Li Cheng-peng, Zhang Meng-si, Liu Jun, Geng Shan, Li Jing, Zhu Jia-hong, Zhang Yan-yan, Jia Yan-yan, Wang Lu, Wang Shun-he, Wang Ya-ping
Zhongguo Zhong Yao Za Zhi. 2014 Nov;39(22):4442-7.
Neurodegenerative disease is common and frequently occurs in elderly patients. Previous studies have shown that ginsenoside Rg1 was able to inhibit senescent of brain, but the mechanism on the brain during the treatment remains elucidated. To study the mechanism of ginsenoside Rg1 in the process of anti-aging of brain, forty male SD rats were randomly divided into normal group, Rg1 normal group, brain aging model group and Rg1 brain aging model group, each group with 10 rats (brain aging model group: subcutaneous injection of D-galactose (120 mg kg(-1)), qd for 42 consecutive days; Rg1 brain aging model group: while copying the same test as that of brain aging model group, begin intraperitoneal injection of ginsenosides Rg1 (20 mg x kg(-1)) qd for 27 d from 16 d. Rg1 normal group: subcutaneous injection of the same amount of saline; begin intraperitoneal injection of ginsenosides Rg1 (20 mg x kg(-1)) qd for 27 d from 16 d. Normal: injected with an equal volume of saline within the same time. Perform the related experiment on the second day after finishing copying the model or the completion of the first two days of drug injections). Learning and memory abilities were measured by Morris water maze. The number of senescent cells was detected by SA-beta-Gal staining while the level of IL-1 and IL-6 proinflammatory cytokines in hippocampus were detected by ELISA. The activities of SOD, contents of GSH in hippo- campus were quantified by chromatometry. The change of telomerase activities and telomerase length were performed by TRAP-PCR and southern blotting assay, respectively. It is pointed that, in brain aging model group, the spatial learning and memory capacities were weaken, SA-beta-Gal positive granules increased in section of brain tissue, the activity of antioxidant enzyme SOD and the contents of GSH decreased in hippocampus, the level of IL-1 and IL-6 increased in hippocampus, while the length of telomere and the activity of telomerase decreased in hippocampus. Rats of Rg1 brain aging group had their spatial learning and memory capacities enhanced, SA-beta-Gal positive granules in section of brain tissue decreased, the activity of antioxidant enzyme SOD and the contents of GSH increased in hippocampus, the level of IL-1 and IL-6 in hippocampus decreased, the length contraction of telomere suppressed while the change of telomerase activity increased in hippocampus. Compared with that of normal group, the spatial learning and memory capacities were enhanced in Rg1 normal group, SA-beta-Gal positive granules in section of brain tissue decreased in Rg1 normal group, the level of IL-1 and IL-6 in hippocampus decreased in Rg1 normal group. The results indicated that improvement of antioxidant ability, regulating the level of proinflammatory cytokines and regulation of telomerase system may be the underlying anti-aging mechanism of Ginsenoside Rg1.
神经退行性疾病很常见，且经常发生于老年患者。先前的研究表明人参皂苷Rg1能够抑制大脑衰老，但治疗期间其对大脑的作用机制仍有待阐明。为了研究人参皂苷Rg1在大脑抗衰老过程中的机制，将40只雄性SD大鼠随机分为正常组、Rg1正常组、脑衰老模型组和Rg1脑衰老模型组，每组10只大鼠（脑衰老模型组：皮下注射D-半乳糖（120 mg·kg⁻¹），每天1次，连续42天；Rg1脑衰老模型组：在复制与脑衰老模型组相同的试验时，从第16天开始腹腔注射人参皂苷Rg1（20 mg·kg⁻¹），每天1次，共27天。Rg1正常组：皮下注射等量生理盐水；从第16天开始腹腔注射人参皂苷Rg1（20 mg·kg⁻¹），每天1次，共27天。正常组：在相同时间内注射等体积生理盐水。在完成模型复制或药物注射前两天结束后的第二天进行相关实验）。通过Morris水迷宫测量学习和记忆能力。通过SA-β-Gal染色检测衰老细胞数量，同时通过ELISA检测海马中IL-1和IL-6促炎细胞因子水平。通过比色法对海马中SOD活性、GSH含量进行定量。分别通过TRAP-PCR和Southern印迹分析进行端粒酶活性和端粒长度的变化检测。结果表明，在脑衰老模型组中，空间学习和记忆能力减弱，脑组织切片中SA-β-Gal阳性颗粒增加，海马中抗氧化酶SOD活性和GSH含量降低，海马中IL-1和IL-6水平升高，而海马中端粒长度和端粒酶活性降低。Rg1脑衰老组大鼠的空间学习和记忆能力增强，脑组织切片中SA-β-Gal阳性颗粒减少，海马中抗氧化酶SOD活性和GSH含量增加，海马中IL-1和IL-6水平降低，端粒长度收缩受到抑制，而海马中端粒酶活性变化增加。与正常组相比，Rg1正常组的空间学习和记忆能力增强，Rg1正常组脑组织切片中SA-β-Gal阳性颗粒减少，Rg1正常组海马中IL-1和IL-6水平降低。结果表明，提高抗氧化能力、调节促炎细胞因子水平和调节端粒酶系统可能是人 参皂苷Rg1潜在的抗衰老机制。
