Korean Mistletoe (Viscum album coloratum) Extract Improves Endurance Capacity in Mice by Stimulating Mitochondrial Activity

被引:25
|
作者
Jung, Hoe-Yune [1 ,2 ,4 ]
Lee, An-Na [4 ]
Song, Tae-Jun [4 ]
An, Hyo-Sun [4 ]
Kim, Young-Hoon [4 ]
Kim, Kyu-Dae [4 ]
Kim, In-Bo [4 ]
Kim, Kyoung-Shim [1 ]
Han, Baek-Soo [1 ]
Kim, Chun-Hyung [3 ]
Kim, Kwang-Soo [1 ,3 ]
Kim, Jong-Bae [4 ]
机构
[1] Korea Res Inst Biosci & Biotechnol, Brain Res Ctr, Taejon, South Korea
[2] Pohang Ctr Evaluaton Biomat, Bioact Nat Prod Reasearch Team, Pohang, South Korea
[3] Harvard Univ, McLean Hosp, Sch Med, Dept Psychiat,Mol Neurobiol Lab, Belmont, MA 02178 USA
[4] Handong Global Univ, Sch Life & Food Sci, Pohang, Gyungbuk, South Korea
关键词
consumption rate; endurance; forced-swim test; mistletoe; oxygen; PGC-1; alpha; SIRT-1; Viscum album coloratum; INSULIN-RESISTANCE; METABOLIC-CONTROL; RECEPTOR-ALPHA; MUSCLE; COACTIVATOR; DYSFUNCTION; EXPRESSION; PGC-1-BETA; ACID; PGC-1-ALPHA;
D O I
10.1089/jmf.2010.1469
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
The beneficial effects of exercise on overall health make it desirable to identify the orally active agents that enhance the effects of exercise in an effort to cure metabolic diseases. Natural compounds such as resveratrol (RSV) are known to increase endurance by potentiating mitochondrial function. Korean mistletoe (Viscum album coloratum) extract (KME) has characteristics similar to those of RSV. In the present study, we determined whether KME could increase mitochondrial activity and exert an anti-fatigue effect. We found that KME treatment significantly increased the mitochondrial oxygen consumption rate (OCR) in L6 cells and increased the expression of peroxisome proliferator-activated receptor gamma coactivator (PGC)-1 alpha and silent mating type information regulation 2 homolog 1 (SIRT1), two major regulators of mitochondria function, in C2C12 cells. In the treadmill test, KME-treated mice could run 2.5-times longer than chow-fed control mice. Additionally, plasma lactate levels of exhausted mice were significantly lower in the KME-treated group. In addition, the swimming time to exhaustion of mice treated with KME was prolonged by as much as 212% in the forced-swim test. Liver and kidney histology was similar between the KME-treated and phosphate-buffered saline-treated animals, indicating that KME was nontoxic. Taken together, our data show that KME induces mitochondrial activity, possibly by activating PGC-1 alpha and SIRT1, and improves the endurance of mice, strongly suggesting that KME has great potential as a novel mitochondria-activating agent.
引用
收藏
页码:621 / 628
页数:8
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