Original Research
Copyright ©The Author(s) 2001. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Oct 15, 2001; 7(5): 667-671
Published online Oct 15, 2001. doi: 10.3748/wjg.v7.i5.667
Effect of cholecystokinin on cytokines during endotoxic shock in rats
Yi-Ling Ling, Ai-Hong Meng, Xiao-Yun Zhao, Bao-En Shan, Jun-Lan Zhang, Xiao-Peng Zhang
Yi-Ling Ling, Ai-Hong Meng, Xiao-Yun Zhao, Jun-Lan Zhang, Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, Hebei Province, China
Bao-En Shan, Research Center of Fourth Hospital, Hebei Medical University, Shijiazhuang 050000, Hebei Province, China
Xiao-Peng Zhang, Department of Chest Surgery of Hebei Provincial People’s Hospital, Shijiazhuang 050000, Hebei Province, China
Author contributions: All authors contributed equally to the work.
Correspondence to: Professor Yi-Ling Ling, Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017, Hebei Province, China. LingYL20@sina.com.cn
Telephone: +86-311-6052263
Received: June 3, 2001
Revised: August 6, 2001
Accepted: August 20, 2001
Published online: October 15, 2001

AIM: To study the effect of cholecystokinin-octapeptide (CCK-8) on systemic hypotension and cytokine production in lipopolysaccharide (LPS)-induced endotoxic shock (ES) rats.

METHODS: The changes of blood pressure were observed using physiological record instrument in four groups of rats: LPS (8 mg•kg¯¹, iv) induced ES; CCK-8 (40 μg•kg¯¹, iv) pretreatment 10 min before LPS (8 mg•kg¯¹); CCK-8 (40 μg•kg¯¹, iv) or normal saline (control) groups. Differences in tissue and circulating specificity of the proinflammatory cytokines (TNF-α, IL-1β and IL-6) were assayed with ELISA kits.

RESULTS: CCK-8 reversed LPS-induced decrease of mean artery blood pressure (MABP) in rats. Compared with control, LPS elevated the serum level of IL-6 significantly (3567 ± 687) ng•L¯¹vs 128 ± 22 ng•L¯¹, P < 0.01), while contents of TNF-αβ elevated significantly (277 ± 86 ng•L¯¹vs not detectable and 43 ± 9 ng•L¯¹vs not detectable, P < 0.01) but less extent than IL-6. CCK-8 significantly inhibited the LPS-induced increase in serum TNF-α, IL-1β and IL-6. LPS elevated spleen and lung content of IL-1β significantly (5184 ± 85 ng•L¯¹vs 1047 ± 21 ng•L¯¹ and 4050 ± 614 ng•L¯¹vs not detectable, P < 0.01), while levels of TNF-α and IL-6 also rose significantly but in less extent than IL-1β. CCK-8 inhibited the LPS-induced increase of the cytokines in spleen and lung. In the heart, CCK-8 significantly inhibited LPS-induced increase of TNF-α (864 ± 123 ng•L¯¹ in CCK-8 + LPS group vs 1599 ± 227 ng•L¯¹ in LPS group, P < 0.01), and IL-1β (282 ± 93 ng•L¯¹ in CCK-8+LPS group vs 621 ± 145 ng•L¯¹ in LPS group, P < 0.01).

CONCLUSION: CCK-8 reverses ES, which may be related to its inhibitory effect on the overproduction of cytokines.

Keywords: sincalide/pharmacology, lipopolysaccharides, shock, septic/drug therapy, shock, septic/blood, tumor necrosis factor/analysis, interleukins/blood, hypotension/drug therapy, hypotension/etiology