Inhibitory effect of cholecystokinin-octapeptide on production of cytokines in the lung of endotoxic shock rats.
- Author:
Ai-Hong MENG
1
;
Yi-Ling LING
;
Xiao-Yun ZHAO
;
Jun-Lan ZHANG
;
Qiu-Hong WANG
Author Information
1. Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017.
- Publication Type:Journal Article
- MeSH:
Animals;
Cytokines;
biosynthesis;
Lung;
metabolism;
Male;
Mitogen-Activated Protein Kinases;
biosynthesis;
physiology;
Rats;
Rats, Sprague-Dawley;
Shock, Septic;
drug therapy;
metabolism;
Sincalide;
pharmacology;
p38 Mitogen-Activated Protein Kinases
- From:
Acta Physiologica Sinica
2002;54(2):99-102
- CountryChina
- Language:Chinese
-
Abstract:
To study the effect of cholecystokinin-octapeptide (CCK-8) on systemic hypotension and cytokine production in serum and lung of endotoxic shock (ES) rats induced by lipopolysaccharide (LPS) and investigate its signal transduction mechanism of p38 mitogen-activated protein kinase (MAPK), the changes in mean arterial pressure (MAP) were observed by using a polygraph in four groups of SD rats: group of LPS (8 mg/kg i.v.) induced ES, group of CCK-8 (40 microg/kg i.v.) pretreatment 10 min before LPS (8 mg/kg) administration, group of CCK-8 (40 microg/kg i.v.) only, and normal saline (control) group; the contents of proinflammatory cytokines (TNF-alpha, IL-1 beta and IL-6) in the lung and serum were assayed using ELISA kits; and p38 MAPK was detected by Western blot. The results showed that CCK-8 alleviated LPS-induced decrease in MAP of rats; compared with the control, LPS elevated the levels of TNF-alpha, IL-1 beta and IL-6 in serum and lung significantly, while CCK-8 significantly inhibited the LPS-induced increases in TNF-alpha, IL-1 beta and IL-6 in serum and lung. The activation of p38 MAPK in the lung of ES rats was enhanced by CCK-8 pretreatment. These results suggest that CCK-8 can alleviate the LPS-induced decrease in MAP of ES rats and exert an inhibitory effect on the overproduction of proinflammatory cytokines, and that p38 MAPK may be involved in its signal transduction mechanisms.
