目的：采用常压间歇性低氧(intermittent hypoxia,IH)大鼠的动物模型，观察间歇性常压低氧预处理的促血管生成作用。方法:成年雄性Wistar大鼠25只，体重210～215 g，随机分为2大组:对照组(C组，n=5)和间歇性低氧预处理组(IH组，n=20)。IH组动物进行间歇性低氧预处理(4 h/d，间歇缺氧1 d者为IH1组，7 d者为IH2组，14 d者为IH3组，28 d者为IH4组)，按计划完成实验后测定心肌血管内皮生长因子(VEGF) 蛋白表达及毛细血管密度。结果：间歇性低氧预处理大鼠心肌VEGF蛋白表达增加，心肌毛细血管密度增高。结论：间歇性低氧预处理能促进大鼠心肌内的血管生成，其机制可能与心肌VEGF表达增高有关。
Objective To study the effects of hypoxic preconditioning on the glucose metabol ism of rat BMSCs and its underlying mechanism so as to provide the theoretical basis for the optimization of the stem-cell based therapy. Methods Density gradient centrifugation method was adopted to isolate rat BMSCs from neonatal SD rats (aged 1-3 days). BMSCs were cultured to 4th passage and divided into 4 groups based on different culture conditions: group A in normoxia condition for 24 hours, group B in 1% O2 for 24 hours, group C in 2-methoxyestradiol (20 μmol/L) for 24 hours before hypoxic preconditioning, and group D in hypoxia-inducible factor 1 (HIF-1) specific siRNA (50 μmol/L) for 12 hours before hypoxicpreconditioning. MTT method was appl ied to evaluate the prol iferation of BMSCs. Biochemical analyzer and Real-timefluorescent quantitative PCR were appl ied to detect the glucose uptake, lactate production, and HIF-1α mRNA and Glut-1mRNA levels of BMSCs. Results MTT showed that the absorbance (A) values were 387.67 ± 58.92, 322.50 ± 50.60, 297.00 ± 53.00, and 286.00 ± 41.00 in groups A, B, C, and D, respectively, showing no significant difference among 4 groups (P gt; 0.05). The levels of glucose uptake and lactate production were higher in group B than in groups A, C, and D, showing significant differences (P lt; 0.05); the levels of groups C and D were higher than those of group A, but showing no significant difference (P gt; 0.05). The mRNA expressions of HIF-1α and Glut-1 elevated significantly in group B when compared with those in group A (P lt; 0.05); groups C and D were significantly lower than group B (P lt; 0.05) and were significantly higher than group A (P lt; 0.05). Conclusion Hypoxic preconditioning can stimulate the glucose uptake and metabol ism of rat BMSCs, whose mechanism is probably related to up-regulating the mRNA expressions of HIF-1α and Glut-1.