Effects of norcantharidin on lipopolysaccharide-induced hepatocyte injury in vitro.
10.3969/j.issn.1672-7347.2012.03.013
- Author:
Jun ZHOU
1
;
Qin WANG
;
Qunwei WANG
;
Wenbin DUAN
Author Information
1. Department of Minimal Invasive Surgery, Second Xiangya Hospital, Central South University, Changsha 410011, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Bridged Bicyclo Compounds, Heterocyclic;
pharmacology;
Cell Proliferation;
Chick Embryo;
DNA-Binding Proteins;
metabolism;
Hepatocytes;
cytology;
metabolism;
pathology;
Interleukin-6;
genetics;
metabolism;
L-Lactate Dehydrogenase;
genetics;
metabolism;
Lipopolysaccharides;
antagonists & inhibitors;
Male;
NF-kappa B;
metabolism;
Primary Cell Culture;
Protective Agents;
pharmacology;
Rats;
Rats, Sprague-Dawley;
Tumor Necrosis Factor-alpha;
genetics;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2012;37(3):285-289
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To study the effects of norcantharidin (NCTD) on lipopolysaccharide (LPS)-induced hepatocyte injury and the expression of TNF-α and IL-6 in vitro.
METHODS:Hepatocytes were isolated from male Sprague-Dawley rats by collagenase perfusion. LPS at concentration of 40 mg/L was used to induce injury to the cultured cells, and NCTD (0.5, 1.0, 2.5 μg/mL) was added at the same time. After 24 h of incubation, the cell proliferation rates were detected by MTT. LDH, TNF-α and IL-6 were measured by appropriate reagent kits.NF-κB DNA binding activity was measured.
RESULTS:40 mg/L LPS caused a 27% growth inhibition in primary hepatocytes. LDH leakage was 20- fold higher in NCTD-treated hepatocytes than in normal ones. TNF-α and IL-6 expression significantly increased. In cells treated with NCTD at doses of 0.5, 1.0 and 2.5 μg/mL, LDH leakage, TNF-α and IL-6 expression, and NF-κB DNA binding activity were attenuated in a dose dependent manner.
CONCLUSION:NCTD protects hepatocytes from injury induced by LPS; the protection is associated with suppression of the inflammatory cytokine TNF-α and IL-6.
