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The pituitary adenylate cyclase-activating polypeptide (PACAP) protects adrenal function in septic rats administered etomidate
| Content Provider | Semantic Scholar |
|---|---|
| Author | Zhang, Yanmin Xiong, Jun-Yu Liu, Shan Lv, Shen |
| Copyright Year | 2016 |
| Abstract | BACKGROUND Both hyperinflammation during sepsis and etomidate can suppress adrenal function. In this study, we explored whether treatment with pituitary adenylate cyclase-activating polypeptide (PACAP) relieves adrenal suppression in cecal ligation and puncture (CLP)-induced septic rats. MATERIALS AND METHODS Female Sprague-Dawley rats were randomly divided into five groups (n=7 per group), including the sham group, sepsis group (CLP group), sepsis and etomidate group (CLP+ETO group), PACAP group, and etomidate alone group (ETO group). Rats were sacrificed on the third day of sepsis, and blood and adrenal gland samples were obtained for further testing. RESULTS The PACAP reduced the apoptosis rate of adrenal cells and peripheral lymphocytes, improving adrenal function, inhibiting the secretion of interferon gamma (IFN-γ) from peripheral lymphocytes, and slightly relieving the suppression of the adrenal function induced by the injection of etomidate in sepsis. CONCLUSION In septic conditions, the PACAP protects the adrenal gland by regulating peripheral inflammation, which slightly relieves the toxic effects of etomidate on adrenal function. |
| Starting Page | 53 |
| Ending Page | 59 |
| Page Count | 7 |
| File Format | PDF HTM / HTML |
| DOI | 10.1016/j.npep.2016.03.005 |
| PubMed reference number | 27103538 |
| Journal | Medline |
| Volume Number | 58 |
| Alternate Webpage(s) | https://api.elsevier.com/content/article/pii/S0143417916300300 |
| Alternate Webpage(s) | https://www.sciencedirect.com/science/article/pii/S0143417916300300?dgcid=api_sd_search-api-endpoint |
| Alternate Webpage(s) | https://doi.org/10.1016/j.npep.2016.03.005 |
| Journal | Neuropeptides |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |