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Acteoside attenuates acute lung injury following administration of cobra venom factor to mice

BACKGROUND: Acteoside, a water-soluble active constituent of diverse valuable medicinal vegetation, has shown strong anti-inflammatory property. However, studies on the anti-inflammatory property of acteoside in complement-induced acute lung injury (ALI) are limited. Therefore, this study aims to ev...

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Autores principales: Guo, Jing, Liu, Qiao-Zhou, Zhu, Fang-Juan, Li, Min, Li, Jiao, Guo, Li, Sun, Qian-Yun, Yang, Qing-Xiong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9674544/
https://www.ncbi.nlm.nih.gov/pubmed/36411899
http://dx.doi.org/10.1016/j.heliyon.2022.e11622
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author Guo, Jing
Liu, Qiao-Zhou
Zhu, Fang-Juan
Li, Min
Li, Jiao
Guo, Li
Sun, Qian-Yun
Yang, Qing-Xiong
author_facet Guo, Jing
Liu, Qiao-Zhou
Zhu, Fang-Juan
Li, Min
Li, Jiao
Guo, Li
Sun, Qian-Yun
Yang, Qing-Xiong
author_sort Guo, Jing
collection PubMed
description BACKGROUND: Acteoside, a water-soluble active constituent of diverse valuable medicinal vegetation, has shown strong anti-inflammatory property. However, studies on the anti-inflammatory property of acteoside in complement-induced acute lung injury (ALI) are limited. Therefore, this study aims to evaluate the anti-inflammatory activity of acteoside in cobra venom factor (CVF)-stimulated human microvascular endothelial cells (HMEC) and in ALI mice model. METHODS: In this study, we investigated the effects of acteoside (20, 10, and 5 μg/mL) in vitro in CVF induced HMECs and the activity of acteoside (100, 50, and 20 mg/kg/day bodyweight) in vivo in CVF induced ALI mice. Each eight male mice were orally administered acteoside or the positive drug PDTC (100 mg/kg/day) for 7 days before CVF (35 μg/kg) injection. After injection for 1 h, the pharmacological effects of acteoside were investigated by spectrophotometry, pathological examination, enzyme-linked immunosorbent assay, and immunohistochemistry. RESULTS: In vitro, acteoside (20, 10, and 5 μg/mL) reduced the protein expression of adhesion molecules and pro-inflammatory cytokines and transcriptional activity of NF-κB (P < 0.01). In vivo studies showed that acteoside dose-dependently alleviated lung histopathologic lesion, inhibited the production of the protein content of BALF, leukocyte cell number, lung MPO activity, and expression levels of IL-6, TNF-α, and ICAM-1, and suppressed the C5b-9 deposition and NF-κB activation in CVF-induced acute lung inflammation in mice (P < 0.05, 0.01). CONCLUSION: This study demonstrates that acteoside exerts strong anti-inflammatory activities in the CVF-induced acute lung inflammation model and suggests that acteoside is a potential therapeutic agent for complement-related inflammatory diseases.
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spelling pubmed-96745442022-11-20 Acteoside attenuates acute lung injury following administration of cobra venom factor to mice Guo, Jing Liu, Qiao-Zhou Zhu, Fang-Juan Li, Min Li, Jiao Guo, Li Sun, Qian-Yun Yang, Qing-Xiong Heliyon Research Article BACKGROUND: Acteoside, a water-soluble active constituent of diverse valuable medicinal vegetation, has shown strong anti-inflammatory property. However, studies on the anti-inflammatory property of acteoside in complement-induced acute lung injury (ALI) are limited. Therefore, this study aims to evaluate the anti-inflammatory activity of acteoside in cobra venom factor (CVF)-stimulated human microvascular endothelial cells (HMEC) and in ALI mice model. METHODS: In this study, we investigated the effects of acteoside (20, 10, and 5 μg/mL) in vitro in CVF induced HMECs and the activity of acteoside (100, 50, and 20 mg/kg/day bodyweight) in vivo in CVF induced ALI mice. Each eight male mice were orally administered acteoside or the positive drug PDTC (100 mg/kg/day) for 7 days before CVF (35 μg/kg) injection. After injection for 1 h, the pharmacological effects of acteoside were investigated by spectrophotometry, pathological examination, enzyme-linked immunosorbent assay, and immunohistochemistry. RESULTS: In vitro, acteoside (20, 10, and 5 μg/mL) reduced the protein expression of adhesion molecules and pro-inflammatory cytokines and transcriptional activity of NF-κB (P < 0.01). In vivo studies showed that acteoside dose-dependently alleviated lung histopathologic lesion, inhibited the production of the protein content of BALF, leukocyte cell number, lung MPO activity, and expression levels of IL-6, TNF-α, and ICAM-1, and suppressed the C5b-9 deposition and NF-κB activation in CVF-induced acute lung inflammation in mice (P < 0.05, 0.01). CONCLUSION: This study demonstrates that acteoside exerts strong anti-inflammatory activities in the CVF-induced acute lung inflammation model and suggests that acteoside is a potential therapeutic agent for complement-related inflammatory diseases. Elsevier 2022-11-14 /pmc/articles/PMC9674544/ /pubmed/36411899 http://dx.doi.org/10.1016/j.heliyon.2022.e11622 Text en © 2022 The Author(s) https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Research Article
Guo, Jing
Liu, Qiao-Zhou
Zhu, Fang-Juan
Li, Min
Li, Jiao
Guo, Li
Sun, Qian-Yun
Yang, Qing-Xiong
Acteoside attenuates acute lung injury following administration of cobra venom factor to mice
title Acteoside attenuates acute lung injury following administration of cobra venom factor to mice
title_full Acteoside attenuates acute lung injury following administration of cobra venom factor to mice
title_fullStr Acteoside attenuates acute lung injury following administration of cobra venom factor to mice
title_full_unstemmed Acteoside attenuates acute lung injury following administration of cobra venom factor to mice
title_short Acteoside attenuates acute lung injury following administration of cobra venom factor to mice
title_sort acteoside attenuates acute lung injury following administration of cobra venom factor to mice
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9674544/
https://www.ncbi.nlm.nih.gov/pubmed/36411899
http://dx.doi.org/10.1016/j.heliyon.2022.e11622
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