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目的观察三七皂甙Rb1对缺氧缺血新生大鼠脑梗死体积、内源性一氧化碳(CO)水平及血红素加氧酶-1(HO-1)表达的影响,探讨三七皂甙Rb1抗脑缺血损伤作用及其可能的分子机制。方法 7日龄新生SD大鼠建立缺氧缺血性脑损伤(HIBD)动物模型,将动物随机分为4组:9 g.L-1盐水组,2 mg.kg-1三七皂甙Rb1组(低剂量组)、10 mg.kg-1三七皂甙Rb1组(中剂量组)、50 mg.kg-1三七皂甙Rb1组(高剂量组)。各组大鼠分别腹腔注射9 g.L-1盐水和不同剂量三七皂甙Rb1。心脏取血,检测全血碳氧血红蛋白(COHb)水平。检测其海马组织HO-1活性变化,采用反转录-PCR检测其海马HO-1 mRNA的表达。结果低剂量组、中剂量组、高剂量组与9 g.L-1盐水组比较,脑缺氧缺血后脑梗死体积显著减少。中剂量组与高剂量组、低剂量组相比,脑缺氧缺血后全血COHb水平显著升高,海马HO-1活性显著增加(Pa<0.05)。中剂量组大鼠海马HO-1 mRNA的表达水平明显高于其他各组(Pa<0.05)。结论三七皂甙Rb1可能通过增加COHb水平和脑局部HO-1活性改善缺氧缺血脑损伤。三七皂甙Rb1在脑缺氧缺血中的脑保护作用可能与增强脑局部HO-1 mRNA表达有关。
Objective To observe the effect of notoginsenoside Rb1 on the infarct volume, the level of endogenous carbon monoxide (CO) and the expression of heme oxygenase-1 (HO-1) in neonatal rats with hypoxic-ischemic brain damage Ischemic injury and its possible molecular mechanism. Methods Hypoxic-ischemic brain damage (HIBD) was induced in 7-day-old SD rats. The animals were randomly divided into 4 groups: 9 gL-1 saline group, 2 mg.kg-1 Panax Notoginseng saponin Rb1 group Dose group), 10 mg.kg-1 notoginsenoside Rb1 group (middle dose group), 50 mg.kg-1 notoginsenoside Rb1 group (high dose group). Rats in each group were intraperitoneally injected with 9 g.L-1 saline and different doses of Panax notoginsenoside Rb1. Blood was taken from the heart and whole blood carboxyhemoglobin (COHb) levels were measured. The activity of HO-1 in hippocampus was detected. The HO-1 mRNA expression in hippocampus was detected by RT-PCR. Results Compared with 9 g · L-1 saline group, the volume of cerebral infarction after hypoxia-ischemia in hypoxia-ischemia group was significantly decreased. Compared with the high-dose group and the low-dose group, the COHb level in the whole blood of hypoxia-ischemia group was significantly increased, and the HO-1 activity in the hippocampus significantly increased (P <0.05). The expression level of HO-1 mRNA in hippocampus of middle-dose group was significantly higher than that in other groups (Pa <0.05). Conclusion Panax notoginsenoside Rb1 may improve hypoxic-ischemic brain damage by increasing COHb level and local HO-1 activity. Cerebral protection of notoginsenoside Rb1 in hypoxic-ischemic brain damage may be related to the enhancement of brain HO-1 mRNA expression.