ArticleExperimental and therapeutic medicine2017
Isoflurane anesthesia induces liver injury by regulating the expression of insulin-like growth factor 1.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 19 citations in OpenAlex.
- Bidirectional Relationship Between Anaesthetic Drugs and Metabolic Syndrome: Clinical Effects and Mechanisms.Journal of cellular and molecular medicine · 2025Review
- Anesthesia and analgesia for common research models of adult mice.Laboratory animal research · 2022Review
- In vivo demonstration of a novel non-invasive model for inducing localized hypothermia to ameliorate hepatotoxicity.Scientific reports · 2021Article
- Inhibition of SUMO2/3 antagonizes isoflurane-induced cancer-promoting effect in hepatocellular carcinoma Hep3B cells.Oncology letters · 2021Article
- Anesthesia-Sepsis-Associated Alterations in Liver Gene Expression Profiles and Mitochondrial Oxidative Phosphorylation Complexes.Frontiers in medicine · 2020Article
- Sevoflurane induces liver injury by modulating the expression of insulin-like growth factor 1 via miR-214.Journal of cellular physiology · 2018Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has been suggested that isoflurane may cause perioperative liver injury. However, the mechanism of its action remains unknown. The purpose of the present study was to determine this possible mechanism. Sprague-Dawley rats were randomly assigned into one of three groups (all n=12): Control group (exposed to mock anesthesia), isoflurane group (exposed to 2% isoflurane for 90 min), and isoflurane + insulin-like growth factor 1 (IGF-1) group (exposed to 2% isoflurane for 90 min and then treated with IGF-1). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and western blotting were conducted to determine the levels of expression of IGF-1 and its receptor IGF-R. Liver necrosis was assessed by histological examination. TUNEL assay was performed to determine the apoptosis of hepatic cells. In addition, the levels of the proteins caspase-3 and B-cell lymphoma-extra large (Bcl-xL) were measured. Compared with the control group, levels of IGF-1 and IGF-1R mRNA and protein were significantly decreased following exposure to isoflurane (all P<0.05). The necrosis rate and liver apoptosis were significantly increased in the group treated with isoflurane alone compared with the control group (P<0.05), but were significantly decreased compared with the isoflurane group following application of IGF-1 (P<0.05). Additionally, isoflurane exposure significantly increased levels of caspase-3 compared with the control group (P<0.05), but decreased levels of Bcl-xL (P<0.05). By contrast, application of IGF-1 reversed these changes. The present study therefore suggests that isoflurane induces liver injury in part by regulating the expression of IGF-1 and that application of IGF-1 may protect against liver injury induced by isoflurane exposure.
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