Protective effect of esculentoside A on lipopolysaccharide-induced acute lung injury in mice

• Published in: The Journal of surgical research Vol. 185; no. 1; pp. 364 - 372
• Main Authors: Zhong, Wei-ting, PhD, Jiang, Lan-xiang, PhD, Wei, Jing-yuan, PhD, Qiao, An-na, BSc, Wei, Miao-miao, MD, Soromou, Lanan-Wassy, PhD, Xie, Xian-xing, BSc, Zhou, Xuan, BSc, Ci, Xin-xin, PhD, Wang, Da-cheng, PhD
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.11.2013
• Subjects: Acute lung injury; Acute Lung Injury - chemically induced; Acute Lung Injury - immunology; Acute Lung Injury - prevention & control; Animals; Bronchoalveolar Lavage Fluid - cytology; Bronchoalveolar Lavage Fluid - immunology; Disease Models, Animal; Drugs, Chinese Herbal - chemistry; Drugs, Chinese Herbal - pharmacology; Esculentoside A; I-kappa B Proteins - immunology; IκBa; Lipopolysaccharides - pharmacology; LPS; Lung - drug effects; Lung - immunology; Lung - metabolism; Male; MAP Kinase Signaling System - drug effects; MAP Kinase Signaling System - immunology; MAPK; Mice; Mice, Inbred BALB C; NF-KappaB Inhibitor alpha; Oleanolic Acid - analogs & derivatives; Oleanolic Acid - chemistry; Oleanolic Acid - pharmacology; Pulmonary Edema - chemically induced; Pulmonary Edema - immunology; Pulmonary Edema - prevention & control; Saponins - chemistry; Saponins - pharmacology; Surgery; Acute lung injury; MAPK; Esculentoside A; LPS; IκBa
• ISSN: 0022-4804; 1095-8673
• DOI: 10.1016/j.jss.2013.05.018

Abstract Background Esculentoside A (EsA) is a saponin isolated from the Chinese herb Phytolacca esculenta . In our study, we sought to investigate the protective effects of EsA on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. Materials and methods To determine the effects of EsA on the reduction of histopathologic changes in mice with ALI, inflammatory cell count in bronchoalveolar lavage fluid (BALF) and lung wet-to-dry weight ratio were measured in LPS-challenged mice, and lung histopathologic changes observed via paraffin section were assessed. Next, cytokine production induced by LPS in BALF was measured by enzyme-linked immunosorbent assay. To further study the mechanism of EsA protective effects on ALI, IκBa, p38, and extracellular signal receptor-activated kinase pathways were investigated in lung tissue of mice with ALI. Results In the present investigation, EsA showed marked effects by reducing inflammatory infiltration, thickening of the alveolar wall, and pulmonary congestion. Levels of tumor necrosis factor α and interleukin 6 elevated by LPS were significantly decreased in BALF in EsA-pretreated ALI model. Furthermore, EsA significantly suppressed phosphorylation of IκBa, p38, and extracellular signal receptor-activated kinase. Conclusions Taken together, our results suggest that EsA suppressed inflammatory responses in LPS-induced ALI through inhibition of the nuclear factor kappa B and mitogen activated protein kinase signaling pathways. EsA may be a promising potential preventive agent for ALI treatment.