Chen Gang, Fu Qiang, Cao Jiangbei, Mi Weidong
Anesthesia and Operation Center, PLA General Hospital, Beijing 100853, China.
Neural Regen Res. 2012 Jul 25;7(21):1645-9. doi: 10.3969/j.issn.1673-5374.2012.21.007.
We intraperitoneally injected 10 and 50 mg/kg of propofol for 7 consecutive days to treat a rat model of chronic cerebral ischemia. A low-dose of propofol promoted the expression of brain-derived neurotrophic factor, tyrosine kinase receptor B, phosphorylated cAMP response element binding protein, and cAMP in the hippocampus of aged rats with chronic cerebral ischemia, but a high-dose of propofol inhibited their expression. Results indicated that the protective effect of propofol against cerebral ischemia in aged rats is related to changes in the expression of brain-derived neurotrophic factor and tyrosine kinase receptor B in the hippocampus, and that the cAMP-cAMP responsive element binding protein pathway is involved in the regulatory effect of propofol on brain-derived neurotrophic factor expression.
我们连续7天腹腔注射10毫克/千克和50毫克/千克的丙泊酚来治疗慢性脑缺血大鼠模型。低剂量丙泊酚促进慢性脑缺血老龄大鼠海马中脑源性神经营养因子、酪氨酸激酶受体B、磷酸化cAMP反应元件结合蛋白和cAMP的表达,但高剂量丙泊酚抑制它们的表达。结果表明,丙泊酚对老龄大鼠脑缺血的保护作用与海马中脑源性神经营养因子和酪氨酸激酶受体B表达的变化有关,且cAMP-cAMP反应元件结合蛋白通路参与丙泊酚对脑源性神经营养因子表达的调节作用。