Effects of astilbin on the expression of TNF alpha and IL-10 in liver warm ischemia-reperfusion injury.
- Author:
Rong-Kai LIN
1
;
Cheng-Hua ZHANG
;
Ning MU
;
Qing-Yong YAO
;
Shao-Liang DONG
;
Qiu-Bao AI
;
Quan-Xing WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Flavonols; pharmacology; Interleukin-10; metabolism; Liver; drug effects; metabolism; Male; Mice; Mice, Inbred C57BL; Reperfusion Injury; etiology; metabolism; Tumor Necrosis Factor-alpha; metabolism; Warm Ischemia
- From: Chinese Journal of Hepatology 2010;18(6):463-466
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVESTo investigate the effects of astilbin on the expressions of TNF alpha and IL-10 during liver warm ischemia-reperfusion injury.
METHODSC57BL/ 6 mice were randomly divided into 4 groups (n = 8): sham-operated group (Sham), model control group(I/R), low dosage of astilbin treatment group (10 mg/kg) and high dosage of astilbin (40 mg/kg) treatment group. The treatment group mice were intraperitoneally injected with 10 or 40 mg/kg astilbin 24 hours and one hour before Ischemia, the hepatic ischemia-reperfusion model were thus established. After jn90 of min ischemia and 6 h reperfusion of the partial hepatic lobe, the expressions of TNF alpha and IL-10 in liver tissues collected from the experimental groups were detected by Western blot and semiquantitative RT-PCR.
RESULTSThe expression of TNF alpha protein in liver tissues gradually decreased in treatment groups (low and high dosages of astilbin treatment groups) as compared to the I/R model control group. Similar results were observed in the mRNA expressions of these genes as determined by semiquantitative RT-PCR (P less than 0.05 for low dosage group; P less than 0.01 for high dosage group). Compared with the I/R model control group, the expression of IL-10 was increased in both treatment groups (low dosage group P less than 0.05; large dosage group P less than 0.01).
CONCLUSIONTreatment with astilbin decreases TNF alpha expression but induces IL-10 expression in liver during warm ischemia-reperfusion injury.