Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6
Background. Under septic conditions, LPS induced lung vascular endothelial cell (EC) injury, and the release of inflammatory mediator launches and aggravates acute lung injury (ALI). There are no effective therapeutic options for ALI. Genistein-3′-sodium sulfonate (GSS) is a derivative of native soy...
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| Format: | Article |
| Language: | English |
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Wiley
2019-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2019/4251394 |
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| author | Lei Yi Zengding Zhou Yijuan Zheng Mengling Chang Xiaoqin Huang Feng Guo Quanming Zhao Jingning Huan |
| author_facet | Lei Yi Zengding Zhou Yijuan Zheng Mengling Chang Xiaoqin Huang Feng Guo Quanming Zhao Jingning Huan |
| author_sort | Lei Yi |
| collection | DOAJ |
| description | Background. Under septic conditions, LPS induced lung vascular endothelial cell (EC) injury, and the release of inflammatory mediator launches and aggravates acute lung injury (ALI). There are no effective therapeutic options for ALI. Genistein-3′-sodium sulfonate (GSS) is a derivative of native soy isoflavone, which exhibits neuroprotective effects via its antiapoptosis property. However, whether GSS protect against sepsis-induced EC injury and release of inflammatory mediators has not been determined. In this study, we found that GSS not only downregulated the levels of TNF-α and IL-6 in the lung and serum of mice in vivo but also inhibited the expression and secretion of TNF-α and IL-6 in ECs. Importantly, we also found that GSS blocked LPS-induced TNF-α and IL-6 expression in ECs via the Myd88/NF-κB signaling pathway. Taken together, our results demonstrated that GSS might be a promising candidate for sepsis-induced ALI via its regulating effects on inflammatory response in lung ECs. |
| format | Article |
| id | doaj-art-270f1f35e8754e28b08b00bc7cb13555 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2019-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-270f1f35e8754e28b08b00bc7cb135552025-02-03T01:30:15ZengWileyMediators of Inflammation0962-93511466-18612019-01-01201910.1155/2019/42513944251394Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6Lei Yi0Zengding Zhou1Yijuan Zheng2Mengling Chang3Xiaoqin Huang4Feng Guo5Quanming Zhao6Jingning Huan7Department of Burn and Plastic Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Burn and Plastic Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Critical Care Medicine, Zhongshan Hospital, Fudan University, Shanghai, ChinaDepartment of Burn and Plastic Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Burn and Plastic Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaDepartment of Plastic Surgery, Shanghai Jiaotong University Affiliated Sixth People’s Hospital, Shanghai, ChinaDepartment of Orthopedic Surgery, The Second Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, ChinaDepartment of Burn and Plastic Surgery, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, ChinaBackground. Under septic conditions, LPS induced lung vascular endothelial cell (EC) injury, and the release of inflammatory mediator launches and aggravates acute lung injury (ALI). There are no effective therapeutic options for ALI. Genistein-3′-sodium sulfonate (GSS) is a derivative of native soy isoflavone, which exhibits neuroprotective effects via its antiapoptosis property. However, whether GSS protect against sepsis-induced EC injury and release of inflammatory mediators has not been determined. In this study, we found that GSS not only downregulated the levels of TNF-α and IL-6 in the lung and serum of mice in vivo but also inhibited the expression and secretion of TNF-α and IL-6 in ECs. Importantly, we also found that GSS blocked LPS-induced TNF-α and IL-6 expression in ECs via the Myd88/NF-κB signaling pathway. Taken together, our results demonstrated that GSS might be a promising candidate for sepsis-induced ALI via its regulating effects on inflammatory response in lung ECs.http://dx.doi.org/10.1155/2019/4251394 |
| spellingShingle | Lei Yi Zengding Zhou Yijuan Zheng Mengling Chang Xiaoqin Huang Feng Guo Quanming Zhao Jingning Huan Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6 Mediators of Inflammation |
| title | Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6 |
| title_full | Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6 |
| title_fullStr | Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6 |
| title_full_unstemmed | Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6 |
| title_short | Suppressive Effects of GSS on Lipopolysaccharide-Induced Endothelial Cell Injury and ALI via TNF-α and IL-6 |
| title_sort | suppressive effects of gss on lipopolysaccharide induced endothelial cell injury and ali via tnf α and il 6 |
| url | http://dx.doi.org/10.1155/2019/4251394 |
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