Protective effects of vasoactive intestinal peptide on septic shock rats.
- Author:
Jiang-feng QIU
1
;
Zhi-qi ZHANG
;
Wei CHEN
;
Zhi-yong WU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Blood Pressure; drug effects; Disease Models, Animal; Enzyme-Linked Immunosorbent Assay; Interleukin-10; blood; Male; Neuroprotective Agents; administration & dosage; therapeutic use; Random Allocation; Rats; Rats, Sprague-Dawley; Shock, Septic; blood; mortality; prevention & control; Survival Rate; Tumor Necrosis Factor-alpha; metabolism; Vasoactive Intestinal Peptide; administration & dosage; therapeutic use
- From: Chinese Journal of Surgery 2007;45(3):196-199
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the protective effects of vasoactive intestinal peptide (VIP) on septic shock rats and explore its possible mechanism.
METHODSCecal ligation and puncture (CLP) was performed to produce septic shock rat model. Thirty adult Sprague-dawley rats were randomly divided into 3 groups with 10 animals in each group: sham operation group, CLP group and VIP group. The rats in VIP group were given intravenous injection of VIP (5 nmol per rat) instantly after the CLP operation. Then the mean arterial pressure (MAP) was monitored consistently and survival rate was observed. Blood samples were obtained from femoral artery for measuring the serum concentrations of tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) by using enzyme-linked immunosorbent assays (ELISA). Organs (lung, kidney and intestine) were harvested for pathological examination.
RESULTSAt each time point after 8 h, the MAP of VIP rats was significantly higher than that in CLP rats (P<0.05). In VIP group rats, the serum TNF-alpha concentration was decreased meanwhile IL-10 level was increased with markedly alleviated organic pathological injuries and the survival rate was obviously raised.
CONCLUSIONSVIP exerts protective effects on septic shock rats through inhibiting production of proinflammatory factors and stimulating the production of anti-inflammatory cytokines.
