4.7 Article

Protective effects of ginsenoside Rb1, ginsenoside Rg1, and notoginsenoside R1 on lipopolysaccharide-induced microcirculatory disturbance in rat mesentery

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LIFE SCIENCES
卷 81, 期 6, 页码 509-518

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PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.lfs.2007.06.008

关键词

Panax notoginseng; microcirculatory disturbance; leukocyte adhesion molecules; hydrogen peroxide; mast cell degranulation; lipopolysaccharide

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Ginsenoside Rb1 (Rb1). ginsenoside Rg1 (Rg1), and notoginsenoside R1 (R1) are major active components of Panalc notoginseng, a Chinese herb that is widely used in traditional Chinese medicine to enhance blood circulation and dissipate blood stasis. To evaluate the effect of these saponins on microcirculatory disturbance induced by lipopolysaccharide (LPS), vascular hemodynamics in rat mesentery was observed continuously during their administration using an inverted microscope and a high speed video camera system. LPS administration decreased red blood cell velocity but Rb1, Rg1, and RI attenuated this effect. LPS administration caused leukocyte adhesion to the venular wall, mast cell degranulation, and the release of cytokines. Rb1, Rg1, and R1 reduced the number of adherent leukocytes, and inhibited mast cell degranulation and cytokine elevation. In vitro experiments using flow cytometry further demonstrated that a) the LPS-enhanced expression of CD11b/CD 18 by neutrophils was significantly depressed by Rb1 and R 1, and b) hydrogen peroxide (H2O2) release from neutrophils in response to LPS stimulation was inhibited by treatment with Rg1 and R1. These results suggest that the protective effect of Rb1 and RI against leukocyte adhesion elicited by LPS may be associated with their suppressive action on the expression of CD11b/CD 18 by neutrophils. The protective effect against mast cell degranulation by Rb1 and R1, and the blunting of H2O2 release from neutrophils by Rg1 and R1 suggest mechanistic diversity in the effects of Panax notoarnseng saponins in the attenuation of microcirculatory disturbance induced by LPS. (c) 2007 Published by Elsevier Inc.

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