Angiotensin-(1–7) treatment blocks lipopolysaccharide-induced organ damage, platelet dysfunction, and IL-6 and nitric oxide production in rats

Abstract Sepsis can lead to shock, multiple organ failure, and even death. Platelets play an active role in the pathogenesis of sepsis-induced multiple organ failure. Angiotensin (Ang)-(1–7), a biologically active peptide, counteracts various effects of Ang II and attenuates inflammatory responses,...

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Autores principales:	Hsin-Jung Tsai, Chih-Chin Shih, Kuang-Yi Chang, Mei-Hui Liao, Wen-Jinn Liaw, Chin-Chen Wu, Cheng-Ming Tsao
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/402d0fcc278347fba3c87beaac688ad5
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spelling	oai:doaj.org-article:402d0fcc278347fba3c87beaac688ad52021-12-02T15:23:03ZAngiotensin-(1–7) treatment blocks lipopolysaccharide-induced organ damage, platelet dysfunction, and IL-6 and nitric oxide production in rats10.1038/s41598-020-79902-x2045-2322https://doaj.org/article/402d0fcc278347fba3c87beaac688ad52021-01-01T00:00:00Zhttps://doi.org/10.1038/s41598-020-79902-xhttps://doaj.org/toc/2045-2322Abstract Sepsis can lead to shock, multiple organ failure, and even death. Platelets play an active role in the pathogenesis of sepsis-induced multiple organ failure. Angiotensin (Ang)-(1–7), a biologically active peptide, counteracts various effects of Ang II and attenuates inflammatory responses, reactive oxygen species production, and apoptosis. We evaluated the effects of Ang-(1–7) on organ injury and platelet dysfunction in rats with endotoxaemia. We treated male Wistar rats with saline or lipopolysaccharide (LPS, 10 mg, intravenously) then Ang-(1–7) (1 mg/kg, intravenous infusion for 3 h beginning 30 min after LPS administration). We analysed several haemodynamic, biochemical, and inflammatory parameters, as well as platelet counts and aggregation. Ang-(1–7) improved hypotension and organ dysfunction, and attenuated plasma interleukin-6, chemokines and nitric oxide production in rats after LPS administration. The LPS-induced reduction in platelet aggregation, but not the decreased platelet count, was restored after Ang-(1–7) treatment. The protein expression of iNOS and IκB, but not phosphorylated ERK1/2 and p38, was diminished in Ang-(1–7)-treated LPS rats. The histological changes in liver and lung were significantly attenuated in Ang-(1–7)-treated LPS rats. Our results suggest that Ang-(1–7) ameliorates endotoxaemic-induced organ injury and platelet dysfunction, likely through the inhibition of the inflammatory response and nitric oxide production.Hsin-Jung TsaiChih-Chin ShihKuang-Yi ChangMei-Hui LiaoWen-Jinn LiawChin-Chen WuCheng-Ming TsaoNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-12 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Hsin-Jung Tsai Chih-Chin Shih Kuang-Yi Chang Mei-Hui Liao Wen-Jinn Liaw Chin-Chen Wu Cheng-Ming Tsao Angiotensin-(1–7) treatment blocks lipopolysaccharide-induced organ damage, platelet dysfunction, and IL-6 and nitric oxide production in rats
description	Abstract Sepsis can lead to shock, multiple organ failure, and even death. Platelets play an active role in the pathogenesis of sepsis-induced multiple organ failure. Angiotensin (Ang)-(1–7), a biologically active peptide, counteracts various effects of Ang II and attenuates inflammatory responses, reactive oxygen species production, and apoptosis. We evaluated the effects of Ang-(1–7) on organ injury and platelet dysfunction in rats with endotoxaemia. We treated male Wistar rats with saline or lipopolysaccharide (LPS, 10 mg, intravenously) then Ang-(1–7) (1 mg/kg, intravenous infusion for 3 h beginning 30 min after LPS administration). We analysed several haemodynamic, biochemical, and inflammatory parameters, as well as platelet counts and aggregation. Ang-(1–7) improved hypotension and organ dysfunction, and attenuated plasma interleukin-6, chemokines and nitric oxide production in rats after LPS administration. The LPS-induced reduction in platelet aggregation, but not the decreased platelet count, was restored after Ang-(1–7) treatment. The protein expression of iNOS and IκB, but not phosphorylated ERK1/2 and p38, was diminished in Ang-(1–7)-treated LPS rats. The histological changes in liver and lung were significantly attenuated in Ang-(1–7)-treated LPS rats. Our results suggest that Ang-(1–7) ameliorates endotoxaemic-induced organ injury and platelet dysfunction, likely through the inhibition of the inflammatory response and nitric oxide production.
format	article
author	Hsin-Jung Tsai Chih-Chin Shih Kuang-Yi Chang Mei-Hui Liao Wen-Jinn Liaw Chin-Chen Wu Cheng-Ming Tsao
author_facet	Hsin-Jung Tsai Chih-Chin Shih Kuang-Yi Chang Mei-Hui Liao Wen-Jinn Liaw Chin-Chen Wu Cheng-Ming Tsao
author_sort	Hsin-Jung Tsai
title	Angiotensin-(1–7) treatment blocks lipopolysaccharide-induced organ damage, platelet dysfunction, and IL-6 and nitric oxide production in rats
title_short	Angiotensin-(1–7) treatment blocks lipopolysaccharide-induced organ damage, platelet dysfunction, and IL-6 and nitric oxide production in rats
title_full	Angiotensin-(1–7) treatment blocks lipopolysaccharide-induced organ damage, platelet dysfunction, and IL-6 and nitric oxide production in rats
title_fullStr	Angiotensin-(1–7) treatment blocks lipopolysaccharide-induced organ damage, platelet dysfunction, and IL-6 and nitric oxide production in rats
title_full_unstemmed	Angiotensin-(1–7) treatment blocks lipopolysaccharide-induced organ damage, platelet dysfunction, and IL-6 and nitric oxide production in rats
title_sort	angiotensin-(1–7) treatment blocks lipopolysaccharide-induced organ damage, platelet dysfunction, and il-6 and nitric oxide production in rats
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/402d0fcc278347fba3c87beaac688ad5
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Angiotensin-(1–7) treatment blocks lipopolysaccharide-induced organ damage, platelet dysfunction, and IL-6 and nitric oxide production in rats

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