@Article{ecn.2019.0431,
AUTHOR = {Yuan Zhao, Gao-Yin Kong, Wan-Min Pei, Bo Zhou, Qin-Qin Zhang, Bing-Bing Pan},
TITLE = {Dexmedetomidine alleviates hepatic injury via the inhibition of oxidative stress and activation of the Nrf2/HO-1 signaling pathway},
JOURNAL = {European Cytokine Network},
VOLUME = {30},
YEAR = {2019},
NUMBER = {3},
PAGES = {88--97},
URL = {http://www.techscience.com/ECN/v30n3/65390},
ISSN = {1952-4005},
ABSTRACT = {Background: Dexmedetomidine (Dex), frequently used as an effective sedative, was reported to play a
critical role in the protection of multiple organs. However, its underlying mechanism of a putative protective effect on
ischemia/reperfusion (I/R)-induced liver injury is still unclear. Methods: A hepatocyte injury model was established by
treating WRL-68 cells with oxygen and glucose deprivation/reoxygenation (OGD/R). Enzyme Linked Immunosorbent
Assay (ELISA) kits were used to determine the level of inflammatory factors (IL-6, IL-1β, and TNF-α), and oxidative
stress indicators (ROS, MDA, GSH-Px, and SOD). MTT assay and flow cytometry analysis were used to determine
the influence of Dex on cell viability and cell apoptosis. Expression of nuclear factor erythroid-derived 2- like 2 (Nrf2),
HO-1, and apoptosis-related proteins (Bax, Bcl-2, caspase3, and caspase9) were detected by qRT-PCR and western
blotting. Results: Dex promoted cell viability and suppressed cell apoptosis in OGD/R-treated WRL-68 cells.
Dex reduced TNF-α, IL-6, IL-1β, ROS, and MDA production, whereas it increased that of SOD and GSH-Px in
OGD/R-treated WRL-68 cells. Moreover, Nrf2, HO-1, and Bcl-2 expression was upregulated, whereas, in contrast,
transcripts for Bax, caspase3, and caspase9 were downregulated following Dex treatment under OGD/R. Knockdown
of Nrf2 reversed the Dex effects on cell proliferation, apoptosis, and expression of TNF-α, IL-6, IL-1β, ROS, MDA,
SOD, and GSH-Px. Conclusion: Dex protects WRL-68 cells against OGD/R-induced injury by inhibiting
inflammation, oxidative stress, and cell apoptosis via the activation of Nrf2/HO-1 signaling pathway, suggesting that
Dex may be a potential protector against hepatic injury.},
DOI = {10.1684/ecn.2019.0431}
}