Abstract | BACKGROUND: 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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Authors | Hyunyoung Lim, Tae Yeon Kim, Soo Yeon Kim, Soo Jin Ro, Su Rim Koh, Sun Ryu, Justin Sangwook Ko, Mi Ae Jeong |
Journal | Transplantation proceedings
(Transplant Proc)
2021 Jan-Feb
Vol. 53
Issue 1
Pg. 427-435
ISSN: 1873-2623 [Electronic] United States |
PMID | 33280824
(Publication Type: Journal Article)
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Copyright | Copyright © 2020. Published by Elsevier Inc. |
Chemical References |
- Adrenergic alpha-2 Receptor Agonists
- Dexmedetomidine
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Topics |
- Adrenergic alpha-2 Receptor Agonists
(pharmacology)
- Animals
- Apoptosis
(drug effects)
- Dexmedetomidine
(pharmacology)
- Liver
(drug effects, pathology)
- Male
- Rats
- Rats, Sprague-Dawley
- Reperfusion Injury
(pathology)
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