Ginsenoside Rd inhibits the expressions of iNOS and COX-2 by suppressing NF-κB in LPS-stimulated RAW264.7 cells and mouse liver.
Ginsenoside Rd inhibits the expressions of iNOS and COX-2 by suppressing NF-κB in LPS-stimulated RAW264.7 cells and mouse liver.
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DOI：
10.5142/jgr.2013.37.54
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发表时间：
2013-03
影响因子：
6.3
通讯作者：
Chung HY
中科院分区：
文献类型：
--
作者：
Kim DH;Chung JH;Yoon JS;Ha YM;Bae S;Lee EK;Jung KJ;Kim MS;Kim YJ;Kim MK;Chung HY
人参皂苷 Rd 是人参根茎的主要成分，已被证明参与糖尿病的调节和肿瘤的形成。报告还表明，人参皂苷 Rd 通过激活抗氧化酶发挥抗氧化作用。人参皂苷 Rd 治疗可降低脂多糖 (LPS) 攻击的 RAW264.7 细胞和 ICR 小鼠肝脏中的一氧化氮和前列腺素 E2 (PGE2)（5 mg/kg LPS；LPS + 人参皂苷 Rd [2、10 和 50 mg/kg]）。此外，这些降低与体外和体内诱导型一氧化氮合酶 (iNOS) 和环氧合酶 (COX)-2 以及核因子 (NF)-κB 活性的下调有关。我们的结果表明，人参皂苷 Rd 处理会降低； 1）一氧化氮产生（抑制40%）； 2）PGE2合成（抑制69%至93%）； 3) NF-κB活性； 4) NF-κB 调节的 iNOS 和 COX-2 表达。综上所述，我们的结果表明人参皂苷 Rd 的抗炎作用是由于 NF-κB 的下调以及随之而来的 iNOS 和 COX-2 的表达抑制所致。
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 E2 (PGE2) 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)-κB activity in vitro and in vivo. Our results indicate that ginsenoside Rd treatment decreases; 1) nitric oxide production (40% inhibition); 2) PGE2 synthesis (69% to 93% inhibition); 3) NF-κB activity; and 4) the NF-κB-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-κB and the consequent expressional suppressions of iNOS and COX-2.