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Cited 5 time in webofscience Cited 3 time in scopus
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The Protective Effects of Dexmedetomidine Preconditioning on Hepatic Ischemia/Reperfusion Injury in Rats

Authors
Lim, HyunyoungKim, Tae YeonKim, Soo YeonRo, Soo JinKoh, Su RimRyu, SunKo, Justin SangwookJeong, Mi Ae
Issue Date
Jan-2021
Publisher
ELSEVIER SCIENCE INC
Citation
TRANSPLANTATION PROCEEDINGS, v.53, no.1, pp.427 - 435
Indexed
SCIE
SCOPUS
Journal Title
TRANSPLANTATION PROCEEDINGS
Volume
53
Number
1
Start Page
427
End Page
435
URI
https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/142446
DOI
10.1016/j.transproceed.2020.10.014
ISSN
0041-1345
Abstract
Background Ischemia/reperfusion (IR) injury is 1 of the major problems in liver surgery. This study aims to evaluate the histologic and biochemical effects of dexmedetomidine on ischemia/reperfusion injury in the liver of rats. Methods Twenty-two Sprague-Dawley male rats were separated into 3 groups: group sham, IR (IR injury), and IR-D (IR with dexmedetomidine). Ischemia was induced for 45 minutes with portal clampage and the reperfusion period was 120 minutes. Group IR-D received 3 μg/kg of dexmedetomidine with loading for 10 minutes and then 3 μg/kg/h of dexmedetomidine was continuously injected intravenously 30 minutes before portal clampage. Biochemical factors (alanine aminotransferase and aspartate aminotransferase), variable cytokines (B cell lymphoma-2 (Bcl-2), Bax, caspase 3, caspase 8, nuclear factor-kappa B, interleukin (IL)-1β, IL-6, IL-10, mixed lineage kinase domain-like protein, and receptor-interacting protein kinase-3), and histologic findings were investigated. Results Dexmedetomidine preconditioning significantly suppressed the histologic damage. In the IR-D group, the expression of IL-6 was decreased and the Bcl-2 was increased when compared with the IR group. Conclusion Dexmedetomidine suppresses hepatic IR injury and the protective mechanism appears to involve the decrease of IL-6 and upregulation of Bcl-2 expression, which result in the attenuation of inflammatory response and the inhibition of apoptosis.
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Jeong, Mi Ae
서울 의과대학 (DEPARTMENT OF ANESTHESIA AND MEDICINE)
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