Glutamine prevents apoptosis in intestinal epithelial cells and induces differential protective pathways in heat and oxidant injury models
| Autor: | Diana K. Stutzman, Alyssa R. Kallweit, Paul E. Wischmeyer, Christine Baird |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
medicine.medical_specialty
Hot Temperature Cell Survival Glutamine HSP27 Heat-Shock Proteins Medicine (miscellaneous) Apoptosis Biology medicine.disease_cause Cell Line Mediator Western blot Internal medicine Heat shock protein medicine Animals HSP70 Heat-Shock Proteins Intestinal Mucosa Cell Proliferation chemistry.chemical_classification Nutrition and Dietetics medicine.diagnostic_test Caspase 3 Cell Differentiation Epithelial Cells Hydrogen Peroxide Molecular biology Amino acid Rats Intestines Oxidative Stress Endocrinology chemistry Cell culture Heme Oxygenase (Decyclizing) Oxidative stress |
| Zdroj: | JPEN. Journal of parenteral and enteral nutrition. 36(5) |
| ISSN: | 1941-2444 |
| Popis: | BACKGROUND Glutamine (GLN) can decrease mortality and length of hospital stay in the critically ill. GLN protects via enhancing protective heat shock proteins (HSPs) in heat stress (HS). GLN's effect on HSPs in oxidant injury and apoptosis remains to be elucidated. The purpose of this study was to determine if GLN protects via decreasing apoptosis during both heat and oxidative stress. METHODS IEC-18 cells were treated (15 minutes) with 0 mM GLN (control cells [CTs]) or 8 mM GLN and exposed to either lethal injury (44°C for 50 minutes or 4 mM H(2)O(2) for 30 minutes) or nonlethal injury (43°C for 45 minutes or 600 µM H(2)O(2) for 30 minutes). Survival was determined via MTS assay. Injured groups were normalized to noninjured controls. HSPs and cleaved caspase-3 (CC3), a key mediator for apoptosis, were evaluated via Western blot following a 3-hour recovery. RESULTS MTS assays showed GLN increased survival 4- to 5-fold (P < .001 vs HS CT or H(2)O(2)). Western blot showed GLN increased all 3 HSPs in HS (P < .001 vs HS CTs) but only HSP32 during oxidant injury (P < .02 vs H(2)O(2) only). GLN decreased CC3 in both injuries (P < .03 vs non-GLN-treated cells). CONCLUSIONS GLN protects intestinal cells from both heat and oxidant injury. HSP25, 32, and 70 levels increased with GLN during HS, but in oxidant injury, only HSP32 increased, suggesting GLN's mechanism of protection may vary in different models of injury. In both injuries, GLN lowered the expression of CC3, indicating prevention of apoptosis may be a key mechanism by which GLN protects. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text