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...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-a, IL-l3 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-1 vs 128_+22 ng.L-1, P＜0.01), while contents of TNF-a and IL- lβ elevated significantly (277 _± 86ng.L-1 vs not detectable and 43 ± 9 ng.L-1 vs notdetectable, P<0.01) but less extent than IL-6, CCK-8significantly inhibited the LPS-induced increase in serum TNF-a, IL-lβ and IL-6. LPS elevated spleen and lung content of IL-Iβ significantly (5184 ± 85 ng.L-1 vs 1047 ±21 ng.L-1 and 4050 ± 614 ng.L-1 vs not detectable,P＜0,01). while levels of TNF-a and IL-6 also rosesignificantly but in less extent than IL-lβ. 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-a (864 ± 123 ng. L-1 in CCK-8 +LPS group vs 1599_-227 ng-L-1 in LPS group, P＜0.01),and IL-lβ (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 relatedto its inhibitory effect on the overproduction of cytokines.展开更多
文摘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-a, IL-l3 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-1 vs 128_+22 ng.L-1, P＜0.01), while contents of TNF-a and IL- lβ elevated significantly (277 _± 86ng.L-1 vs not detectable and 43 ± 9 ng.L-1 vs notdetectable, P<0.01) but less extent than IL-6, CCK-8significantly inhibited the LPS-induced increase in serum TNF-a, IL-lβ and IL-6. LPS elevated spleen and lung content of IL-Iβ significantly (5184 ± 85 ng.L-1 vs 1047 ±21 ng.L-1 and 4050 ± 614 ng.L-1 vs not detectable,P＜0,01). while levels of TNF-a and IL-6 also rosesignificantly but in less extent than IL-lβ. 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-a (864 ± 123 ng. L-1 in CCK-8 +LPS group vs 1599_-227 ng-L-1 in LPS group, P＜0.01),and IL-lβ (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 relatedto its inhibitory effect on the overproduction of cytokines.
