Vitexin attenuates lipopolysaccharide-induced acute lung injury by controlling the Nrf2 pathway.
A major feature of acute lung injury (ALI) is excessive inflammation in the lung. Vitexin is an active component from medicinal plants which has antioxidant and anti-inflammatory activities. Oxidative stress and inflammation play important roles in the pathophysiological processes in ALI. In the cur...
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2018-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC5942793?pdf=render |
| _version_ | 1811225336205017088 |
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| author | Ying Lu Ting Yu Jingyao Liu Lina Gu |
| author_facet | Ying Lu Ting Yu Jingyao Liu Lina Gu |
| author_sort | Ying Lu |
| collection | DOAJ |
| description | A major feature of acute lung injury (ALI) is excessive inflammation in the lung. Vitexin is an active component from medicinal plants which has antioxidant and anti-inflammatory activities. Oxidative stress and inflammation play important roles in the pathophysiological processes in ALI. In the current study, we investigate the effect and potential mechanisms of Vitexin on lipopolysaccharide (LPS)-induced ALI.ALI was induced by LPS intratracheal instillation in C57BL/6 wild-type mice and Nrf2 gene knocked down (Nrf2-/-) mice. One hour before LPS challenge, Vitexin or vehicle intraperitoneal injection was performed. Bronchoalveolar lavage fluid and lung tissues were examined for lung inflammation and injury at 24 h after LPS challenge.Our animal study's results showed that LPS-induced recruitment of neutrophils and elevation of proinflammatory cytokine levels were attenuated by Vitexin treatment. Vitexin decreased lung edema and alveolar protein content. Moreover, Vitexin activated nuclear factor erythroid-2-related factor 2 (Nrf2), and increased the activity of its target gene heme oxygenase (HO)-1. The LPS-induced reactive oxygen species were inhibited by Vitexin. In addition, the activation of the nucleotide-binding domain and leucine-rich repeat PYD-containing protein 3 (NLRP3) inflammasome was suppressed by Vitexin. However, these effects of Vitexin were abolished in the Nrf2-/- mice. Our cell studies showed that Vitexin enhanced the expression of Nrf2 and HO-1 activity. Moreover, reactive oxygen species (ROS) and IL-1β productions were reduced in Vitexin-treated cells. However, knockdown of Nrf2 by siRNA in RAW cells reversed the benefit of Vitexin.Vitexin suppresses LPS-induced ALI by controlling Nrf2 pathway. |
| first_indexed | 2024-04-12T09:04:17Z |
| format | Article |
| id | doaj.art-e041215cad4b401da5406aab818e4f73 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-04-12T09:04:17Z |
| publishDate | 2018-01-01 |
| publisher | Public Library of Science (PLoS) |
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| series | PLoS ONE |
| spelling | doaj.art-e041215cad4b401da5406aab818e4f732022-12-22T03:39:08ZengPublic Library of Science (PLoS)PLoS ONE1932-62032018-01-01134e019640510.1371/journal.pone.0196405Vitexin attenuates lipopolysaccharide-induced acute lung injury by controlling the Nrf2 pathway.Ying LuTing YuJingyao LiuLina GuA major feature of acute lung injury (ALI) is excessive inflammation in the lung. Vitexin is an active component from medicinal plants which has antioxidant and anti-inflammatory activities. Oxidative stress and inflammation play important roles in the pathophysiological processes in ALI. In the current study, we investigate the effect and potential mechanisms of Vitexin on lipopolysaccharide (LPS)-induced ALI.ALI was induced by LPS intratracheal instillation in C57BL/6 wild-type mice and Nrf2 gene knocked down (Nrf2-/-) mice. One hour before LPS challenge, Vitexin or vehicle intraperitoneal injection was performed. Bronchoalveolar lavage fluid and lung tissues were examined for lung inflammation and injury at 24 h after LPS challenge.Our animal study's results showed that LPS-induced recruitment of neutrophils and elevation of proinflammatory cytokine levels were attenuated by Vitexin treatment. Vitexin decreased lung edema and alveolar protein content. Moreover, Vitexin activated nuclear factor erythroid-2-related factor 2 (Nrf2), and increased the activity of its target gene heme oxygenase (HO)-1. The LPS-induced reactive oxygen species were inhibited by Vitexin. In addition, the activation of the nucleotide-binding domain and leucine-rich repeat PYD-containing protein 3 (NLRP3) inflammasome was suppressed by Vitexin. However, these effects of Vitexin were abolished in the Nrf2-/- mice. Our cell studies showed that Vitexin enhanced the expression of Nrf2 and HO-1 activity. Moreover, reactive oxygen species (ROS) and IL-1β productions were reduced in Vitexin-treated cells. However, knockdown of Nrf2 by siRNA in RAW cells reversed the benefit of Vitexin.Vitexin suppresses LPS-induced ALI by controlling Nrf2 pathway.http://europepmc.org/articles/PMC5942793?pdf=render |
| spellingShingle | Ying Lu Ting Yu Jingyao Liu Lina Gu Vitexin attenuates lipopolysaccharide-induced acute lung injury by controlling the Nrf2 pathway. PLoS ONE |
| title | Vitexin attenuates lipopolysaccharide-induced acute lung injury by controlling the Nrf2 pathway. |
| title_full | Vitexin attenuates lipopolysaccharide-induced acute lung injury by controlling the Nrf2 pathway. |
| title_fullStr | Vitexin attenuates lipopolysaccharide-induced acute lung injury by controlling the Nrf2 pathway. |
| title_full_unstemmed | Vitexin attenuates lipopolysaccharide-induced acute lung injury by controlling the Nrf2 pathway. |
| title_short | Vitexin attenuates lipopolysaccharide-induced acute lung injury by controlling the Nrf2 pathway. |
| title_sort | vitexin attenuates lipopolysaccharide induced acute lung injury by controlling the nrf2 pathway |
| url | http://europepmc.org/articles/PMC5942793?pdf=render |
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