Effect of Dexamethasone on NF-kB Activation, Tumor Necrosis Factor Formation, and Glucose Dyshomeostasis in Septic Rats
| Autor: | William Schumer, Sheila Llanes, Cheow K. Chang |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Blood Glucose
Male endocrine system medicine.medical_specialty Time Factors medicine.drug_class medicine.medical_treatment Peritonitis Biology Dexamethasone Rats Sprague-Dawley Sepsis chemistry.chemical_compound Internal medicine medicine Animals Homeostasis RNA Messenger Glucocorticoids Base Sequence Glycogen Tumor Necrosis Factor-alpha NF-kappa B Nuclear Proteins Blotting Northern medicine.disease Rats Disease Models Animal Steroid hormone Glucose Endocrinology Cytokine Gene Expression Regulation Liver chemistry Corticosteroid Surgery Tumor necrosis factor alpha Oligonucleotide Probes Phosphoenolpyruvate carboxykinase Phosphoenolpyruvate Carboxykinase (ATP) hormones hormone substitutes and hormone antagonists medicine.drug |
| Zdroj: | Journal of Surgical Research. 72:141-145 |
| ISSN: | 0022-4804 |
| Popis: | Glucocorticoids are potent anti-inflammatory and immunosuppressive therapeutic agents. The protective effect of dexamethasone (DEX) on hepatic phosphoenolpyruvate carboxykinase (PEPCK) transcript level, hepatic NF-kB (nuclear factor-kB) activation, and serum tumor necrosis factor α (TNF) formation was investigated in peritoneal sepsis induced by cecal incision in rats. For the control the rats were sham-operated with laparotomies only. Each group (N= 6) was pretreated with either normal saline (NS) or DEX before surgery (NS/Sham, NS/Sepsis, DEX/Sham, and DEX/Sepsis). At 3 hr post cecal incision, DEX treatment inhibited sepsis-induced hepatic NF-kB activation by 23%, suppressed circulating TNF by 50%, reduced serum glucose by 36%, reduced hepatic glycogen depletion by 76%, and attenuated PEPCK mRNA level. These findings suggested that DEX treatment was beneficial in attenuating glucose dyshomeostasis and significantly inhibited two sepsis-induced inflammatory mediators, NF-kB and TNF, in the early phase of peritoneal sepsis. However, in the late (6 hr) septic phase, DEX treatment inhibited serum TNF by 69%, but had no effect on NF-kB activation, glycogen depletion, and PEPCK mRNA level suggesting liver function failure injury. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Full Text from ScienceDirect