• The Korean Journal of Food And Nutrition
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• v.29 no.6
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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.

• The Korean Journal of Food And Nutrition
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• v.30 no.6
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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).

• Korean Journal of Food Science and Technology
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• v.45 no.1
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• pp.97-103
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• 2013

Pine bark extract is made from the bark of Pinus densiflora which naturally contains occurring phytochemicals such as phenolic compounds. PineXol$^{(R)}$ from products of pine bark extract is sold under the brand name. The aim of this study was to evaluate the total phenol, total flavonoids contents and antioxidant activity of the PineXol$^{(R)}$ as well as to assess the lipid accumulation during adipogenesis of 3T3-L1 cells. Our results demonstrate that the total phenolic and flavonoids contents of the PineXol$^{(R)}$ were $717.40{\pm}6.86$ GAE mg/mL and $54.44{\pm}0.01$ RE mg/mL, respectively. The antioxidative activities of the PineXol$^{(R)}$ were significantly increased in a dose dependent manner on DPPH (1,1-Diphenyl-2-picryl hydrazyl) radical scavenging, ABTS (2,2'-Azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) diammonium salt) radical scavenging, FRAP (ferric reducing antioxidant power) activity, reducing power, nitrite radical scavenging activity and ORAC (Oxygen radical absorbance capacity) value. In addition, the PineXol$^{(R)}$ inhibited the adipocyte differentiation of 3T3-L1 preadipocytes. Exposure to 200 ${\mu}g/mL$, PineXol$^{(R)}$ significantly reduced lipid accumulation (~80%) in 3T3-L1 cells compared to control cells.

• Journal of Microbiology and Biotechnology
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• v.27 no.4
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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.

• Korean Journal of Pharmacognosy
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• v.47 no.3
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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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• v.27 no.11
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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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• v.28 no.5
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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.