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| 1 | Effect of cholecystokinin on cytokines during endotoxic shock in rats显示文摘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. | Yi-Ling Ling~1 Ai-Hong Meng~1 Xiao-Yun Zhao~1 Bao-En Shan~2 Jun-Lan Zhang~1 Xiao-Peng Zhang~3 1 Department of Pathophysiology,Hebei Medical University,Shijiazhuang 050017,Hebei Province,China2 Research Center of Fourth Hospital,Hebei Medical University,Shijiazhuang 050000,Hebei Province,China3 Department of Chest Surgery of Hebei Provincial People’s Hospital,Shijiazhuang 050000,Hebei Province,China | 2001 | World Journal of Gastroenterology2001，7，5： | 31 |
| 2 | Levels of vasoactive intestinal peptide,cholecystokinin and calcitonin gene-related peptide in plasma and jejunum of rats following traumatic brain injury and underlying significance in gastrointestinal dysfunction显示文摘AIM:To study the alterations of brain-gut peptides following traumatic brain injury (TBI) and to explore the underlying significance of these peptides in the complicated gastrointestinal dysfunction.METHODS:Rat models of focal traumatic brain injury were established by impact insult method,and divided into 6 groups (6 rats each group) including control group with sham operation and TBI groups at postinjury 3,12,24,72h,and d 7.Blood and proximal jejunum samples were taken at time point of each group and gross observations of gastrointestinal pathology were recorded simultaneously.The levels of vasoactive intestinal peptide (VIP) in plasma,calcitonin gene-related peptide (CGRP) and cholecystokinin (CCK) in both plasma and jejunum were measured by enzyme immunoassay (EIA). Radioimmunoassay (RIA) was used to determine the levels of VIP in jejunum.RESULTS:Gastric distension,delayed gastric emptying and intestinal dilatation with a large amount of yellowish effusion and thin edematous wall were found in TBI rats through 12h and 72h, which peaked at postinjury 72h. As compared with that of control group (247.8±29.5ng/L), plasma VIP levels were significantly decreased at postinjury 3,12 and 24h (106.7±34.1ng/L, 148.7±22.8ng/L,132.8±21.6ng/L,respectively),but significantly increased at 72h (405.0±29.8ng/L) and markedly declined on d 7 (130.7±19.3ng/L).However,Plasma levels CCK and CGRP were significantly increased through 3h and 7d following TBI (126-691% increases),with the peak at 72 h.Compared with control (VIP, 13.6±1.4ng/g;CGRP,70.6±17.7ng/g);VIP and CGRP levels in jejunum were significantly increased at 3h after TBI (VIP,35.4±5.0ng/g;CGRP,103.8±22.1ng/g),and declined gradually at 12 h and 2d h (VIP,16.5±1.8ng/g,5.5±1.4ng/g;CGRP,34.9±9.7ng/g, 18.5±7.7ng/g),but were significantly increased again at 72 h (VIP, 48.7±9.5ng/g; CGRP,142.1±24.3ng/g),then declined in various degrees on d 7 (VIP, 3.8±1.1ng/g; CGRP, 102.5±18.1ng/g).The CCK levels in jejunum were found to change in a similar trend as that in plasma with the concentrations of CCK significantly increased following TBI (99-517% increases) and peaked at 72h.CONCLUSION:Traumatic brain injury can lead to significant changes of brain-gut peptides in both plasma and small intestine, which may be involved in the pathogenesis of complicated gastrointestinal dysfunction. | Chun-HuaHang Ji-XinShi Jie-ShouLi WeiWu wei-QinLi Hong-XiaYin | 2004 | World Journal of Gastroenterology2004，10，6： | 25 |
| 3 | Significance of changes of gastrointestinal peptides in blood and ileum of experimental spleen deficiency rats显示文摘AIM: To explore the mechanism of spleen deficiency (SD)by studying the relationship of gastro-intestinal peptides level and ileal electro-mechanical activity of SD rats and cold restrain rats.METHODS: (1) spleen deficiency (SD) model was established by feeding Houpou:Zhishi: Dahuang in the ratio of 3:3:2,3 ml/time, for 42 days. (2) The cold restrain stress model:Animals were restrained on grille and placed in a cool water at 18 °C for 3 h. (3) Substance P (SP) and vasoactive intestinal peptide (VIP) levels in all layers of initial part of ileum and blood in rats were measured by radioimmunoassays (RIA)while changes of electric activity and motility in ileum of rats were recorded with electrode and strain gauge.RESULTS: SP levels in ileum and blood of experimental SD rats were significantly higher than that of the control groups (9.89±5.65 vs 1.22±1.18, P<0.005, in ileum; 22.7±3.95 vs6.60±1.47, P<0.001, in blood) while the VIP levels of theSD rats were significantly lower than that of the controls (3.50±2.01 vs9.10±4.91, P<0.05, in ileum; 229.8±62.4 vs560.4±151.3, P<0.001, in blood). As compared with the controls, the average frequency of slow electric waves (21.3±0.96 vs18.2±2.28, P<0.05) and motility (21.5±0.58vs 18±2.65, P<0.005) of SD rats increased obviously and the frequency of fast waves of SD rat also increased. In spontaneous recovery cases, SP levels recovered significantly (compared with the SD groups, 2.99±0.62 vs 9.89±5.65,P<0.001, in ileum; 14.4±4.22 vs 22.7±3.95, P<0.001, in blood) but did not drop to normal. After the SD rats treated with Chinese herbs (Jiawei Sijun zi Tang), SP improved (compared with SD cases, 2.20±1.25 vs9.89±5.65, (P<0.001),in ileum; 10.7±1.88 vs 22.7±3.95, (P<0.001), in blood)and VIP in blood also improved (compared with SD rats,485.7±229.0 vs 229.8±62.4, P<0.01) while the amplitude of motility decreased apparently (compared with the SD rats,0.64±0.096 vs0.89±0.15, P<0.01). The ileal SP levels of cool stress didn't change while the ileal VIP levels of cool stress became significantly lower than that of the control groups (2.87±0.87 vs 9.10±4.91, P<0.01). The blood SP levels of cool stress were significantly higher (15.60±1.83vs 6.60±1.47, P<0.001) whereas the blood VIP levels of cool stress were significantly lower than that of the control group (153.4±70.46 vs 560.4±151.30, P<0.001).CONCLUSION: Changes of SP and VIP levels in initial part of ileum and blood of SD rats and cool stress rats may be closely related to the gastrointestinal motility disorders presented in SD and cool stress rats. the Chinese herbs (Jiawei Sijun zi Tang) currently used have partially therapeutic effect. | Li-Sheng Li Rui-Yao Qu Wei Wang Hua Guo Department of Physiology,Capital University of Medical Sciences,100054,Beijing,China | 2003 | World Journal of Gastroenterology2003，9，3： | 17 |
| 4 | Anti-intlammatory effect of cholecystokinin ana its signal transduction mechanism in endotoxic shock rat显示文摘AIM: To study the anti-inflammatory effects ofcholecystokinin-octapeptide (CCK-8) onlipopolysaccharide (LPS)-induced endotoxic shock (ES)and further investigate its signal transduction pathwaysinvolving p38 mitogen-activated protein kinase (MAPK)METHODS: Eighty-four rats were divided randomly intofour groups: LPS (8 mg @ kg-1, iv) induced ES; CCK-8(40 μg @ kg-1, iv) pretreatment 10 min before LPS (8mg @ kg-1); CCK-8(40 μ g @ kg-1, iv) or normal saline(control) groups.The inflammatory changes of lung andspleen, phagocytic function of alveolar macrophage,quantification of inflammatory calls in bronchoalveolarlavage (BAL) were investigated in rats by usinghematoxylin and eosin (HE) staining, phagocytosis ofCandida albicans and differential cell counting. Nitricoxide (NO) production in serum, lung and spleen wasmeasured with the Griess reaction. The mechanisminvestigated by Western blot.RESULTS: Inflammatory changes of lung and spleeninduced by LPS were alleviated by CCK-8, the increaseof NO induced by LPS in serum, lung and spleen wassignificantly inhibited and the neutrophil infiltration inBAL was significantly reduced by CCK-8. The numberof neutrophils was (52±10)× 106 cells. L-1 in LPS group,while it decreased to (18±4)×106 cells@ L-1 in CCK-8+LPS (P<0.01). The phagocytic rate of CCK-8 groupincreased to (62.49±9.49) %, compared with controlgroup (48.16±14.20) %, P<0.05. The phagocytosisrate was (85.14±4.64) % in LPS group, which reducedto (59.33±3.14) % in CCK-8+LPS group (P<0.01). Theresults of phagocytosis indexes showed similar changes.CCK-8 may play an important role in increasing theexpression of p38 MAPK and decreasing the degradation of IκB-αin Iung and spleen of ES rats.CONCLUSION: CCK-8 can result in anti-inflammatoryeffects, which may be related to activation of p38 MAPK and inhibition on the degradation of IκB-α. | Ai-Hong Meng Yi-Ling Ling Jun-Lan Zhang Department of Pathophysiology,Hebei Medical University,Shijiazhuang 050017,Hebei Province,China Xiao-Peng Zhang Department of Cardiothoracic Surgery,Hebei Provincial People’s Hospital,Shijiazhuang 050071,Hebei Province,China | 2002 | World Journal of Gastroenterology2002，8，4： | 15 |
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