Ginsenoside Rd inhibits the expressions of iNOS and COX-2 by suppressing NF-κB in LPS-stimulated RAW264.7 cells and mouse liver

被引:132
作者
Kim, Dae Hyun [1 ]
Chung, Jae Heun [1 ]
Yoon, Ji Sung [1 ]
Ha, Young Mi [1 ]
Bae, Sungjin [1 ]
Lee, Eun Kyeong [2 ]
Jung, Kyung Jin [3 ]
Kim, Min Sun [4 ]
Kim, You Jung [5 ]
Kim, Mi Kyung [6 ]
Chung, Hae Young [1 ,6 ]
机构
[1] Pusan Natl Univ, Coll Pharm, Mol Inflammat Res Ctr Aging Intervent MRCA, Pusan 609735, South Korea
[2] Dongnam Inst Radiol & Med Sci, Res Ctr, Pusan 619953, South Korea
[3] Korea Inst Toxicol, Inhalat Toxicol Ctr, Jeongeup 580185, South Korea
[4] Sunchon Natl Univ, Dept Pharm, Coll Pharm, Sunchon 540742, South Korea
[5] Busan Womens Coll, Dept Dent Hyg, Pusan 614734, South Korea
[6] Pusan Natl Univ, Longev Life Sci & Technol Inst, Pusan 609735, South Korea
关键词
Panax ginseng; Ginsenoside Rd; Inducible nitric oxide synthase; Cyclooxygenase-2; Prostaglandin E-2;
D O I
10.5142/jgr.2013.37.54
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Ginsenoside Rd is a primary constituent of the ginseng rhizome and has been shown to participate in the regulation of diabetes and in tumor formation. Reports also show that ginsenoside Rd exerts anti-oxidative effects by activating anti-oxidant enzymes. Treatment with ginsenoside Rd decreased nitric oxide and prostaglandin E-2 (PGE(2)) in lipopolysaccharides (LPS)-challenged RAW264.7 cells and in ICR mouse livers (5 mg/kg LPS; LPS + ginsenoside Rd [2, 10, and 50 mg/kg]). Furthermore, these decreases were associated with the down-regulations of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2 and of nuclear factor (NF)-kappa B activity in vitro and in vivo. Our results indicate that ginsenoside Rd treatment decreases; 1) nitric oxide production (40% inhibition); 2) PGE(2) synthesis (69% to 93% inhibition); 3) NF-kappa B activity; and 4) the NF-kappa B-regulated expressions of iNOS and COX-2. Taken together, our results suggest that the anti-inflammatory effects of ginsenoside Rd are due to the down-regulation of NF-kappa B and the consequent expressional suppressions of iNOS and COX-2.
引用
收藏
页码:54 / 63
页数:10
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