• 한국식품영양학회지
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• 제29권6호
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• pp.923-929
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• 2016

The purpose of this study was to evaluate the protective effect of $PineXol^{(R)}$ on $H_2O_2$-induced cell death in SK-N-MC cells, and in early stage focal ischemia rodent model. SK-N-MC cells were pre-treated with $200{\mu}M$ $H_2O_2$ or various concentrations of $PineXol^{(R)}$ (10, 30, and 50 pg/mL) for 24 h, and then exposed to $H_2O_2$ for 3 h. Cell death was assessed by the CCK-8 assay, reactive oxygen species (ROS) assay, and lactate and dehydrogenase (LDH) release assay. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) expressions were also analyzed by western blotting. Focal ischemia rodent model was used as the in vivo model, and different concentrations of $PineXol^{(R)}$ (1, 10, and 100 mg/kg) were administered. One week after administration, reduction of infarct volume was analyzed by TTC staining. Cell viability of $H_2O_2$-treated SK-N-MC cells significantly increased by pre-treatment of $PineXol^{(R)}$ (p<0.05). $PineXol^{(R)}$ pre-treatment also induced significant decrease of ROS and LDH expressions. However, $PineXol^{(R)}$ did not affect the infarct volume. These results suggest that $PineXol^{(R)}$ has significant neuroprotective effect in vitro, but statistical significance was not confirmed in the in vivo focal ischemia model.

• 한국식품영양학회지
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• 제30권6호
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• pp.1279-1285
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• 2017

$Amyloid-{\beta}$ protein ($A{\beta}$) is known to increase free radical production in neuronal cells, leading to cell death by oxidative stress. The purpose of this study was to evaluate the protective effects of $PineXol^{(R)}$ on $A{\beta}_{25-35}$ induced neuronal cell death. Rat pheochromocytoma (PC-12) cells were pre-treated with $100{\mu}g/mL$ of $PineXol^{(R)}$ for 2 h. The cells were exposed to single dose of $30{\mu}M$ $A{\beta}_{25-35}$ for 24 h. Cell death was assessed by a cell count kit-8 (CCK-8) assay, lactate and dehydrogenase (LDH) release assay. An Apoptotic process was analyzed by a protein expression of the Bcl-2 family using western blotting. Cell viability increased in PC-12 cells treated with both $A{\beta}_{25-35}$ and $PineXol^{(R)}$, compared to the control group. $PineXol^{(R)}$ induced a decrease of the Bcl-2 protein expression (p<0.05), while Bax and Sod1 increased (p<0.05), indicating attenuation of $A{\beta}_{25-35}$ induced apoptosis. These results suggest that $PineXol^{(R)}$ may be a good candidate for the prevention of Alzheimer's disease(AD).

• 한국식품과학회지
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• 제45권1호
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• pp.97-103
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• 2013

소나무 껍질 추출물은 높은 항산화 활성을 가지는 것으로 많은 연구 결과를 통해 조사되어 왔으며, 해외에서는 이미 프랑스 해송 껍질 추출물인 피크노제놀(pycnogenol)에 관한 연구가 많이 이루어진 반면, 우리나라 적송 껍질 추출물(PineXol$^{(R)}$)의 생리활성 효과에 대해서는 아직 연구가 많이 이루어지지 못했다. 따라서 본 연구에서는 우리나라 적송 껍질 추출물인 PineXol$^{(R)}$의 항산화 활성 및 anti-adipogenic 활성을 평가하였다. PineXol$^{(R)}$의 총 페놀 및 플라보노이드 함량은 각각 $717.40{\pm}6.86$ GAE mg/g 및 $54.44{\pm}0.01$ RE mg/g으로 측정되었다. 또한 다양한 항산화 평가 모델(DPPH, ABTS, FRAP, 환원력)을 통하여 PineXol$^{(R)}$의 항산화 활성을 측정한 결과, 농도가 증가함에 따라 항산화 활성이 유의적으로 증가하였으며, 대조군으로 사용한 동일한 농도의 아스코르빈산과 유사한 항산화 활성을 나타내었다. 또한 ORAC value는 $693.97{\pm}14.13{\mu}M$ TE/g으로 측정되었고, 1.0 mg/mL의 농도에서 55.39%의 아질산염소거능을 나타내었다. PineXol$^{(R)}$은 3T3-L1 지방세포에서 세포독성을 나타내지 않았으며, 분화과정동안 50, 100 및 200 ${\mu}g/mL$의 농도에서의 지방축적량은 각각 $66.85{\pm}5.87$, $44.59{\pm}5.71$ 및 $20.85{\pm}2.78%$의 농도가 증가함에 따른 유의적인 억제효과를 보였다. 이상의 결과로부터, PineXol$^{(R)}$은 항산화 활성 및 지방세포 분화억제 효능을 갖으며, 천연물 유래 항산화제로써 활용 가능성이 높은 것으로 기대된다.

• Journal of Microbiology and Biotechnology
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• 제27권4호
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• pp.660-667
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• 2017

PineXol, extracted from Korean red pine bark, has beneficial effects, such as antioxidant, antiinflammatory, and antilipogenic activities in vitro. We tested the hypothesis that PineXol supplementation could have anti-obesity effects on mice fed a high-fat diet (HFD). Four-week-old male C57BL/6 mice were fed normal chow (18% kcal from fat) or a HFD (60% kcal from fat). HFD-fed animals were also subjected to PineXol treatment at a dose of 10 or 50 mg/kg body weight (BW) (PX10 or PX50, respectively) body weight. The body weight and body fat mass in the PX50 group were statistically lower than those in the HFD group (p < 0.05 and p < 0.001, respectively). The concentration of hepatic triglycerides, total cholesterol, and low-density lipoprotein cholesterol were reduced in the PX50 group compared with the HFD group (p < 0.01). Acetyl CoA carboxylase (p < 0.01), elongase of very long chain fatty acids 6 (p < 0.01), stearoyl CoA desaturase 1 (p < 0.05), microsomal triglyceride transfer protein (p < 0.01), and sterol regulatory element-binding protein 1 (p < 0.05) were significantly decreased in the PX50 group compared with that in the HFD group. In white adipose tissue, CCAAT-enhancer-binding protein alpha (p < 0.05), peroxisome proliferator-activated receptor gamma (p < 0.001), and perilipin (p < 0.01) were decreased in the PX50 group compared with those in the HFD group. Therefore, the current study implies the potential of PineXol for the prevention and/or amelioration of obesity, in part by inhibition of both hepatic lipid synthesis and adipogenesis in white adipose tissue.

• 생약학회지
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• 제47권3호
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• pp.246-250
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• 2016

Pinus densiflora contained diverse phenol compounds like flavonoid, phenylpropanoid and tannin. PineXol$^{(R)}$ is nutraceutical preparation which was treated from bark of Pinus densiflora. Validation and contents determination of taxifolin, (+)-catechin and procyanidion B1 for the preparation of Pinus densiflora (PineXol$^{(R)}$) were confirmed using High-Performance Liquid Chromatography (HPLC). As a result, content of taxifolin, (+)-catechin and procyanidin B1 were, respectively 4.90%, 2.35% and 8.19%. These analysis method and results could be used as important basic data for the preparation of Pinus densiflora.

• Journal of Microbiology and Biotechnology
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• 제27권11호
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• pp.1925-1931
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• 2017

Korean red pine (Pinus densiflora) bark extract, PineXol (PX), was investigated for its potential antioxidant and anti-inflammation effects in vitro. It was hypothesized that PX treatment ($25-150{\mu}g/ml$) would reduce the lipid synthesis in HepG2 hepatocytes as well as lipid accumulation in 3T3-L1 adipocytes. Hepatocytes' intracellular triglycerides and cholesterol were decreased in the PX $150{\mu}g/ml$ treatment group compared with the control (p < 0.05). Consequently, de novo lipogenic proteins (acetyl-CoA carboxylase 1, stearoyl-CoA desaturase 1, elongase of very long chain fatty acids 6, glycerol-3-phosphate acyltransferase 1, and sterol regulatory element-binding protein 1) were significantly decreased in hepatocytes by PX $150{\mu}g/ml$ treatment compared with the control (p < 0.05). In differentiated 3T3-L1 adipocytes, the lipid accumulation was significantly attenuated by all PX treatments (p < 0.01). Regulators of adipogenesis, including CCAAT-enhancer-binding proteins alpha, peroxisome proliferatoractivated receptor gamma, and perilipin, were decreased in PX $100{\mu}g/ml$ treatment compared with the control (p < 0.05). In conclusion, PX might have anti-obesity effects by blocking hepatic lipogenesis and by inhibiting adipogenesis in adipocytes.

• Journal of Microbiology and Biotechnology
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• 제28권5호
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• pp.679-687
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• 2018

Korean red pine (Pinus densiflora) is one of the major Pinus species in Korea. Red pine bark is removed prior to the chipping process in the wood industry and discarded as waste. However, red pine bark contains a considerable amount of naturally occurring phenolics, including flavonoids, and therefore may have a variety of biological effects. In this study, we investigated if Korean red pine bark extract (KRPBE) could protect neuronal PC-12 cells from oxidative stress and inhibit cholinesterase activity. Analysis of reversed-phase high-performance liquid chromatography results revealed four phenolics in KRPBE: vanillin, protocatechuic acid, catechin, and taxifolin. The total phenolic and flavonoid contents of KRPBE were 397.9 mg gallic acid equivalents/g dry weight (DW) and 248.7 mg catechin equivalents/g DW, respectively. The antioxidant capacities of KRPBE measured using ABTS, DPPH, and ORAC assays were 697.3, 521.8, and 2,627.7 mg vitamin C equivalents/g DW, respectively. KRPBE and its identified phenolics protected against $H_2O_2$-induced oxidative cell death in a dose-dependent manner. Acetylcholinesterase and butyrylcholinesterase, which degrade the neurotransmitter acetylcholine to terminate neurotransmission in synaptic clefts, were inhibited by treatment with KRPBE and its identified phenolics. Taken together, these results suggest that KRPBE and its constituent antioxidative phenolics are potent neuroprotective agents that can maintain cell viability under oxidative stress and inhibit cholinesterase activity.