Protective effects of propofol pretreatment on rat neurons against anoxic-reoxygenated injury
- VernacularTitle:异丙酚预先给药对缺氧复氧鼠脑神经元的保护作用
- Author:
Jun CHEN
;
Guolin WANG
- Publication Type:Journal Article
- Keywords:
Propofol;
Neurons;
Cell hypoxia;
Nitric oxide;
Heat shock proteins 70;
Oxygen
- From:
Chinese Journal of Anesthesiology
1996;0(08):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of propofol on cultured primary neurons isolated from fetal Wistar rats against anoxic-reoxygenated injury and its neuro-protective mechanisms at cellular level. Methods Neuronal cells were isolated from brains of fetal Wistar rats and cultured for 12 days. The cultured neuronal cells were randomly divided into 4 groups : (Ⅰ) control group; (Ⅱ) anoxic-reoxygenated group in which neurons were exposed to 95% N2 + 5% CO2 at 37?for 3O min; (Ⅲ) propofol pretreatmenl group in which propofol was added to the culture medium (the final concentrations of propofol were 14 ?mol?L-1) 1 h before exposure to anoxia. (Ⅳ) propofol pretreatment group (the final concentrations of propofol were 56 ?mol?L-1) . Neuronal activity was detected by MTT analysis and NO output was assayed with nitrate reductase method at 1, 2, 4, 6 and 24 h after reoxygenation. The synthesis of heat shock protein (Hsp)70 mRNA was measured by in situ hybridization technique and the synthesis of Hsp70 was measured by immuno-histochemical technique at 1, 3, 8, 24, 48 h and 72 h after reoxygenation.Results (1) 30-min anoxia decreased neuronal activity, increased NO output and significantly increased the synthesis of Hsp70 mRNA and Hsp70. The expression of Hsp70 mRNA reached its peak at 24 h after reoxygenation and that of Hsp70 at 48 h after reoxygenation. (2) Propofol pretreatment significantly increased neuronal activity at 1, 2, 4, 6 and 24 h after reoxygenation and decreased NO output at 1, 2 and 4 h after reoxygenation compared with those in anoxia-reoxygenated group. (3) The synthesis of Hsp70 mRNA was significantly increased and accelerated by pretreatment with both concentrations of propofol but the synthesis of Hsp70 was significantly increased and accelerated by pretreatment with 56?mol?L-1 propofol only. Conclusion Propofol pretreatment can inhibit anoxia-reoxygenation injury to neurons by decreasing NO output and increasing expression of Hsp70 through inducing the synthesis of Hsp70 at both transcription and translation levels.
