• 한국융합학회논문지
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• 제12권8호
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• pp.309-315
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• 2021

소나무 수피에서 추출한 Pycnogenol은 항균활성과 항산화 효과가 뛰어난 성분으로 항염, 혈압조절기능, 면역조절, 암세포 성장억제 등 다양한 의학적 효능과 함께 천연 소염제로 응용되고 있지만 화장품 관련 연구는 미비한 상황이므로 본 연구는 Pycnogenol 성분이 피부에 미치는 효과를 임상학적 접근한 연구이다. Pycnogenol 성분 첨가, 무첨가한 화장품을 각 각 10명의 임상자가 6주간 사용하게 한 후 피부 상태 변화를 살펴보았으며 모공의 감소, 눈가주름의 감소, 처진모공의 개수와 각도의 감소, 색소침착이 감소하는 효과가 있었다. 그러므로 Pycnogenol 성분을 함유한 화장품은 노화피부에서 나타나는 피부 문제를 개선하는 효과가 있다.

• 한국식품위생안전성학회지
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• 제23권1호
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• pp.68-72
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• 2008

Antimicrobial stability of grape seed extract ($ActiVin^{TM}$), pine bark extract ($Pycnogenol^{(R)}$), and oleoresin rosemary ($Herbalox^{(R)}$) on the growth of Aeromonas hydrophila was investigated in cooked ground beef. When compared to the control, the populations of A. hydrophila were most effectively reduced by 4.06 log CFU/g for 1% $Pycnogenol^{(R)}$ added after cooking at 10 days of refrigerated storage, followed by 3.06 log CFU/g for 1% $Pycnogenol^{(R)}$ added before cooking and 1.36 log CFU/g for $ActiVin^{TM}$. Bacteriostatic and bactericidal activities were observed for $Pycnogenol^{(R)}$ added before and after cooking, respectively. $Pycnogenol^{(R)}$ consists of heat-labile and heat-stable compounds. $ActiVin^{TM}$ and $Pycnogenol^{(R)}$ could be considered for use as multifunctional preservatives in meat and meat products.

• 디지털융복합연구
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• 제20권3호
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• pp.487-495
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• 2022

프랑스 해송 껍질추출물인 피크노제놀은 항염, 항혈전, 혈압조절 효과, 면역조절 효과 등의 다양한 의학적 연구결과를 바탕으로 건강식품 소재로 활용되고 있으며 최근 화장품 소재로도 활용되고 있지만 피부 유효성에 관한 임상연구는 미미한 실정이다. 본 연구는 피크노제놀 성분을 화장품에 적용하여 10~20대 여드름 피부에 미치는 효과를 피부임상학적으로 접근하여 그 유효성을 연구하고자 하였으며, 피크노제놀 0.2% 첨가 화장품과 무첨가 화장품을 각 그룹별 11명의 임상자가 참여하여 6주 동안 사용하게 한 후 여드름 피부 상태변화를 살펴보았다. 피크노제놀을 함유한 화장품을 사용한 그룹에서 여드름 균(P-Acnes)의 대사산물인 포비린 지수가 감소하였으며 홍조와 색소침착 지수가 감소하는 효과가 있었다. 본 연구를 통하여 피크노제놀 성분이 여드름 균을 감소시키고 여드름 피부에 나타나는 홍조와 색소침착 증상을 완화하는 효과가 있는 화장품 소재인 것을 확인하였다.

• 대한화장품학회지
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• 제28권1호
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• pp.58-70
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• 2002

Retinol에 대한 합성물질과 천연물질의 항산화력을 비교하였다. 수용성 합성 항산화제 tertiary butylhydroquulone(TBHQ)와 수용성 천연 항산화제 $\alpha$-glycosyl rutin($\alpha$-G rutin), licorice, pycnogenol, 지용성 합성 항산화제 butylated hydroxytoluene(BHT)와 지용성 천연 항산화제 $\alpha$-lipoic acid, ferulic acid, natural concentrated tocopherol(no-tocopherol)를 각각 0.0, 0.0l, 0.02, 0.05, 0.l0wt% 사용하여 리포좀에 봉입하였으며, 4$^{\circ}C$, $25^{\circ}C$, 5$0^{\circ}C$에서 8주 동안 retinol의 잔류량 변화를 HPLC로 측정하였다. 사용된 항산화제는 retinol에 대하여 모두 산화억제효과를 나타내었으며, 수용성 항산화제는 licorice>pycnogenol>TBHQ>$\alpha$-G rutin 순으로, 지용성 항산화제는 $\alpha$-lipoic acid>BHT>no-tocopherol>ferulic acid 순으로 나타났다. 또한 $\alpha$-lipolc acid, BHT, licorice, pycnogenol을 흔합하여 retinol에 대한 항산화력 상승효과를 알아보았다. $\alpha$-lipoic acid와 BHT를 혼합하여 사용하였을 때 retinol에 대한 항산화력이 가장 좋게 나타났다.

• 한국식품영양학회지
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• 제24권3호
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• pp.422-433
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• 2011

The objective of this study was to evaluate their effects as the meat antioxidant and on the antioxidant enzymes like superoxide dismutase(SOD) and catalase during the refrigeration storage of ground beef, respectively. Ground beef loin was treated by three natural antioxidants(pycnogenol, catechin, ${\alpha}$-tocopherol) and the synthetic antioxidant(BHT) at the level of 0.01%(w/w) of total fat. Samples were refrigerated at $4{\sim}6^{\circ}C$ for 3, 5, 7 and 10 days to evaluate the color and the pH as the quality parameters, TBA value and fatty acid composition as the parameters of lipid peroxidation, and the activities of SOD and catalase. This study showed that catechin and pycnogenol were excellent in terms of meat color, pH and delaying lipid peroxidation and also maintained the activity of in vivo SOD and catalase better than ${\alpha}$-tocopherol and BHT. These results suggested that the duration of the refrigeration of ground beef may be prolonged up to 10 days in catechin and pycnogenol treated ones in terms of the lipid peroxidation, but 5 days of refrigeration will be more adequate if considering the microbial safety as food, too.

• Journal of Microbiology
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• 제41권1호
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• pp.28-33
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• 2003

Pycnogenol (PYC) is believed to have potential as a therapeutic agent against free radical-mediated oxidative stress. It is important, therefore, to understand the interactions between PYC and cellular defenses against oxidative stress. Toward this end, we analyzed the survival rates on the gene expression responses of E. coli sod katG mutants to PYC after pre-treatment of PQ or H$_2$O$_2$-mediated stress under aerobic conditions. We identified SOD induced by PYC, but not HP1 in sod hate mutants. A striking result was the PYC induction of SOD with antioxidant property in single katG mutant cells, particularly MnSOD and CuZnSOD. These inductions were further increased with oxidative stress, while HP1 was not induced in these conditions. The effects of pycnogenol treatment on these cells depend in part on its concentration on the stress response. Protective effects of PYC exposure which affected gene expression in cells were consistent with cell survival rates. Our results demonstrate that pycnogenol may alter the stress response gene expression in a specific manner such as SOXRS because PYC induction of single mutant only worked under increased PQ stress. All together our data indicate that SOD activity is essential for the cellular defense against PQ-mediated oxidative stress, suggesting that PYC may not be effective as an antioxidant in only oxidative stress conditions. On the other hand, it was expected that PYC may play a role as a pro-oxidant and if it is available for use, it should be evaluated carefully.

• Nutrition Research and Practice
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• 제8권5호
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• pp.533-538
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• 2014

BACKGROUND/OBJECTIVES: We investigated the effect of Pycnogenol (Pyc) on survival and immune dysfunction of C57BL/6 mice induced by low micronutrient supplementation. MATERIALS/METHODS: Female C57/BL/6 mice were fed a diet containing 7.5% of the recommended amount of micronutrients for a period of 12 wks (immunological assay) and 18 wks (survival test). For immunological assay, lymphocyte proliferation, cytokine regulation, and hepatic oxidative status were determined. RESLUTS: Pyc supplementation with 50 and $100mg{\cdot}kg^{-1}{\cdot}bw{\cdot}d^{-1}$ resulted in partial extension of the median survival time. Pyc supplementation led to increased T and B cell response against mitogens and recovery of an abnormal shift of cytokine pattern designated by the decreased secretion of Th1 cytokine and increased secretion of Th2 cytokine. Hepatic vitamin E level was significantly decreased by micronutrient deficiency, in accordance with increased hepatic lipid peroxidation level. However, Pyc supplementation resulted in a dose-dependent reduction of hepatic lipid peroxidation, which may result from restoration of hepatic vitamin E level. CONCLUSION: Findings of this study suggest that Pyc supplementation ameliorates premature death by restoring immune dysfunction, such as increasing lymphocyte proliferation and regulation of cytokine release from helper T cells, which may result from the antioxidative ability of Pyc.

• Preventive Nutrition and Food Science
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• 제10권2호
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• pp.161-166
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• 2005

We investigated the effect of pycnogenol (PYC) supplementation on retarding the immune dysfunction of CS7BL/6 mice after murine AIDS (MAIDS) development. Dysfunction of T and B cell mitogenesis from primary cultured splenocytes has been observed with retrovirus infection and PYC supplementation partially recovered the dysfunction of T and B cells. There was an abnormal shift of cytokine pattern with retrovirns infection, which was designated by the decreased secretion of Th1 cytokines and increased secretion of Th2 cytokines. PYC supplementation increased IL-2 and $IFN-\gamma$ secretion and decreased IL-4, IL-6, and $TNF-\alpha$ secretion, but it was not sufficient enough to maintain the normal level of these cytokines. Hepatic vitamin E level was significantly decreased by retrovirns infection, in accordance with increased hepatic lipid peroxidation level, whereas PYC supplementation normalized the hepatic level of vitamin E and lipid peroxidation. This study suggests that PYC supplementation may partially help retard the incidence of symptoms during MAIDS.

• Applied Microscopy
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• 제43권4호
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• pp.133-139
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• 2013

This study was carried out to investigate the effects of pycnogenol (PYC) on the cutaneous wound healing of the mice. The wounds were extracted on days 1, 3, 5, and 7 post-injury for histomorphometrical analysis including wound area, infiltrating inflammatory cells, wound contracture including collagen deposition. As the result, the wound area of PYC-treated group was larger than the control group on days 1 to 7. Inflammatory cells in the PYC-treated wounds were decreased at day 1 compared to the control wound tissue. From day 3 to 7, there was no significant difference between the control and the PYC-treated skin wounds. Though the degree of contraction in the PYC-treated group was lower than that of the control group from days 1 to 5, but appeared significantly higher on day 7. Compared to the control group, collagen accumulation in the PYC-treated group was higher than that of the control group from days 5 to 7. From this result, it may support the possibility that PYC would be useful agent for early inflammatory response and matrix remodeling phase of the skin wounds.

• Laboraroty Animal Research
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• 제33권2호
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• pp.76-83
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• 2017

Chronic obstructive pulmonary diseases (COPD) is an important disease featured as intense inflammation, protease imbalance, and air flow limitation and mainly induced by cigarette smoke (CS). In present study, we explored the effects of $Pycnogenol^{(R)}$ (PYC, pine bark extract) on pulmonary fibrosis caused by CS+lipopolysaccharide (LPS) exposure. Mice were treated with LPS intranasally on day 12 and 26, followed by CS exposure for 1 h/day (8 cigarettes per day) for 4 weeks. One hour before CS exposure, 10 and 20 mg/kg of PYC were administered by oral gavage for 4 weeks. PYC effectively reduced the number of inflammatory cells and proinflammatory mediators caused by CS+LPS exposure in bronchoalveolar lavage fluid. PYC inhibited the collagen deposition on lung tissue caused by CS+LPS exposure, as evidenced by Masson's trichrome stain. Furthermore, transforming growth $factor-{\beta}1$ ($TGF-{\beta}1$) expression and Smad family member 2/3 (Smad 2/3) phosphorylation were effectively suppressed by PYC treatment. PYC markedly reduced the collagen deposition caused by CS+LPS exposure, which was closely involved in $TGF-{\beta}1$/Smad 2/3 signaling, which is associated with pulmonary fibrotic change. These findings suggest that treatment with PYC could be a therapeutic strategy for controlling COPD progression.