ArticleExperimental and therapeutic medicine2019
Dexmedetomidine activates the PI3K/Akt pathway to inhibit hepatocyte apoptosis in rats with obstructive jaundice.
Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Could Different Doses of Dexmedetomidine Be as Effective as Amifostine Against Radiotherapy-Induced Liver Injury in Rats? Evidence from Mitotic, Apoptotic, Oxidative, and Neurogenic Insights.Journal of clinical medicine · 2025Article
- Meta-analysis comparing dexmedetomidine versus standard of care for sedation in patients with sepsis.Proceedings (Baylor University. Medical Center) · 2022Review
- Better detoxifying effect of ripe forsythiae fructus over green forsythiae fructus and the potential mechanisms involving bile acids metabolism and gut microbiota.Frontiers in pharmacology · 2022Article
- Dexmedetomidine ameliorates lipopolysaccharide-induced acute lung injury by inhibiting the PI3K/Akt/FoxO1 signaling pathway.Journal of anesthesia · 2021Article
- Dexmedetomidine reduces ventilator-induced lung injury via ERK1/2 pathway activation.Molecular medicine reports · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Obstructive jaundice (OJ) is a common disease in clinical surgery. The present study aimed to determine the effects of dexmedetomidine (Dex) on hepatocyte apoptosis in rats with OJ and also to explore the underlying mechanism. A total of 30 adult male Sprague Dawley rats were randomly divided into 3 groups: Sham group, bile duct ligation (BDL) group, and BDL+Dex group. The serum liver function index, expression levels of serum inflammatory factor interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α), and the liver pathological changes were compared amongst groups. The serum liver function index and expression levels of inflammatory factors in the BDL group and BDL+Dex group were higher compared with the sham group. The serum liver function index and expression levels of inflammatory factors were lower in the BDL+Dex group compared with the BDL group. The severity of hepatic injury was diminished in the BDL+Dex group compared with the BDL group. Compared with the sham group, the hepatocyte apoptosis rate increased significantly in the BDL group and BDL+Dex group. The present findings suggested that Dex improved the liver function of rats with OJ, reduced the production of inflammatory factors and inhibited the apoptosis of hepatocytes. Dex demonstrated a protective effect on liver damage potentially via activation of the phosphoinositide 3-kinase/protein kinase B signaling pathway.
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