高效液相色谱法同时测定三七总皂苷中人参皂苷Rg_1、Re、Rb_1与三七皂苷R_1含量

目的建立高效液相色谱法同时测定三七总皂苷中人参皂苷Rg1、Re、Rb1与三七皂苷R1的方法。方法采用高效液相色谱法 ,固定相为氨基键合相 ,流动相为乙腈 水 ( 81∶1 9,V∶V) ,检测波长2 0 3nm。结果三七总皂苷中人参皂苷Rg1、Re、Rb1和三七皂苷R1与其他成分分离良好 ,保留时间分别约为 5 7min、8 9min、2 5 1min和 9 9min。人参皂苷Rg1在 80～ 2 80mg/L(r =0 9992 )、Re在 2 0～ 1 80mg/L(r=0 9993 )、Rb1在 95～ 2 85mg/L(r=0 9991 )、三七皂苷R1在1 8～ 1 4 6mg/L(r=0 9991 )内线性关系良好 ,人参皂苷Rg1、Re、Rb1和三七皂苷R1的回收率分别为 99 1 %、98 4 %、98 6%和 97 1 % ,RSD分别为 2 1 %、2 0 %、2 2 %、2 8%。结论本法可用于三七的质量控制     

正交试验优化超高压提取人参中人参皂苷的工艺研究

目的　研究超高压提取人参中人参皂苷的最佳工艺。方法　采用超高压技术常温提取,正交试验优化,分光光度法检测人参总皂苷的含量。结果　超高压提取人参皂苷的最佳提取工艺参数为:提取溶剂为5 0 %乙醇,固液比为1∶75 ,提取压力为5 0 0 MPa,提取时间2 m in,人参皂苷的得率高达7.76 %。结论　超高压提取工艺具有提取效率高、时间短、能耗低、杂质含量少等优点。     

人参皂苷CK对人肝癌细胞HepG2迁移及侵袭的影响

目的探讨人参皂苷CK对人肝癌细胞增殖、迁移、侵袭的影响及其可能机制。方法取对数生长期的Hep G2细胞,用不同浓度人参皂苷CK(0、10、20、40、80μmol·L^-1)处理,MTT法检测人参皂苷CK对细胞增殖的影响;细胞划痕实验、Transwell实验检测人参皂苷CK对肝癌细胞迁移、侵袭的影响;Western blot检测人参皂苷CK对Hep G2细胞中E-cadherin、N-cadherin及信号分子p-ERK、ERK、p-Akt、Akt水平的影响。结果 MTT检测结果显示,人参皂苷CK对肝癌Hep G2细胞生长有抑制作用;划痕和Transwell实验结果显示,人参皂苷CK可抑制Hep G2细胞的迁移和侵袭;Western blot结果显示人参皂苷CK可降低N-cadherin表达,明显升高E-cadherin表达水平,同时抑制ERK和Akt信号的磷酸化。结论人参皂苷CK可抑制肝癌细胞的迁移和侵袭过程,可能与抑制ERK和Akt信号有关。     

去甲肾上腺素对神经细胞胆碱酯酶活性的促进作用

鸡胚脑神经细胞培养的第5天给去甲肾上腺素(NE)2μg/ml,培养第10天的神经细胞胆碱酯酶活性为对照的2.3倍,且较对照提前3天达到高峰。在神经细胞培养的第5天同时给 NE2μg/ml 和人参皂甙87μg/ml 时,第7天的胆碱酯酶活性为单给 NE的190.7%。氨甲基喋呤能明显降低神经细胞的胆碱酯酶活性,NE 能减轻氨甲基喋呤对神经细胞胆碱酯酶活性的降低。初步认为 NE 促进培养神经细胞胆碱酯酶活性的增强是因为它促进了神经细胞的成熟和胆碱酯酶的合成。     

人参三醇皂甙促进人白细胞介素6转译的生物学效应

将PHA激活淋巴结细胞作为研究对象,观察了人参三醇皂甙(PTGS)对人白细胞介素6(IL-6)分泌的促进效应。应用同位素示踪技术观察细胞RNA合成和蛋白质合成与IL-6分泌的关系,结合IL-6mRNA体外转译体系,探讨了PTGS促IL-6诱生的机理。结果表明PTGS对IL-6基因的转录环节无明显作用,但对IL-6基因的转译环节具明显促进效应。     

蒸参水化学成分的研究

本文阐述了蒸参水的化学成分。实验结果表明,蒸参水含有人参总皂甙(1.90g/L),多种氨基酸和多种维生素。     

高效液相色谱法测定三七中人参皂苷Rd的含量

目的:考察三七中人参皂苷Rd的含量,为该药材质量标准的修订提供依据。方法:应用高效液相色谱法,采用All-tech C_(18)色谱柱(4.6 mm×150 mm,5 μm),乙腈-水(35:65)作为流动相,流速:1.0 mL·min~(-1),检测波长为203 nm,进样量10 μL。结果:方法学考察结果表明,人参皂苷Rd的范围为2.061～12.88 μg,加样回收率为98.23％(n=6);三七药材中的人参皂苷Rd的含量在0.36％～1.47％之间。结论:以高效液相色谱法测定三七中人参皂苷Rd含量的方法可行,人参皂苷Rd可以作为控制三七质量的一个指标成分。     

Protective Effect of Ginsenoside Rd on Lipopolysaccharide‑Induced Acute Lung Injury through its Anti‑Inflammatory and Anti‑Oxidative Activity

Background: Inflammation and oxidation stress are key factors in the mechanism of acute lung injury(ALI). Therefore, suppression of the inflammatory response and oxidative stress could be a potential strategy to treat lipopolysaccharide(LPS)-induced ALI. Ginsenoside Rd(Rd), a natural Ginseng extract, alleviates inflammation and oxidative stress in several diseases such as Alzheimer's disease and cerebral ischemia, but its effect on ALI is still unclear. Aims and Objectives: To explore the protective effect of Rd on LPS-induced ALI and explored associated mechanisms. Materials and Methods: Mice were divided into five groups: A sham-operated group, a LPS-induced ALI group, and three LPS groups pretreated with Rd doses of 20, 40, and 80 mg/kg, respectively. The pathological changes of lung, collagen deposition, pulmonary edema, inflammatory cytokine, oxidative stress and the expression levels of TLR4 and NF-κB were detected. Results: The oral administration of Rd dose dependently attenuated histopathologic changes in the lung, lung edema, pulmonary collagen deposition, protein concentration in bronchoalveolar lavage fluid(BALF), myeloperoxidase(MPO) activity, and inflammatory cell infiltration. In addition, Rd suppressed the LPS-induced inflammatory cytokines tumor necrosis factor-α, interleukin(IL)-6, and IL-1 β in BALF. The productions of oxidative stress-related enzymes(catalase, superoxide dismutase, and glutathione peroxidase) in lung tissue were significantly upregulated by Rd administration. However, malondialdehyde and pulmonary MPO activity was reduced in the Rd-pretreated groups when compared with LPS-induced ALI group. Rd treatment also dose dependently suppressed LPS-induced NF-κB activation and TLR4 expression. Conclusion: Overall, these findings provide evidence that Rd pretreatment inhibits LPS-induced ALI through anti-inflammatory and antioxidative actions, suggesting that it could be a promising protective drug for LPS-induced ALI.     

Ginsenoside Rg1 reverses stress‐induced depression‐like behaviours and brain‐derived neurotrophic factor expression within the prefrontal cortex

Depression is a major neuropsychiatric disorder that exerts deleterious effects upon public health. However, the neuronal mechanisms of depression remain largely uncharacterized, which has retarded the identification and development of effective therapeutic tools for the treatment of this disorder. The aim of this study was to explore the neuronal mechanisms underlying the protective effects of ginsenoside Rg1, a natural steroidal saponin found in ginseng, against chronic stress‐induced depression.The results showed that chronic administration of ginsenoside Rg1 (40 mg/kg, i.p., 5 weeks) significantly ameliorated depression‐like behaviours in rats as assessed in the sucrose preference and forced swim tests. Furthermore, chronic stress decreased the phosphorylation levels of the extracellular signal‐regulated kinase and cAMP‐response element‐binding protein in the prefrontal cortex as well as producing a reduction of brain‐derived neurotrophic factor expression. Of particular importance, all reductions in these parameters were significantly reversed by pre‐treatment with ginsenoside Rg1. Taken together, the results of the present study suggest that the antidepressant‐like effect of ginsenoside Rg1 might be mediated, at least in part, by activating the cAMP‐response element‐binding protein–brain‐derived neurotrophic factor system within the prefrontal cortex. These findings not only reveal some of the underlying neuronal mechanisms of depression, but also the therapeutic potential of ginsenoside Rg1 as a preventive agent in the treatment of depression.