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Anti-inflammatory effects of Esomeprazole in septic lung injury by mediating endoplasmic reticulum stress.

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Title: Anti-inflammatory effects of Esomeprazole in septic lung injury by mediating endoplasmic reticulum stress.
Authors: Wang, Peng1 (AUTHOR), Li, Hui1 (AUTHOR), Wu, Wencheng1 (AUTHOR) WenchengWu12@163.com
Source: Journal of Bioenergetics & Biomembranes. Jun2025, Vol. 57 Issue 2, p173-182. 10p.
Subjects: Endoplasmic reticulum stress, Transcription factors, Lactate dehydrogenase, Immunostaining, Hematoxylin & eosin staining
Abstract: Acute lung injury characterized by overactive pulmonary inflammation is a common and serious complication of sepsis. Esomeprazole (ESO), a potent proton pump inhibitor (PPI), has been demonstrated as a promising anti-inflammatory agent in treating sepsis at high concentrations, the efficacy of which in sepsis-induced lung injury has not been explored. This research aimed to investigate the role of ESO in septic lung injury and the potential mechanism. The mice were pretreated by ESO prior to the construction of cecal ligation and puncture (CLP) sepsis model. MH-S lung macrophages were exposed to lipopolysaccharide (LPS) to induce inflammatory injury. The severity of lung damage was detected by H&E staining, measurement of lactic dehydrogenase (LDH) and lung wet/dry weight (W/D) ratio. The levels of inflammatory cytokines were detected by ELISA and Western blotting. The number of inflammatory cells was counted. Macrophage distribution was measured by immunohistochemical staining of macrophage markers. Western blotting also determined the expression of endoplasmic reticulum stress (ERS) and NLR family pyrin domain containing 3 (NLRP3) inflammasome-related proteins. CCK-8 method was used to detect cell viability. ESO concentration-dependently mitigated the pathological damage of lung tissues, reduced LDH activity, lung W/D ratio, decreased inflammatory cell counts and F4/80 expression in the lung tissues of sepsis mice. Besides, ESO suppressed inflammatory response, NLRP3 inflammasome activation and inactivated activating transcription factor 6 (ATF6)-CCAAT-enhancer-binding protein homologous protein (CHOP)-mediated ERS signaling both in vitro and in vivo. ATF6 overexpression partially reversed the impacts of ESO on NLRP3 inflammasome and the levels of inflammatory cytokines in LPS-induced MH-S cells. Anyway, ESO may inhibit ATF6/CHOP pathway to protect against inflammation in septic lung injury. [ABSTRACT FROM AUTHOR]
Copyright of Journal of Bioenergetics & Biomembranes is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
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  Label: Title
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  Data: Anti-inflammatory effects of Esomeprazole in septic lung injury by mediating endoplasmic reticulum stress.
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  Data: <searchLink fieldCode="AR" term="%22Wang%2C+Peng%22">Wang, Peng</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Li%2C+Hui%22">Li, Hui</searchLink><relatesTo>1</relatesTo> (AUTHOR)<br /><searchLink fieldCode="AR" term="%22Wu%2C+Wencheng%22">Wu, Wencheng</searchLink><relatesTo>1</relatesTo> (AUTHOR)<i> WenchengWu12@163.com</i>
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  Data: <searchLink fieldCode="JN" term="%22Journal+of+Bioenergetics+%26+Biomembranes%22">Journal of Bioenergetics & Biomembranes</searchLink>. Jun2025, Vol. 57 Issue 2, p173-182. 10p.
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  Data: <searchLink fieldCode="DE" term="%22Endoplasmic+reticulum+stress%22">Endoplasmic reticulum stress</searchLink><br /><searchLink fieldCode="DE" term="%22Transcription+factors%22">Transcription factors</searchLink><br /><searchLink fieldCode="DE" term="%22Lactate+dehydrogenase%22">Lactate dehydrogenase</searchLink><br /><searchLink fieldCode="DE" term="%22Immunostaining%22">Immunostaining</searchLink><br /><searchLink fieldCode="DE" term="%22Hematoxylin+%26+eosin+staining%22">Hematoxylin & eosin staining</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Acute lung injury characterized by overactive pulmonary inflammation is a common and serious complication of sepsis. Esomeprazole (ESO), a potent proton pump inhibitor (PPI), has been demonstrated as a promising anti-inflammatory agent in treating sepsis at high concentrations, the efficacy of which in sepsis-induced lung injury has not been explored. This research aimed to investigate the role of ESO in septic lung injury and the potential mechanism. The mice were pretreated by ESO prior to the construction of cecal ligation and puncture (CLP) sepsis model. MH-S lung macrophages were exposed to lipopolysaccharide (LPS) to induce inflammatory injury. The severity of lung damage was detected by H&E staining, measurement of lactic dehydrogenase (LDH) and lung wet/dry weight (W/D) ratio. The levels of inflammatory cytokines were detected by ELISA and Western blotting. The number of inflammatory cells was counted. Macrophage distribution was measured by immunohistochemical staining of macrophage markers. Western blotting also determined the expression of endoplasmic reticulum stress (ERS) and NLR family pyrin domain containing 3 (NLRP3) inflammasome-related proteins. CCK-8 method was used to detect cell viability. ESO concentration-dependently mitigated the pathological damage of lung tissues, reduced LDH activity, lung W/D ratio, decreased inflammatory cell counts and F4/80 expression in the lung tissues of sepsis mice. Besides, ESO suppressed inflammatory response, NLRP3 inflammasome activation and inactivated activating transcription factor 6 (ATF6)-CCAAT-enhancer-binding protein homologous protein (CHOP)-mediated ERS signaling both in vitro and in vivo. ATF6 overexpression partially reversed the impacts of ESO on NLRP3 inflammasome and the levels of inflammatory cytokines in LPS-induced MH-S cells. Anyway, ESO may inhibit ATF6/CHOP pathway to protect against inflammation in septic lung injury. [ABSTRACT FROM AUTHOR]
– Name: AbstractSuppliedCopyright
  Label:
  Group: Ab
  Data: <i>Copyright of Journal of Bioenergetics & Biomembranes is the property of Springer Nature and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1007/s10863-025-10055-0
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            NameFull: Wang, Peng
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            NameFull: Li, Hui
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              M: 06
              Text: Jun2025
              Type: published
              Y: 2025
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