Ethanol Extract of Pinus koraiensis Leaves Mitigates High Fructose-Induced Hepatic Triglyceride Accumulation and Hypertriglyceridemia

被引:3
|
作者
Lee, Min-Ho [1 ]
Park, Sunyeong [2 ]
Xu, Yinzhu [3 ]
Kim, Jung-Eun [3 ]
Han, Hengmin [4 ]
Lee, Jae-Hyeon [4 ]
Paik, Jean Kyung [5 ]
Lee, Hyo-Jeong [3 ,4 ]
机构
[1] Eulji Univ, Dept Food Sci & Serv, Seongnam 13135, South Korea
[2] Dain Nat Co Ltd, Seoul 04788, South Korea
[3] Kyung Hee Univ, Coll Korean Med, Grad Sch, Dept Sci Korean Med, 26 Kyungheedae Ro, Seoul 02447, South Korea
[4] Kyung Hee Univ, Coll Korean Med, Grad Sch, Dept Canc Prevent Mat Dev, 26 Kyungheedae Ro, Seoul 02447, South Korea
[5] Eulji Univ, Dept Food & Nutr, Seongnam 13135, South Korea
来源
APPLIED SCIENCES-BASEL | 2022年 / 12卷 / 13期
关键词
Pinus koraiensis; de novo lipogenesis; hypertriglyceridemia; high fructose diet; non-alcoholic fatty liver; FATTY LIVER-DISEASE; DE-NOVO LIPOGENESIS; INSULIN-RESISTANCE; STEATOSIS; DIET; CHREBP; INFLAMMATION; GLUCOSE; MICE; INHIBITION;
D O I
10.3390/app12136745
中图分类号
O6 [化学];
学科分类号
0703 ;
摘要
Pinus koraiensis is a valuable plant source of functional health foods and medicinal materials. Hypertriglyceridemia affects about 15-20% of adults and is related to stroke, metabolic syndromes, cardiovascular diseases, and diabetes mellitus. Dietary fructose, a risk factor for developing hypertriglyceridemia, significantly increases postprandial triglyceride (TG) levels and aggravates non-alcoholic fatty liver disease. In this study, we aimed to analyze the effect of ethanol extract from P. koraiensis needles (EPK) on fructose (Fr)-induced cell culture and animal models, respectively. Our team determined the bioactivity, such as anti-cancer, anti-obesity, anti-diabetic, and anti-hyperlipidemic functions, of P. koraiensis needle extract. The EPK markedly reduced TG levels in the liver and serum and enhanced TG excretion through feces in high-fructose-fed rats. Furthermore, the EPK inhibited de novo lipogenesis and its markers-carbohydrate response element-binding protein (ChREBP), sterol regulatory element-binding protein 1 (SREBP-1), fatty acid synthase (FAS), 3-Hydroxy-3-Methylglutaryl-CoA Reductase (HMGCR), and tumor necrosis factor-alpha (TNF-alpha), a pro-inflammatory marker. Consistent with the results of the in vivo experiment, the EPK decreased SREBP-1, ChREBP, HMGCR, FAS, TNF-alpha, and iNOS expression levels, resulting in slower lipid accumulation and lower TG levels in Fr-induced HepG2 cells. These findings suggest that EPK mitigates hypertriglyceridemia and hepatic TG accumulation by inhibiting de novo lipogenic and pro-inflammatory factors.
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页数:13
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