ArticleJournal of translational medicine2016
Propofol attenuated liver transplantation-induced acute lung injury via connexin43 gap junction inhibition.
Article in Journal of translational medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 25 citations in OpenAlex.
- Molecular mechanism of propofol in reducing kidney injury induced by autologous orthotopic liver transplantation.Frontiers in immunology · 2026Article
- Ciprofol prevents ferroptosis in LPS induced acute lung injury by activating the Nrf2 signaling pathway.BMC pulmonary medicine · 2024Article
- Downregulation of connexin 43-based gap junctions underlies propofol-induced excessive relaxation in hypertensive vascular smooth muscle cells.Cell communication and signaling : CCS · 2023Article
- The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023Review
- A new side-effect of sufentanil: increased monocyte-endothelial adhesion.BMC anesthesiology · 2021Article
- Propofol Regulates the TLR4/NF-κB Pathway Through miRNA-155 to Protect Colorectal Cancer Intestinal Barrier.Inflammation · 2021Article
- Oxidative stress under general intravenous and inhalation anaesthesia.Arhiv za higijenu rada i toksikologiju · 2020Review
- Improved multiparametric scrape loading-dye transfer assay for a simultaneous high-throughput analysis of gap junctional intercellular communication, cell density and viability.Scientific reports · 2020Article
- Dexmedetomidine Attenuates Monocyte-Endothelial Adherence via Inhibiting Connexin43 on Vascular Endothelial Cells.Mediators of inflammation · 2020Article
- Ulinastatin attenuates monocyte-endothelial adhesion via inhibiting ROS transfer between the neighboring vascular endothelial cells mediated by Cx43.American journal of translational research · 2020Article
- Dexmedetomidine Attenuates LPS-Induced Monocyte-Endothelial Adherence via Inhibiting Cx43/PKC-Oxidative medicine and cellular longevity · 2020Article
- Dexmedetomidine and propofol sedation requirements in an autistic rat model.Korean journal of anesthesiology · 2019Article
- Cx43 Inhibition Attenuates Sepsis-Induced Intestinal Injury via Downregulating ROS Transfer and the Activation of the JNK1/Sirt1/FoxO3a Signaling Pathway.Mediators of inflammation · 2019Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPostoperative acute lung injury (ALI) is a severe complication after liver transplantation, which influences patient survival rate obviously. However, its mechanisms are unclear and effective therapies are still lacking. The current study focused on effects of propofol on liver transplantation-induced ALI and whether its underlying mechanism was relative with connexin43 (Cx43) alternation. The authors postulated that endotoxin induced enhancement of Cx43 gap junction (GJ) plays a critical role in mediating post liver transplantation ALI and that pretreatment with the anesthetic propofol, known to inhibit gap junction, can confer effective protection.
methodsMale Sprague-Dawley rats underwent autologous orthotopic liver transplantation (AOLT) in the absence or presence of treatments with the selective Cx43 inhibitor, enanthol (0.1 mg/kg) and propofol (50 mg/kg), a commonly used anesthetic in clinical anesthesia. In vitro study, BEAS-2B cells, a kind of lung epithelial cell line expressing Cx43, exposed to lipopolysaccharide (LPS), which mainly contributed to ALI. Function of Cx43 GJ was regulated by Cx43 specific inhibitors, gap26 (300 μM) or enhancer, retinoic acid (10 μM) and two specific siRNAs.
resultsCompared with the sham group, AOLT results in ALI obviously with plasma endotoxin increase. Cx43 inhibition decreased ALI through inflammatory reaction reduction. In vitro studies, LPS-induced BEAS-2B cells damage was attenuated by Cx43 function inhibition, but amplified by enhancement. Another important finding was propofol reduced Cx43 function and protected against LPS-mediated BEAS-2B cells damage or AOLT-induced ALI, mechanisms of which were also associated with inflammatory reaction decrease.
conclusionCx43 plays a vital role in liver transplantation-induced ALI. Propofol decreased Cx43 function and protected against ALI in vivo and in vitro. This finding provide a new basis for targeted intervention of organ protection in liver transplantation, even in other kinds of operations.
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