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Dehydroepiandrosterone (DHEA)와 Pycnogenol의 상승작용이 Old Mice의 면역계에 미치는 영향
박건영,황권택,이정민 대한암예방학회 2005 Journal of cancer prevention Vol.10 No.1
Oxidative stress plays a critical role in aging process, especially immune dysfunction, due to exhaustion of antioxidative molecules. Antioxidant hormone dehydroepiandrosterone (DHEA) and pycnogenol (PYC) were tested to restore immune dysfunction in 16 month old mice and to determine their synergism. T and B cell response to mitogen was partially normalized by combined treatment of DHEA and PYC. It was caused by normalization of Th1/Th2 type cytokine balance. In particular, IL-2, IL-4, and IL-6 was increased by combined treatment of DHEA and PYC whereas IFN-γ and TNF-α were decreased. Hepatic lipid peroxidation was decreased by combined treatment of DHEA and PYC whereas hepatic vitamin E level was maintained as normal. Our study suggests that combined treatment of DHEA and PYC can more effectively prevent immune dysfunction in old mice than DHEA or PYC treatment alone. (Cancer Prev Res 10, 48-53, 2005)
Lee, Jeong-Min,Hwang, Kwon-Taek,Lee, Jong-Moon,Kim, Sun-Ho,Watson, Ronald R.,Park, Kun-Young The Korean Society of Food Science and Nutrition 2004 Preventive Nutrition and Food Science Vol.9 No.1
Side-stream cigarette smoke (SSCS) is a major component of environmental tobacco smoke. The purpose of this study was to investigate the development of lung injury and lipid peroxidation in the lung and liver of immunodeficient (Nude) mice exposed to acute SSCS (a total 5 hours of exposure). The effects of French maritime bark extract (Pycnogeno $l^{ⓡ}$) supplementation of the mice were also determined. SSCS increased pulmonary resistance and lipid peroxidation in these mice. Pycnogeno $l^{ⓡ}$ supplementation increased vitamin E levels in lung and liver. In addition, Pycnogeno $l^{ⓡ}$ attenuated SSCS-mediated lung injury and lipid peroxidation. It appears that the enhanced resistance against SSCS-induced lung injury and lipid peroxidation may be primarily due to the antioxidant property of Pycnogeno $l^{ⓡ}$ in supplemented mice.
Ko, Je-Won,Shin, Na-Rae,Park, Sung-Hyeuk,Kim, Joong-Sun,Cho, Young-Kwon,Kim, Jong-Choon,Shin, In-Sik,Shin, Dong-Ho Korean Association for Laboratory Animal Science 2017 Laboratory Animal Research Vol.33 No.2
<P>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® (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-β1 (TGF-β1) 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-β1/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.</P>
Ko, Je-Won,Park, So-Won,Shin, Na-Rae,Kim, Woong-Il,Kim, Jong-Choon,Shin, In-Sik,Shin, Dong-Ho Korean Association for Laboratory Animal Science 2018 Laboratory Animal Research Vol.34 No.3
<P>Benign prostate hyperplasia (BPH) is a male reproductive disease that has gained increasing importance in recent years. The present study investigated whether Pycnogenol® (PYC), a standardized French maritime pine bark extract, could prevent BPH induced by testosterone propionate (TP) in rats. Male Sprague-Dawley rats were randomly divided into five groups of six rats. One group was used as a normal control rats and the other groups received subcutaneous injections of TP for 4 weeks to induce BPH. In the two treatment groups, PYC (20 or 40 mg/kg) was administered daily for 4 weeks by oral gavage concurrently with the induction of TP. All rats were sacrificed at the scheduled termination time, the prostates were weighed, and histopathologic examinations were conducted. Dihydrotestosterone (DHT) levels in serum and the prostate were measured, and the expression of proliferating cell nuclear antigen (PCNA) and Ki-67 proteins was investigated. BPH-treated animals showed increases in the relative weight of the prostate, higher concentrations of DHT in serum and the prostate, and higher expression of PCNA and Ki-67 in the prostate; in contrast, PYC-treated animals had significant reductions in these factors compared with the BPH animals. These findings indicated that PYC inhibited the development of BPH and that this was closely associated with a reduction in DHT concentration.</P>
( Omid Nikpayam ),( Mohammad Hossein Rouhani ),( Makan Pourmasoumi ),( Neda Roshanravan ),( Ehsan Ghaedi ),( Hamed Mohammadi ) 한국임상영양학회 2018 Clinical Nutrition Research Vol.7 No.2
Pycnogenol is a standardized extract from the bark of the French maritime pine. The aim of the present systematic review and meta-analysis was to clarify the effect of Pycnogenol supplementation on C-reactive protein (CRP) concentration. To identify eligible studies in order to find clinical trials which examined the effect of Pycnogenol supplementation on the level of CRP in adult participants, PubMed, Scopus, and Google Scholar were systematically searched until December 2017. Mean of CRP was collected to estimate the effect size of the supplementation. Potential sources of heterogeneity were explored by subgroup analysis. Five trials including 324 participants were included in this meta-analysis. Pooled effect size showed significant effect of Pycnogenol supplementation on CRP (-1.22 mg/dL, 95% confidence interval, -2.43, -0.003; I<sup>2</sup> = 99%, p<sub>heterogeneity</sub> < 0.001). When the meta-analysis was subgrouped by dose of Pycnogenol, heterogeneity was attenuated in > 150 mg/d category (I<sup>2</sup> = 0.0%, p = 0.42). There was significant difference between-subgroup heterogeneity (p < 0.001). Furthermore, no evidence of publication bias for CRP (p = 0.27, Begg's test and p = 0.62, Egger's test) was seen. Present systematic review and meta-analysis suggested Pycnogenol consumption can decrease the level of CRP and have anti-inflammatory effect. So, Pycnogenol as an anti-inflammatory agent might be a priority in interventions. Further studies with large-scale and better design are needed to confirm this result.
JeongAYoum,YoungGonKim 한국미생물학회 2003 The journal of microbiology Vol.41 No.1
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 H2O2-mediated stress under aerobic conditions. We identified SOD induced by PYC, but not HP1 in sod katG 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.
피크노제놀 성분이 한국 10~20대 여드름 피부에 미치는 영향
김경연 한국디지털정책학회 2022 디지털융복합연구 Vol.20 No.3
Pycnogenol is used as a dietary supplement based on various medical research studies suggesting health benefits. In recent years, it has also been used in cosmetic products, but the clinical research on its dermatologic effects has been insufficient. This study was designed to determine the effectiveness of pycnogenol topically applied to skin of individuals with acne in their teens and twenties. Cosmetics containing 0.2% pycnogenol were applied to a group of 11 clinical subjects for 6 weeks and their skin conditions were assessed. The group that used cosmetics with pycnogenol showed decrease in P-Acnes, acne causing bacteria, phorphyrin index, a metabolite, and the pigmentation and redness index. This study confirms that pycnogenol extract is effective dermatologically in decreasing acne bacteria and reducing redness and pigmentation of skin affected by acne. 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 임상 연구는 미미한 실정이다. 본 연구는 피크노제놀 성분을 화장품에 적용하여 10~20대 여드름 피부에 미치는 효과를 피부 임상학적으로 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.
Youm, Jeong-A,Kim, Young-Gon The Microbiological Society of Korea 2003 The journal of microbiology Vol.41 No.1
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.