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Published on: May 21, 2018
Isoflurane attenuates LPS-induced acute lung injury by targeting miR-155-HIF1-alpha
Rong Hu1, Ying Zhang1, Xiaohua Yang1
1Department of Anesthesiology, Shanghai Ninth People�s Hospital affiliated to Shanghai Jiao Tong University, School of Medicine, No. 639, Zhi Zao Ju Road, Shanghai, China.
Abstract:
Isoflurane alleviates the inflammatory response in endotoxin-induced acute lung injury (ALI). In this study, we investigated the protective mechanism of isoflurane postconditioning in lipopolysaccharide (LPS)induced ALI. Exposure to isoflurane decreased miR-155 and upregulated HIF-1 alpha and HO-1 mRNA and protein. The effects of isoflurane on HIF-1 alpha mRNA and protein could be inhibited by overexpression of miR-155. Furthermore, mice overexpressing miR-155 had higher levels of TNF-alpha and IL-1 beta in BALF when exposed to isoflurane after LPS challenge.Conversely, downregulation of miR-155 promoted isoflurane effects on HIF-1 alpha expression. These results suggest that isoflurane posttreatment hr alleviates LPS-induced ALI and cell injury by triggering miR-155-HIF-1 alpha pathway, leading to upregulation of HO-1.
Insights
Isoflurane postconditioning protects against acute lung injury (ALI) by regulating miR-155 and HIF-1 alpha. This mechanism involves HO-1 upregulation, reducing inflammation and cell damage.
Area of Science:
- Anesthesiology
- Pulmonary Medicine
- Molecular Biology
Background:
- Acute lung injury (ALI) is a critical condition with significant mortality.
- Endotoxin-induced ALI is a common experimental model to study lung inflammation.
- Isoflurane is an anesthetic agent with known anti-inflammatory properties.
Purpose of the Study:
- To investigate the protective mechanism of isoflurane postconditioning in lipopolysaccharide (LPS)-induced ALI.
- To elucidate the role of the miR-155/HIF-1 alpha pathway in isoflurane's protective effects.
- To determine the downstream effects on HO-1 expression and inflammatory markers.
Main Methods:
- Induction of ALI in a mouse model using lipopolysaccharide (LPS).
- Administration of isoflurane as a postconditioning treatment.
- Measurement of miR-155, HIF-1 alpha, and HO-1 at mRNA and protein levels.
- Manipulation of miR-155 expression (overexpression and downregulation).
- Assessment of inflammatory cytokines (TNF-alpha, IL-1 beta) in bronchoalveolar lavage fluid (BALF).
Main Results:
- Isoflurane exposure decreased miR-155 expression while upregulating HIF-1 alpha and HO-1 (mRNA and protein).
- Overexpression of miR-155 inhibited the effects of isoflurane on HIF-1 alpha and increased TNF-alpha and IL-1 beta levels.
- Downregulation of miR-155 enhanced isoflurane's effects on HIF-1 alpha expression.
- Isoflurane posttreatment alleviated LPS-induced ALI and cell injury.
Conclusions:
- Isoflurane posttreatment alleviates LPS-induced ALI and cell injury.
- The protective mechanism involves the miR-155/HIF-1 alpha pathway, leading to HO-1 upregulation.
- This pathway modulation by isoflurane offers a potential therapeutic strategy for ALI.
