Function of STAT3 activation in the proliferation of rat biliary epithelial cells induced by lipopolysaccharide
- VernacularTitle:STAT3活化在脂多糖刺激大鼠胆管上皮细胞增殖中的作用
- Author:
Liping CHEN
;
Yibin GUO
;
Ruiwu DAI
;
Kun LI
;
Shuguang WANG
;
Jiahong DONG
- Publication Type:Journal Article
- Keywords:
Lipopolysaccharides;
Bile ducts;
Epithelial cells;
Interleukin-6;
Signal transduction
- From:
Chinese Journal of Pathophysiology
1989;0(05):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the significance of signal transducers and activation of transcription 3 (STAT3) in proliferation of rat intrahepatic biliary epithelial cell (BEC) induced by LPS. METHODS: Male Wistar rats were randomly divided into three groups: normal control, endotoxemia (LPS) group and rapamycin (RPM) group. Plasma LPS was detected by kinetic turbidimetric limulus test at 6 h, 12 h, 24 h, 48 h, and 72 h after injury. IL-6 secretion in liver homogenate was determined by ELISA. P-STAT3 expression in BEC was analyzed by laser scan confocal microscopy. Proliferation of BEC was detected by immunohistochemistry. RESULTS: Plasm LPS level was maximum at 6 h [(318?115) EU/L] after injury and descended closely to control level at 48 h [(29?11) EU/L]. IL-6 expression peaked at 12 h (653.4 ng/g?168.8 ng/g protein) and closed to control level at 72 h (0.013 ng/g?0.006 ng/g protein). In LPS group, significant direct correlation between p-STAT3 expression in BEC and IL-6 level in liver homogenate was found. BEC proliferation was induced by LPS at 12 h (5.2?0.5) and reached the maximum level at 24 h, which was higher than the control level even at 72 h, while RPM abrogated STAT3 activation and BEC proliferation induced by LPS. CONCLUSION: LPS induces liver IL-6 expression, which might activate BEC proliferation through STAT3 pathway.
