• Animal cells and systems
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• v.6 no.3
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• pp.253-261
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• 2002

Although cardiac distribution of specific receptors for atrial natriuretic peptide (ANP) was mainly observed in the ventricular endocardium, the modulation of ANP receptors in relation to cardiac development is not defined. The present study was undertaken to investigate ANP receptor modulation in rat during development. In the developmental stages examined (fetus, after postnatal 3-days, 1-, 2-, 3-, 4-, and 8-week-old Sprague Dawley rats) specific ANP binding sites were localized in the right and left ventricular endo-cardia by quantitative in vitro receptor autoradiography using (equation omitted)-rat ANP as labeled ligand. The specific bindings to endocardium were much higher in the right than the left ventricle. The binding affinities of ANP were much higher in the right than the left ventricular endocardium. The difference of these binding affinities among various developmental stages was not observed in the right ventricle, whereas the binding affinity in left ventricle was gradually increased with aging and reached the peak value at 8 weeks. No significant difference in maximal binding capacities of endocardial bindings was observed in the right and left ventricular endocardia during developmental stages. Also, cGMP production via activation of particulate guanylyl cyclase-coupled receptor subtypes in the ventricular membranes was gradually decreased with close relationship to aging. Therefore, the present study show that the endocardial ANP receptor is modulated with close relationship to cardiac development in the left ventricle rather than the right ventricle, and may be involved in regulating myocardial contractility in left heart.

• Proceedings of the Ginseng society Conference
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• 1988.08a
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• pp.11-18
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• 1988

The cosmetic effects of epicutaneous treatment with extracts of Panax ginseng C.A. Meyer have been poorly investigated. The little published data found in cosmetic literature emphasize the activating effects on sagging and wrinkled skin and some favorable activities on dry and/or greasy skin. Earlier observations have shown the excellent skin tolerability of some liposomal ginseng extract preparations. No moisturizing and seboregulatory effects were demonstrated. but eutrophic effects on subjects with aging skin have been observed. The present study concerned the preparation of a special extract derivative obtained by Physical-chemical interactions of ginseng saponins and some phospholipids. which we have called 'fitosoma.' These complexes have been characterized by NMR spectroscopy and electron microscopy. Furthermore, these complexes are new. stable. and water microdispersible, forming liposomal structures in water. The cosmetic activities of these compounds have been examined by means of corneometry and elastometry to study their influence on aging skin. on skin layer hydration. and to determine skin elasticity.

• Journal of Periodontal and Implant Science
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• v.36 no.2
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• pp.361-373
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• 2006

치주질환의 진행이 나이에 의해 영향을 받는다는 사실은 알려져 있으나 노화에 따른 치주조직 세포의 기능적인 변화에 관한 사실은 많이 알려져 있지 않다. 노화에 따른 세포의 노화가 치주질환의 진행에 어떠한 여향을 끼치는가를 아는 것은 중요하다. 염증 상태에서 nitric oxide (NO)는 조직 파괴에 관여하는 인자로 작용하여 치주질환의 진행에 관여하는 것으로 알려져 있다. 따라서 이 연구는 사람의 치은에서 배양된 치은섬유아세포를 이용하여 세포의 노화에 따른 NO와 이의 합성효소인 inducible nitric oxide synthase (iNOS)의 발현을 알아봄으로써 세포의 노화가 치주질환의 진행에 끼치는 영향에 대해 알아보고자 하였다. 10세의 환자와 55세의 환자에서 각각 채취한 치은에서 배양된 세포와 10세의 환자에서 채취한 세포를 계속적인 계대배양을 통해 얻은 실험실 상 노화된 세포를 포함하여 총 3 종류의 치은섬유세포를 실험에 이용하였다. Hot phenol-water extraction을 통해 추출된 Porphyromonas, gingivalis ATCC 33277 lipopolysaccharide (LPS)와 재조합 $IFN-{\gamma}$ 를 세포에 적용시켜 Griess assay를 통해 조건화된 배지에서 NO를 측정하였다. 20세와 55세의 환자에서 채취된 치은 조직과 총 3 종류의 배양된 세포에 NOS-II 항체를 적용시켜 iNOS 단백질 발현을 관찰하였다. Total RNA를 추출하여 RT-PCR를 통해 iNOS mRNA의 발현을 분석하였다. 치은섬유아세포에서 NO는 자발적으로 발생되었고, 이러한 발현은 젊은 세포보다 노화된 세포에서 강하였다. P, gingivalis LPS와 제조합 $IFN-{\gamma}$는 치은섬유아세포에서 NO의 발현을 증가시켰고, 이러한 발현은 젊은 세포보다 노화된 세포에서 강하였다. 면역조직화학 염색에서 iNOS 단백질은 젊은 사람과 노화된 사람의 치은 조직 모두에서 치은섬유아세포와 상피의 기저층 세포와 염증세포에서 발현되었으나 노화에 따른 발현의 차이를 구별할 수는 없었다. 세포의 면역염색에서 iNOS 단백질은 노화된 세포에서 강하게 발현되었고 이러한 발현은 LPS와 $IFN-{\gamma}$ 에 의해 강화되었다. LPS와 $INF-{\gamma}$ 의 조건이 주어지지 않은 상태에서 iNOS mRNA는 젊은 세포에서보다 노화된 세포에서 강하게 발현되었다. 이러한 결과를 통해 세포의 노화가 NO와 iNOS 발현을 증가시킴으로서 치주질환의 진행에 영향을 끼칠 수 있음을 시사하였다.

• International Journal of Oral Biology
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• v.44 no.4
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• pp.173-181
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• 2019

The CC chemokine receptor 5 (CCR5) is a G protein-coupled receptor that regulates chemotaxis and effector functions of immune cells. It also serves as the major co-receptor for the entry of human immunodeficiency virus (HIV). Recently, CCR5 inhibitors have been developed and used for the treatment or prevention of HIV infections. Additionally, it has been identified that CCR5 controls bone homeostasis by regulating osteoclastogenesis and the communication between osteoblasts and osteoclasts. However, the effects of CCR5 inhibition on bone tissue in elderly patients are unknown. This study aimed to examine the bone phenotype of aged CCR5 knockout (KO) mice. Femoral and tibial bones were isolated from 12-month and 18-month old wild-type (WT) and CCR5 KO mice, and microcomputed tomography and histology analyses were performed. Twelve-month-old CCR5 KO mice exhibited a decreased trabecular bone mass and cortical bone thickness in both femoral and tibial bones compared with age-matched WT mice. Eighteen-month-old mice also showed a decreased trabecular bone mass in femurs compared with control WT mice, but not in tibial bones. Unlike in 12-month-old mice, the cortical margin of femurs and tibias in 18-month-old mice were rough, likely because they were aggravated by the deficiency of CCR5. Overall, our data suggest that the deficiency of CCR5 with aging can cause severe bone loss. When CCR5 inhibitors or CCR5 inactivating technologies are used in elderly patients, a preventive strategy for bone loss should be considered.

• Biomolecules & Therapeutics
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• v.25 no.5
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• pp.511-518
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• 2017

Ultraviolet (UV) irradiation is a relevant environment factor to induce cellular senescence and photoaging. Both autophagy- and silent information regulator T1 (SIRT1)-dependent pathways are critical cellular processes of not only maintaining normal cellular functions, but also protecting cellular senescence in skin exposed to UV irradiation. In the present studies, we investigated whether modulation of autophagy induction using a novel synthetic SIRT1 activator, heptasodium hexacarboxymethyl dipeptide-12 (named as Aquatide), suppresses the UVB irradiation-induced skin aging. Treatment with Aquatide directly activates SIRT1 and stimulates autophagy induction in cultured human dermal fibroblasts. Next, we found that Aquatide-mediated activation of SIRT1 increases autophagy induction via deacetylation of forkhead box class O (FOXO) 1. Finally, UVB irradiation-induced cellular senescence measured by $SA-{\beta}-gal$ staining was significantly decreased in cells treated with Aquatide in parallel to occurring SIRT1 activation-dependent autophagy. Together, Aquatide modulates autophagy through SIRT1 activation, contributing to suppression of skin aging caused by UV irradiation.

• Journal of Life Science
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• v.29 no.8
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• pp.888-894
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• 2019

Cartilage diseases, such as rheumatoid arthritis (RA) and osteoarthritis (OA), are associated with the loss of chondrocytes and degradation of articular cartilage. Recent studies revealed that inflammatory reactive oxygen species (ROS) and age-related oxidative stress can affect chondrocyte activity and cartilage homeostasis. We investigated changes in the levels of intracellular antioxidants during cellular senescence of primary chondrocytes from rat articular cartilages. Cellular senescence was induced by serial subculture (passages 0, 2, 4, and 8) of chondrocytes and measured using specific senescence-associated ${\beta}$-galactosidase ($SA-{\beta}-gal$) staining. ROS production increased significantly in the senescent chondrocytes. In addition, total glutathione (GSSG/GSH) and superoxide dismutase (SOD) levels and heme oxygenase-1 (HO-1) expression increased in senescent chondrocytes induced by serial subculture. Analysis of changes in intracellular antioxidant levels in articular cartilage from rats of different ages (5, 25, 40, and 72 wk) revealed that total glutathione levels were highest after 40 wk and slightly decreased after 72 wk as compared with those after 25 wk. SOD and HO-1 expression levels increased in accordance with age. Based on these results, we conclude that intracellular antioxidants may be associated with cartilage protection against excessive oxidative stress in the process of chondrocyte senescence and age-related cartilage degeneration in an animal model.

• Development and Reproduction
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• v.5 no.1
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• pp.59-71
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• 2001

Since the first radioimmunoassay (RIA) was developed in 1970s, many conventional RIAs and non-isotopic immunoassays (NIA) had been developed in which the degree of precision, accuracy, specificity and practicability have progressively increased. Recently ultrasensitive assay method at femtogram to determine testosterone in serum, saliva and feces is required for the study of sexual dysfunctions in male and female, monitoring the psychological stress and conditions, aging process such as menopause and partial androgen deficiency in aging male, the hormonal changes of small experimental animals etc. This review discussed the recentd evelopments of steroid assay methods, based upon the testosterone assay results of authors far 20 years, and the problems associated the assay set-up, the characterizations and applications of the established procedures, and desifls of assay, reliablity criteria, and the practical aspects of assay set-up and application, based upon the data of the authors. The present study demonstrates the general problems methods to be consider in order to set up the highly sensitive assay methods and to increase the assay quality and the necessity of assay quality control program. To improve the assay quality of each laboratory and to compare the assay results in homeland, the national QC programs should be organized.

• The Korean Journal of Food And Nutrition
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• v.28 no.6
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• pp.941-946
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• 2015

Photoaging is the main extrinsic aging factor that is induced due to UVB. Many studies have revealed that application of hyaluronic acid to the skin is effective in healing photoaging. However, the effect of hyaluronic acid through oral administration is unclear. The aim of this research was to investigate the effect on skin photoaging after oral administration of hyaluronic acid. During a ten week study, hyaluronic acid was fed to hairless mice, which were illuminated by UV radiation. After ten weeks, wrinkle indicator and histological changes were determined. Compared with the control group, the sample group had a decrease in wrinkle depth, thickness, and number. Especially, the HA 160 mg/kg group had a similar value of wrinkle depth ($19.44{\pm}0.75{\mu}m$), number ($654.00{\pm}98.34$), and thickness ($1.35{\pm}0.08mm$), when compared with the RA (retinoic acid) group ($19.28{\pm}0.95{\mu}m$, $653.57{\pm}83.54$, and $1.34{\pm}0.07mm$ respectively). Also, the treated group showed improved elastosis and decreased collagen degradation resulting from UV irradiation. Thus, we can conclude that hyaluronic acid has a positive effect in improving skin photoaging induced by UV radiation. Hyaluronic acid therefore has the potential to be an ingredient in skin health function foods.

• Journal of Life Science
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• v.31 no.12
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• pp.1110-1119
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• 2021

The purpose of this study was to investigate whether the inflammatory response in lipopolysaccharide (LPS)-treated RAW 264.7 macrophages could be promoted by particulate matter 2.5 (PM_2.5) stimulation. To this end, the levels of inflammatory parameters, reactive oxygen species (ROS) and inflammation-regulating genes were investigated in RAW 264.7 cells treated with PM_2.5 in the presence or absence of LPS. Our results showed that the production levels of pro-inflammatory mediators (nitric oxide and prostaglandin E₂) and cytokines (interleukin-6 and -1β) were significantly increased by PM_2.5 stimulation in LPS-treated RAW 264.7 cells, which was correlated with increased expression genes involved in their production. In addition, when LPS-treated RAW 264.7 cells were exposed to PM_2.5, nuclear factor-kappaB (NF-κB) expression was further increased in the nucleus, and the expression of inhibitor of NF-κB as well as NF-κB in the cytoplasm was decreased. These results suggest that the co-treatment of PM_2.5 and LPS further increases the activation of the NF-κB signaling pathway compared to each treatment alone, thereby contributing to the promotion of transcriptional activity of inflammatory genes. Furthermore, although the generation of ROS was greatly increased by PM_2.5 in LPS-treated RAW 264.7 cells, the NF-κB inhibitor did not reduce the generation of ROS. In addition, when the generation of ROS was artificially suppressed, the production of inflammatory mediators and the activation of NF-κB were both abolished. Therefore, our results suggest that the increase in the NF-κB-mediated inflammatory response induced by PM_2.5 in LPS-treated RAW 264.7 macrophages was a ROS generation-dependent phenomenon.

• Journal of Ginseng Research
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• v.47 no.4
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• pp.561-571
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• 2023

Background: Escalating evidence shows that ginseng possesses an antiaging potential with cognitive enhancing activity. As mountain cultivated ginseng (MCG) is cultivated without agricultural chemicals, MCG has emerged as a popular herb medicine. However, little is known about the MCG-mediated pharmacological mechanism on brain aging. Methods: As we demonstrated that glutathione peroxidase (GPx) is important for enhancing memory function in the animal model of aging, we investigated the role of MCG as a GPx inducer using GPx-1 (a major type of GPx) knockout (KO) mice. We assessed whether MCG modulates redox and cholinergic parameters, and memory function in aged GPx-1 knockout KOmice. Results: Redox burden of aged GPx-1 KO mice was more evident than that of aged wild-type (WT) mice. Alteration of Nrf2 DNA binding activity appeared to be more evident than that of NFκB DNA binding activity in aged GPx-1 KO mice. Alteration in choline acetyltransferase (ChAT) activity was more evident than that in acetylcholine esterase activity. MCG significantly attenuated reductions in Nrf2 system and ChAT level. MCG significantly enhanced the co-localization of Nrf2-immunoreactivity and ChAT-immunoreactivity in the same cell population. Nrf2 inhibitor brusatol significantly counteracted MCG-mediated up-regulation in ChAT level and ChAT inhibition (by k252a) significantly reduced ERK phosphorylation by MCG, suggesting that MCG might require signal cascade of Nrf2/ChAT/ERK to enhance cognition. Conclusion: GPx-1 depletion might be a prerequisite for cognitive impairment in aged animals. MCG-mediated cognition enhancement might be associated with the activations of Nrf2, ChAT, and ERK signaling cascade.