Effect of dexmedetomidine hydrochloride on H2O2-induced oxidative stress and inflammatory response in Kupffer cells.
10.11817/j.issn.1672-7347.2016.05.005
- Author:
Jinmei SHEN
1
;
Li LI
1
;
Lili JIANG
2
;
Gan FU
3
Author Information
1. Department of Anesthesiology, Second Xiangya Hospital, Central South University, Changsha 410011, China.
2. Department of Anesthesiology, Affiliated Hospital of Qingdao University, Qingdao 266071, China.
3. Department of Hematology, Xiangya Hospital, Central South University, Changsha 410008, China.
- Publication Type:Journal Article
- MeSH:
Adrenergic alpha-2 Receptor Antagonists;
pharmacology;
Cell Survival;
Cells, Cultured;
Dexmedetomidine;
pharmacology;
Humans;
Hydrogen Peroxide;
pharmacology;
Kupffer Cells;
cytology;
drug effects;
L-Lactate Dehydrogenase;
metabolism;
Malondialdehyde;
metabolism;
Oxidative Stress;
drug effects;
Receptors, Adrenergic, alpha-2;
metabolism;
Tumor Necrosis Factor-alpha;
metabolism;
Yohimbine;
pharmacology
- From:
Journal of Central South University(Medical Sciences)
2016;41(5):477-481
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To evaluate whether dexmedetomidine hydrochloride, an α(2)-adrenergic receptor agonist, can prevent H(2)O(2)-induced oxidative stress and inflammatory response in Kupffer cells.
METHODS:H(2)O(2)-induced oxidative damage model of Kupffer cell was established. Kupffer cells were pre-conditioned by dexmedetomidine hydrochloride or Yohimbine for 24 h. MTT colorimetry was used to demonstrate the survival rate of Kupffer cells. The levels of lactate dehydrogenase (LDH), malonaldehyde (MDA) and TNF-α in the culture medium were assessed by corresponding kits.
RESULTS:Dexmedetomidine hydrochloride protected Kupffer cells from H(2)O(2)-induced oxidative damage, showing an increase in the cell survival rate while a decrease in LDH, MDA and TNF-α release in the culture supernatant. Yohimbine, an α(2)-adrenergic receptor antagonist, completely neutralized the protective effect of Dexmedetomidine hydrochloride on Kupffer cells. Yohimbine itself had no effect on H(2)O(2)-induced oxidative damage and inflammatory response.
CONCLUSION:Dexmedetomidine hydrochloride can prevent H(2)O(2)-induced oxidative stress and inflammatory response in Kupffer cells through activation of α(2)-adrenergic receptors.
