understanding of autophagy process will lead us to not only elucidate the conundrum how autophagy plays dual roles in the regulation of cellular senescence but also helps the development of new therapeutic strategies for many human diseases associated with cellular senescence. We address the pro-senescence and anti-senescence roles of autophagy while focusing on the potential mechanistic aspects of this complex relationship between autophagy and cellular senescence.