Pinus koraiensis.  松 子 仁 Sōng zǐ rén   Korean pine, Chinese pinenut  Family: Pinaceae   
PART USED: Nut
Nature: Warm  FLAVOR: Sweet  CHANNELS: Liver, Lung and Large intestine
FUNCTIONS
1. Moisten the lung and lubricate the intestine.[1]
INDICATIONS
1. Cough due to lung dryness, chronic constipation.[1]
CONTRAINDICATIONS: Damp phlegm.[2]
PREPARATIONS:
Decoction 10-15 g, or made into pills or paste.[1]
COMBINATIONS
- Constipation due to Dryness of the Intestines: Moistens the Intestines and unblocks the bowels Five seeds combination- Wu ren wan.
    
References
Inner Path can not take any responsibility for any adverse effects from the use of plants. Always seek advice from a professional before using a plant medicinally.
Research

Essential Oil of Pinus koraiensis Exerts Antiobesic and Hypolipidemic Activity via Inhibition of Peroxisome Proliferator-Activated Receptors Gamma Signaling
Hyun-Suk Ko, Hyo-Jeong Lee, Hyo-Jung Lee, Eun Jung Sohn, Miyong Yun, Min-Ho Lee, and Sung-Hoon Kim
Abstract
Our group previously reported that essential oil of Pinus koraiensis (EOPK) exerts antihyperlipidemic effects via upregulation of low-density lipoprotein receptor and inhibition of acyl-coenzyme A. In the present study, we investigated the antiobesity and hypolipidemic mechanism of EOPK using in vitro 3T3-L1 cells and in vivo HFD-fed rats. EOPK markedly suppressed fat accumulation and intracellular triglyceride associated with downregulation of adipogenic transcription factor expression, including PPARγ and CEBPα in the differentiated 3T3-L1 adipocytes. Additionally, EOPK attenuated the expression levels of FABP and GPDH as target genes of PPARγ during adipocyte differentiation. Furthermore, PPARγ inhibitor GW9662 enhanced the decreased expression of FABP and PPARγ and fat accumulation induced by EOPK. To confirm the in vitro activity of EOPK, animal study was performed by administering normal diet, HFD, and/or EOPK at the dose of 100 or 200 mg/kg for 6 weeks. Consistently, EOPK significantly suppressed body weight gain, serum triglyceride, total cholesterol, LDL cholesterol, and AI value and increased HDL cholesterol in a dose-dependent manner. Immunohistochemistry revealed that EOPK treatment abrogated the expression of PPARγ in the liver tissue sections of EOPK-treated rats. Taken together, our findings suggest that EOPK has the antiobesic and hypolipidemic potential via inhibition of PPARγ-related signaling. Evid Based Complement Alternat Med. 2013; 2013: 947037.
Published online 2013 Aug 13. doi: 10.1155/2013/947037
PMCID: PMC3753736 ncbi.nlm.nih.gov

Influence of Korean pine (Pinus koraiensis)-seed oil containing cis-5,cis-9,cis-12-octadecatrienoic acid on polyunsaturated fatty acid metabolism, eicosanoid production and blood pressure of rats.
Sugano M, Ikeda I, Wakamatsu K, Oka T.
Abstract
The effects of dietary Korean pine (Pinus koraiensis)-seed oil containing a peculiar trienoic acid (cis-5,cis-9,cis-12-18:3, pinolenic acid, approximately 18%) on various lipid variables were compared in rats with those of flaxseed (Linum usitatissimum L.) oil, safflower (Carthamus tinctorius L.) oil and evening primrose (Oenothera biennis L.) oil under experimental conditions where the effects of different polyunsaturated fatty acids could be estimated. In Sprague-Dawley rats fed on diets containing 100 g fat and 5 g cholesterol/kg, the hypocholesterolaemic activity of pinolenic acid was intermediate between alpha-linolenic and linoleic acids. Analysis of the fatty acid composition of liver phosphatidylcholine indicated that, in contrast to alpha-linolenic acid, pinolenic acid does not interfere with the desaturation of linoleic acid to arachidonic acid. However, the effects on ADP-induced platelet aggregation and aortic prostacyclin production were comparable. When spontaneously hypertensive rats were fed on diets containing 100 g fat/kg but free of cholesterol, gamma-linolenic and pinolenic acids, as compared with linoleic acid, increased prostacyclin production and tended to reduce platelet aggregation. In addition, pinolenic acid attenuated the elevation of blood pressure after 5 weeks of feeding. Thus, the results of the present studies indicate the beneficial effects of pinolenic acid on various lipid variables.
PMID: 7826999 Br J Nutr. 1994 Nov;72(5):775-83. ncbi.nlm.nih.gov

Essential oil of Pinus koraiensis inhibits cell proliferation and migration via inhibition of p21-activated kinase 1 pathway in HCT116 colorectal cancer cells
Sun-Mi Cho, Eun-Ok Lee, Sung-Hoon Kim, and Hyo-Jeong Leecorresponding author
Abstract
Background
The essential oil of Pinus koraiensis (EOPK) is biologically active compound obtained from the leaves of P. koraiensis. The goal of this study was to investigate the anti-cancer mechanism of EOPK in HCT116 colorectal cancer cells.
Methods
HCT116 cell proliferation was assessed by conducting crystal violet and BrdU assays. To assess the effects of EOPK on cell migration, we performed a wound-healing assay. Further, the contribution of PAK1 to EOPK-induced AKT and extracellular signal-regulated kinase (ERK) suppression was assessed by siRNA-mediated PAK1 knockdown. Changes to the expression and phosphorylation of PAK1 and its effectors were determined by western blotting, and changes to the actin cytoskeleton were determined by performing an immunofluorescence assay.
Results
EOPK significantly decreased HCT116 cell proliferation and migration, and induced G1 arrest without affecting normal cells. Additionally, EOPK suppressed the expression of PAK1, and decreased ERK and AKT phosphorylation in HCT116 cells. Finally, EOPK suppressed β-catenin, cyclin D1, and CDK4/6 expression.
Conclusions
Our studies indicate that EOPK significantly reduced proliferation and migration of colorectal cancer cells. Furthermore, EOPK suppressed PAK1 expression in a dose-dependent manner, and this suppression of PAK1 led to inhibition of ERK, AKT, and β-catenin activities. Our findings suggest that EOPK exerts its anticancer activity via the inhibition of PAK1 expression, suggesting it may be a potent chemotherapeutic agent for colorectal cancer. BMC Complement Altern Med. 2014; 14: 275.
Published online 2014 Jul 30. doi: 10.1186/1472-6882-14-275
PMCID: PMC4138364 ncbi.nlm.nih.gov