论文部分内容阅读
AIM To study the effect of cholecystokinin-octapeptide(CCK-8)on systemic hypotension and cytokine productionin lipopolysaccharide(LPS)-induced endotoxic shock(ES)rats.METHODS The changes of blood pressure were observedusing physiological record instrument in four groups ofrats:LPS(8mg·kg~(-1),iv)induced ES;CCK-8(40μg·kg~1,iv)pretreatment 10min before LPS(8mg.kg~(-1));CCK-8(40μg·kg~(-1),iv)or normal saline(control)groups.Differences in tissue and circulating specificity of theproinflammatory cytokines(TNF-α,IL-1β and IL-6)wereassayed with ELISA kits.RESULTS CCK-8 reversed LPS-induced decrease of meanartery blood pressure(MABP)in rats.Compared withcontrol,LPS elevated the serum level of IL-6 significantly(3567±687ng·L~(-1) vs 128±22ng·L~1,P<0.01),whilecontents of TNF-α and IL-1β elevated significantly(277±86ng.L~1 vs not detectable and 43±9ng·L~1 vs notdetectable,P<0.01)but less extent than IL-6.CCK-8significantly inhibited the LPS-induced increase in serumTNF-α,IL-1β and IL-6.LPS elevated spleen and lungcontent of IL-1β significantly(5184±85ng·L~1 vs 1047±21ng·L~1 and 4050±614ng·L~1 vs not detectable.P<0.01),while levels of TNF-α and IL-6 also rosesignificantly but in less extent than IL-1β.CCK-8 inhibitedthe LPS-induced increase of the cytokines in spleen andlung.In the heart,CCK-8 significantly inhibited LPS-induced increase of TNF-α(864±123ng·L~1 in CCK-8+LPS group vs 1599±227ng·L~1 in LPS group,P<0.01),and IL-1β(282±93ng·L~1 in CCK-8+LPS group vs 621±145ng·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.
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 animals: LPS (8 mg · kg -1), iv) induced ES; CCK-8 (40 μg · kg -1, iv) pretreatment for 10 min before LPS (8 mg · kg -1) (-1), iv) or normal saline (control) groups. Differences in tissue and circulating specificity of the proinflammatory cytokines (TNF-α, IL-1β and IL-6) wereassayed with ELISA kits .RESULTS CCK-8 reversed LPS-induced LPS elevated the serum level of IL-6 significantly (3567 ± 687ng · L -1 vs 128 ± 22ng · L -1, P <0.01), whilecontents (MABP) (277 ± 86 ng.L ~ 1 vs not detectable and 43 ± 9 ng · L ~ 1 vs notdetectable, P <0.01) but less extent than IL-6.CCK-8 was significantly inhibited by the LPS -induced increase in serum TNF-α, IL-1β a nd IL-6.LPS elevated spleen and lung content of IL-1β 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 while levels of TNF-α and IL-6 also ROSEignificantly but in less extent than IL-1β.CCK-8 inhibited the LPS-induced increase of the cytokines in spleen and fluid.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.