OBJECTIVE: To explore the effect of somatostatin on serum interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha in lipopolysaccharide (LPS)-induced septic shock. METHODS: 24 male Wistar rats were randomly divided into 2 groups: intervention group (injected with LPS of Escherichia coli via femoral vein to induce septic shock) and control group (injected with LPS of Escherichia coli and then injected with somatostatin). The mean arterial pressure (MAP), heart rate, respiration rater, and mortality rate were observed before the injection of LPS, and 30, 90, and 360 min after the injection, and the serum IL-6 and TNF-alpha level were detected before the injection of LPS, 30, 90, and 360 min after the injection, or after the death. RESULTS: The IL-6 levels 30 min, 90 min, and 360 min after the injection of the somatostatin intervention group were 233 +/- 47, 212 +/- 33, and 217 +/- 26 mg/L respectively, all significantly lower then those of the control group (308 +/- 56, 260 +/- 32, and 230 +/- 92 mg/L, all P < 0.05). The TNF-alpha level 30 min, 90 min, and 360 min after the injection of the somatostatin intervention group were 450 +/- 82, 417 +/- 92, and 440 +/- 49 mg/L, all significantly lower than those of the control group (607 +/- 149, 517 +/- 74, and 474 +/- 219 mg/L, all P < 0.05). In addition, compared with the control group, the MAP of the somatostatin intervention group increased after 90 min. Two rats in the control group died 30 to 90 min later and 4 rats died 90 to 360 min later, however, 360 min later all rats in the somatostatin intervention group were alive (P = 0.0054). CONCLUSION: Somatostatin can inhibit the level of serum IL-6 and TNF-alpha in septic shock induced by LPS and improve the survival rate.
OBJECTIVE: To explore the effect of somatostatin on serum interleukin (IL)-6 and tumor necrosis factor (TNF)-alpha in lipopolysaccharide (LPS)-induced septic shock. METHODS: 24 male Wistar rats were randomly divided into 2 groups: intervention group (injected with LPS of Escherichia coli via femoral vein to induce septic shock) and control group (injected with LPS of Escherichia coli and then injected with somatostatin). The mean arterial pressure (MAP), heart rate, respiration rater, and mortality rate were observed before the injection of LPS, and 30, 90, and 360 min after the injection, and the serum IL-6 and TNF-alpha level were detected before the injection of LPS, 30, 90, and 360 min after the injection, or after the death. RESULTS: The IL-6 levels 30 min, 90 min, and 360 min after the injection of the somatostatin intervention group were 233 +/- 47, 212 +/- 33, and 217 +/- 26 mg/L respectively, all significantly lower then those of the control group (308 +/- 56, 260 +/- 32, and 230 +/- 92 mg/L, all P < 0.05). The TNF-alpha level 30 min, 90 min, and 360 min after the injection of the somatostatin intervention group were 450 +/- 82, 417 +/- 92, and 440 +/- 49 mg/L, all significantly lower than those of the control group (607 +/- 149, 517 +/- 74, and 474 +/- 219 mg/L, all P < 0.05). In addition, compared with the control group, the MAP of the somatostatin intervention group increased after 90 min. Two rats in the control group died 30 to 90 min later and 4 rats died 90 to 360 min later, however, 360 min later all rats in the somatostatin intervention group were alive (P = 0.0054). CONCLUSION:Somatostatin can inhibit the level of serum IL-6 and TNF-alpha in septic shock induced by LPS and improve the survival rate.
Authors: Mitra Khumbatta; Bahrom Firozgary; David John Tweardy; Joel Weinstock; Gohar Firozgary; Zal Bhatena; Tushar Bulsara; Ricardo Siller; Prema Robinson Journal: Biomed Res Int Date: 2014-07-09 Impact factor: 3.411