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AIM:To study the effect of sulfated cholecystokinin-octapeptide(CCK-8)on systemic hypotension,gene andprotein expression of TNF-α in spleen of lipopolysaccharide(LPS)-induced endotoxic shock(ES)rats,and furtherinvestigate the signal transduction mechanism of p38mitogen-activated protein kinase(MAPK).METHODS:The changes of blood pressure were observedusing physiological record instrument in four groups of rats:LPS(S mg·kg~(-1),iv),CCK-8(40μg·kg~(-1),iv)pretreatment10 rain before LPS(8 mg·kg~(-1)),CCK-8(40μg·kg~(-1),iv)ornormal saline(control)group.The content of TNF-αinspleen was assayed 2 h after LPS administration usingELISA kit and the expression of TNF-α mRNA was examined30 min,2 h and 6 h after LPS administration by reversetranscribed polymerase chain reaction(RT-PCR).Activationof p3S MAPK was detected with Western blot 30 min afterLPS administration.RESULTS:CCK-8 reversed LPS-induced decrease of meanarterial pressure(MAP)in rats.The content of TNF-α inspleen was(282±30)ng·L~(-1)in control group,while itincreased to(941±149)ng·L~(-1)in LPS group,P<0.01.CCK-8 significantly inhibited the LPS-induced increase ofTNF-α content in spleen.It decreased to(462±87)ng·L~(-1)inCCK-8+LPS group,P<0.01.The expression of TNF-αmRNA 30 min and 2 h after treatment was stronger in LPSgroup,while it was lowered after CCK-8 pretreatment.Thep38 MAPK expression increased significantly in LPS group(5.84 times of control)and CCK-8 increased the activationof p38 MAPK in ES rats(10.74 times of control).CONCLUSION:CCK-8 reverses the decrease of MAP in ESrats and has inhibitory effect on the gene and proteinexpression of TNF-α in spleen,and p38 MAPK may beinvolved in its signal transduction mechanisms.
AIM: To study the effect of sulfated cholecystokinin-octapeptide (CCK-8) on systemic hypotension, gene and protein expression of TNF-α in spleen of lipopolysaccharide (LPS) -induced endotoxic shock (ES) rats, and further investigated the signal transduction mechanism of METHODS: The changes of blood pressure were observed using physiological record instrument in four groups of rats: LPS (S mg · kg -1, iv), CCK-8 (40 μg · kg -1) (-1), iv) pretreatment10min before LPS (8mg · kg -1), CCK-8 (40μg · kg -1, iv) ornormal saline (control) group.The content of TNF- αinspleen was assayed 2 h after LPS administration using ELISA kit and the expression of TNF-α mRNA was 30 min, 2 h and 6 h after LPS administration by reversetranscribed polymerase chain reaction (RT-PCR). Activation of p3S MAPK was detected with Western blot 30 min after LPS administration .RESULTS: CCK-8 reversed LPS-induced decrease of meanarterial pressure (MAP) in rats. The content of TNF-α inspleen was (282 ± 30) ng · L -1 in control group, while it was increased to (941 ± 149) ng · L -1 in LPS group, P <0.01.CCK-8 significantly inhibited the LPS-induced increase of TNF-α content in spleen. I decreased to (462 ± 87) ng · L -1 inCCK-8 + LPS group, P <0.01. The expression of TNF-α mRNA was 30 min and 2 h after treatment was stronger in LPS group, while it was reduced after CCK-8 pretreatment. p38 MAPK expression increased significantly in LPS group (5.84 times of control) and CCK-8 increased the activation of p38 MAPK in ES rats (10.74 times of control) .CONCLUSION: CCK-8 reverses the decrease of MAP in ESrats and has inhibitory effect on the gene and proteinexpression of TNF-α in spleen, and p38 MAPK may be in viral signal transduction mechanisms.