Abstract

Objective To explore the possible mechanisms of the neuroprotective effect of dexamethasone(DEX) on neonatal rats with cerebral bypoxia-ischemia. Methods Sprague-Dawley (SD) pregnant rats were made to hypoxic ischemic brain damage (HIBD) model and randomly divided into: pretreatment groups of different doses (L-Dexl group, H-Dexl group); treatment groups of different doses (L-Dex2 group, H-Dex2 group); isotonic saline group (NS group) and normal group (NOR). The expressions of interleukin-1β(IL-1β) and myelin basic protein (MBP) in serum and brain tissue were measured, the number of apoptosis cells in brain tissue was counted, and the pathological changes of brain tissue in HIBD were observed. Results Compared with the NS group, the pathological changes of brain tissue in the pretreatment and treatment groups with different DEX doses were mild with neuron dendrite involution and Nissl body increase. The contents of MBP, IL-1β in serum and brain tissue in NS group 3 days after HIBD were (5.88 4±0. 46,34.25± 4. 65 ; 127. 97± 16.60,1060. 33±42.22)and the numbers of apoptosis were 13.27±0. 90 and 11.05±1.23, which were significantly higher than the NOR group (2.01±0. 12,10. 24±1.75; 41.21±4. 02,221.10± 30. 57; 0. 75±0. 17,P<0. 05). On 7 days after HIBD, the above parameters were decreased in the NS group, but remained higher than the NOR group (P<0. 05). The contents of MBP and IL-1β in in serum and brain Dex pretreated rats were (4. 30±0. 73,24. 10±3. 36,and 59. 89±6. 16,393. 68±31.46) and those in the treated groups(4. 48±0. 49,16. 98±1.32 and 50. 81±8. 32,405. 15±29. 02) were significantly lower than those in the NS group(5.88±0. 46,34. 25±4. 65 and 127.97±16. 60,1060. 33 ±42. 22,P<0. 05). No significant difference was shown between Dexl and Dex2 groups with the same dose. The apoptosis cell count in DEX pretreated and treated groups(7. 92± 1.64 and 8. 97± 0.81) were significantly less than those in the NS group (13. 27±0. 90, P<0. 05). Compared with thc pretreated groups, levels of apoptosis in treated groups were higher (P<0.05) and was dose dependent. Conclusions Variations of serum MBP reflect the degree of white matter damage. DEX might protect the brain from injury by inhibiting overexpression of IL-1β followed by alleviated systemic inflammatory reactions. Key words: Hypoxia-ischemia, brain; Dexamethasone; Apoptosis; Myelin basic proteins; Interleukin-1

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