Ginsenoside ameliorated ventilator-induced lung injury in rats
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RESEARCH
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Ginsenoside ameliorated ventilator-induced lung injury in rats Woo Hyun Cho1†, Yun Hak Kim2†, Hye Jin Heo2, Dohyung Kim3, Tae Won Kwak4, Kwang Ho Kim4 and Hye Ju Yeo1*
Abstract Background: Ginsenosides have antioxidant and anti-inflammatory features. This study aimed to evaluate the biologic effects of ginsenoside Rb2 pretreatment on ventilator-induced lung injury (VILI) in rats. Methods: Rats were divided into four groups with 12 rats per group: control; low tidal volume (TV), TV of 6 mL/kg, VILI, TV of 20 mL/kg, positive end-expiratory pressure of 5 cm H2O, and respiratory rate of 60 breaths per minute for 3 h at an inspiratory oxygen fraction of 0.21; and ginsenosides, treated the same as the VILI group but with 20 mg/ kg intraperitoneal ginsenoside pretreatment. Morphology was observed with a microscope to confirm the VILI model. Wet-to-dry weight ratios, protein concentrations, and pro-inflammatory cytokines in the bronchoalveolar lavage fluid were measured. RNA sequencing of the lung tissues was conducted to analyze gene expression. Results: High TV histologically induced VILI with alveolar edema and infiltration of inflammatory cells. Ginsenosides pretreatment significantly reduced the histologic lung injury score compared to the VILI group. Wet-to-dry weight ratios, malondialdehyde, and TNF-α in bronchoalveolar lavage fluid were significantly higher in the VILI group and ginsenoside pretreatment mitigated these effects. In the immunohistochemistry assay, ginsenoside pretreatment attenuated the TNF-α upregulation induced by VILI. We identified 823 genes differentially presented in the VILI group compared to the control group. Of the 823 genes, only 13 genes (Arrdc2, Cygb, Exnef, Lcn2, Mroh7, Nsf, Rexo2, Srp9, Tead3, Ephb6, Mvd, Sytl4, and Ube2l6) recovered to control levels in the ginsenoside group. Conclusions: Ginsenosides inhibited the inflammatory and oxidative stress response in VILI. Further studies are required on the 13 genes, including LCN2. Keywords: Ginsenosides, Ventilator-induced lung injury, Tumor necrosis factor-alpha, LCN2, NGAL
Background Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are fatal diseases [1]. Mechanical ventilation is essential for overcoming life-threatening hypoxia and hypercapnia. Despite the lifesaving effects, * Correspondence: [email protected] † Woo Hyun Cho and Yun Hak Kim contributed equally to this work. 1 Division of Pulmonary, Allergy and Critical Care Medicine, Department of Internal Medicine, Research Institute for Convergence of Biomedical Science and Technology, Pusan National University Yangsan Hospital, Geumo-ro 20, Beomeo-ri, Mulgeum-eup, Yangsan-si, Gyeongsangnam-do 626-770, Republic of Korea Full list of author information is available at the end of the article
mechanical ventilation may induce or deteriorate lung injury, a state noted as ventilator-induced lung injury (VILI) [2]. VILI involves neutrophil activation, high permeability pulmonary edema, increased vascular permeability, and inflammation [2].
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