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目的:探讨人参皂甙Rb1(GRb1)对香烟烟雾诱导的大鼠神经细胞凋亡和细胞内Ca2+浓度的影响。方法:雄性Wistar大鼠48只,随机分为对照组、吸烟组和GRb1组,每组16只。吸烟组和GRb1组连续吸烟12周制作吸烟大鼠模型,期间每周给予GRb1组和吸烟组大鼠分别腹腔注射40mg/kg的GRb1和等量生理盐水,对照组不做任何处理。提取大鼠大脑皮层组织,TUNEL法检测各组细胞凋亡情况,荧光分光光度法检测细胞内Ca2+浓度变化情况。结果:TUNEL法检测表明,未经香烟烟雾处理的对照组大鼠大脑皮层细胞自然凋亡率为2.54±0.92个/视窗。连续吸烟12周,吸烟组大鼠大脑皮层细胞凋亡率较对照组显著升高,达20.62±2.13个/视窗(q=35.72,P<0.01)。GRb1组细胞凋亡率虽也有增加,为11.48±2.37个/视窗,明显低于吸烟组(q=15.39,P<0.01)。对照组、吸烟组和GRb1组大鼠大脑皮层细胞内Ca2+浓度分别为236.62±12.52ng/L、636.37±18.63 ng/L和353.61±13.72 ng/L,GRb1组Ca2+浓度显著低于吸烟组(q=54.73,P<0.01)。结论:GRb1对吸烟大鼠脑损伤的保护作用可能与抑制细胞内的Ca2+超载、降低香烟烟雾诱导的神经细胞凋亡有关。
Objective: To investigate the effects of ginsenoside Rb1 (GRb1) on cigarette smoke-induced neuronal apoptosis and intracellular Ca2 + concentration in rats. Methods: Forty-eight male Wistar rats were randomly divided into control group, smoking group and GRb1 group, 16 rats in each group. The smoking group and GRb1 group were smoked continuously for 12 weeks to make smoking rat model. GRb1 group and smoking group were given intraperitoneal injection of 40 mg / kg GRb1 and the same amount of saline respectively, while the control group did not do any treatment. The cerebral cortex tissues of rats were extracted, the apoptosis of the cells in each group was detected by TUNEL method, and the change of intracellular Ca2 + concentration was detected by fluorescence spectrophotometry. Results: TUNEL assay showed that the apoptotic rate of cerebral cortex cells in control group without cigarette smoke was 2.54 ± 0.92 cells / window. After smoking for 12 weeks, the apoptosis rate of cerebral cortex in smoking group was significantly higher than that in control group (20.62 ± 2.13 / window, q = 35.72, P <0.01). The apoptosis rate of GRb1 group was 11.48 ± 2.37 / window, which was significantly lower than that of smoking group (q = 15.39, P <0.01). The Ca2 + concentrations in cerebral cortex of control group, smoking group and GRb1 group were 236.62 ± 12.52ng / L, 636.37 ± 18.63ng / L and 353.61 ± 13.72ng / L, respectively. The Ca2 + concentration of GRb1 group was significantly lower than that of smoking group = 54.73, P <0.01). Conclusion: The protective effect of GRb1 on brain injury in smoking rats may be related to the inhibition of intracellular Ca2 + overload and the decrease of cigarette smoke-induced neuronal apoptosis.