Attenuating effect of Ginsenoside Rb1 on LPS-induced lung injury in rats.

Qing Yuan,Lei Pan,Ting-Ting Ma,Qiu-Hong Fang,Yan-Wen Jiang

doi:10.1186/s12950-014-0040-5

Qing Yuan, Lei Pan + Show 3 more

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https://doi.org/10.1186/s12950-014-0040-5

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Abstract

BackgroundSepsis causes neutrophil sequestration in the lung which leads to acute lung injury (ALI). Radix Ginseng (RG), a traditional herb used as herbal remedy in eastern Asia for thousands of years, which has been traditionally used in China to improve blood circulation and ameliorate pathological hemostasis. This study investigated whether Ginsenoside Rb1, the main components of RG, can attenuate ALI induced by LPS.MethodsIn vivo, 30 male Wistar rats were divided into three groups (n = 10 each groups) on the basis of the reagent used, which were subjected to LPS injection with or without Ginsenoside Rb1 (5 mg/kg) treatments to induce ALI model. Lung injury was assessed by pulmonary histology, lung wet-weight to dry-weight (W/D) ratio, the number of myeloperoxidase (MPO) positive cells, immunohistochemical analysis of intercellular adhesion molecule-1 (ICAM-1), gene expression of ICAM-1, ultrastructure changes of pulmonary microvasculature, concentration of inflammatory markers and in plasma. In vitro, pulmonary microvascular endothelial cells (PMVECs) were stimulated with LPS in the presence and absence of Ginsenoside Rb1 (50 mM), nuclear factor-κB (NF-κB) p65 was measured by immunocytochemistry staining and western blotting.ResultsInfusion of LPS induced lung injury, in vivo, as demonstrated by pulmonary edema with infiltration of neutrophils and hemorrhage, the increase in lung W/D ratio, the number of MPO positive cells, the level of inflammatory markers such as TNF-α, MCP-1 and IL-8, enhanced expression of ICAM-1 and ICAM-1 gene. Moreover, resulted in the changes of intercellular junctions in the endothelial cells of pulmonary microvasculature. In vitro, the significant increased release of NF-κB p65 and its subsequent translocation into the nucleus in PMVECs were observed. In contrast, Ginsenoside Rb1 treatment significantly ameliorated the LPS-induced lung injury, as judged by the marked improvement in all these indices.ConclusionsThese results indicate that Ginsenoside Rb1 attenuated LPS-induced lung injury through an inhibition of the inflammatory signaling pathway, besides the direct inhibitory effect on proinflammatory molecules.

Highlights

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) in their most severe forms are still major challenges in modern intensive care medicine that significantly contribute to morbidity and mortality of critically ill patients
We previously identified that Ginsenoside Rb1, which is isolated from Notoginseng and Ginseng in Chinese herbal medicine efficiently can attenuate LPSinduced intestinal injury by inhibiting nuclear factor-κB (NF-κB) activation [6]
Histologic examination of the lung and W/D ratio We examined the effect of Ginsenoside Rb1 treatment on lung injury after LPS infusion

Summary

Introduction

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) in their most severe forms are still major challenges in modern intensive care medicine that significantly contribute to morbidity and mortality of critically ill patients. A recent epidemiological study indicate that ALI leads to 75,000 deaths annually in the United States [1]. Respiratory failure is caused by an excessive inflammatory response to both pulmonary and extrapulmonary stimuli, Pulmonary microvascular endothelial cells(PMVECs) are critically involved in the pathogenesis of acute lung injury. PMVECs can be stimulated by pro-inflammatory cytokines including TNF-α to express adhesion molecules such as intercellular cell adhesion molecule-1 (ICAM-1). Increased expression of adhesion molecules on PMVECs leads to leukocyte recruitment via interactions with their cognate ligands on leukocytes at the sites of atherosclerosis. Sepsis causes neutrophil sequestration in the lung which leads to acute lung injury (ALI). This study investigated whether Ginsenoside Rb1, the main components of RG, can attenuate ALI induced by LPS

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