人参皂甙Rb1,Rg1和维生素E保护氧化损伤的牛视网膜色素上皮细胞生长的研究

目的 检验人参皂甙Rb1,Rg1和维生素E是否能抑制次黄嘌呤 (HX) /黄嘌呤氧化酶 (XO)对培养的牛视网膜色素上皮 (RPE)细胞的氧化损伤作用。方法 建立牛眼RPE细胞培养体系以及RPE细胞氧化损伤模型。利用MTT法观察人参皂甙Rb1、Rg1和维生素E对氧化损伤的牛RPE细胞增殖的影响。结果 加入不同浓度的Rb1后测得的细胞OD值普遍较HX/XO组的OD值高 ,但无显著性差异 ;当Rg1=0 1和 1μg/ml,维生素E =1和 10 μg/ml时测得的OD值与HX/XO组的OD值相比有显著性差异 (P <0 0 5 )。结论 Rg1和维生素E能对抗氧自由基对体外培养的牛RPE细胞生长的抑制作用 ,而Rb1的作用不明显。

人参皂甙Rg1、Rb1和维生素E对氧化损伤的牛RPE细胞p53表达的影响

目的：检验氧化损伤的牛RPE细胞是否存在p53基因表达的变化和人参皂甙Rg1、Rb1和维生素E对其的影响，以期进一步研究RPE细胞氧化损害的机理.方法：建立牛RPE细胞氧化损伤模型，原位杂交技术测定RPE细胞p53mRNA的表达，免疫组化技术测定p53蛋白表达.结果：p53蛋白表达阳性的牛RPE细胞的细胞核染成黄色，与次黄嘌吟／黄嘌吟氧化酶（HX／XO）组p53蛋白阳性的细胞数相比较，正常对照组，Rg1（0.1mg.L-1）组及VitE（10mg.L-1）组存在显著性差异（P＜0.05），而与Rb1（10mg.L-1）组无显著性差异.原位杂交法测定P53mRNA表达，牛RPE细胞P53mRNA表达阳性可在细胞浆内见到位于细胞周边部的蓝紫色絮状物，分别与HX／XO组阳性的细胞相比较，正常对照组，Rg1组及VitE组存在显著性差异（P＜0.05），而与Rb1组无显著性差异.结论：氧化损伤可导致基因P53mRNA及其蛋白在RPE细胞内的表达明显增加.人参皂甙Rg1和VitE对抗氧自由基对RPE细胞损伤的机制可能是通过清除氧自由基，影响凋亡基困p53的表达，从而有效地抑制氧自由基对RPE细胞的损伤.

人参皂甙Rb1对ATP诱导大鼠海马脑片毒性损伤的影响

目的:研究人参皂甙Rb1对ATP诱导大鼠海马脑片毒性损伤的影响及其作用机制。方法:采用SD大鼠离体海马脑片模型,随机分为正常对照组、人参皂甙Rb1对照组、ATP损伤组、人参皂甙Rb1(20μmol/L、40μmol/L、60μmol/L)组、亮蓝G(BBG)组、亮蓝G+人参皂甙Rb1组、2'-3'-O-(4-苯甲酰-苯甲酰)腺苷三磷酸三乙烷胺盐(Bz ATP)组和Bz ATP+人参皂甙Rb1组。测定脑片孵育液中乳酸脱氢酶(LDH)释放率,免疫组化测定海马CA1区和齿状回神经型一氧化氮合酶(n NOS)表达,Western blot测定海马磷酸化c-Jun氨基末端激酶(p-JNK1/2)蛋白表达。结果:人参皂甙Rb1(40μmol/L、60μmol/L)组可明显降低ATP诱导的LDH释放,人参皂甙Rb1(60μmol/L)亦降低海马p-JNK1/2以及CA1区和齿状回n NOS的表达,人参皂甙Rb1(60μmol/L)对由P2X7受体激动剂Bz ATP诱导的LDH释放和n NOS、p-JNK1/2表达亦有明显抑制作用。P2X7受体抑制剂亮蓝G可明显减低ATP诱导的LDH释放,但BBG联合应用人参皂甙Rb1(60μmol/L)并未增强人参皂甙Rb1的保护作用。结论:人参皂甙Rb1可明显抑制ATP诱导的大鼠海马脑片毒性损伤,其作用机制与抑制P2X7受体,进而减少nNOS和p-JNK1/2的表达有关。

人参皂苷Rg1对腹主动脉缩窄致大鼠心肌肥厚和TLR4的影响

目的:探讨人参皂苷Rg1对腹主动脉缩窄(AAC)致心肌肥厚的抑制作用及其机制。方法:大鼠采用腹主动脉结扎的方法制备AAC模型,1周后ig给予大鼠人参皂苷Rg1 4,2,1 mg/kg,每天1次,共11周。计算心脏质量指数(HMI)和左心室质量指数(LVMI);测定左心室收缩压(LVSP)、左心室舒张末压(LVEDP)和左心室内压最大升降速率(±dp/dt max),HE染色观察大鼠左室心肌形态学改变;采用逆转录-聚合酶链反应(RT-PCR)测定心肌ANP和TLR4 mRNA表达;采用Western blot测定p65和IκBα的蛋白表达,采用ELISA测定血清中TNF-α和IL-1β的表达。结果:与假手术组相比,AAC模型组的大鼠IκBα明显降低,其他指标均显著增高。与模型组相比,人参皂苷Rg1 4 mg/kg组HMI,LVMI,LVSP,LVEDP和±dp/dt max均显著降低(P<0.05);人参皂苷Rg1 4,2 mg/kg组ANP mRNA,TLR4 mRNA,p65蛋白表达,血清中TNF-α和IL-1β表达明显下降(P<0.05),IκBα蛋白表达明显升高(P<0.05)。结论:人参皂苷Rg1能够有效抑制AAC大鼠心肌肥厚并改善炎症反应,其机制可能与抑制TLR4/NF-κB信号通路表达有关。

人参皂苷Rg3通过干预细胞周期和诱导凋亡影响人食管癌Eca9706细胞生长

目的：研究人参皂苷Rg3对人食管癌细胞生长的抑制作用及其机制。方法：MTT法检测人参皂苷Rg3对人食管癌细胞Eca9706增殖的抑制,用流式细胞仪分别检测细胞周期和凋亡情况。结果：在25~200μg/ml范围内,不同浓度人参皂苷Rg3能抑制Eca9706细胞增殖,且呈剂量依赖性。53μg/ml、86μg/ml、141μg/ml人参皂苷作用Eca9706细胞48h,细胞周期在S期的比例明显增多,细胞凋亡率明显增加。结论：人参皂苷Rg3可能通过干预细胞周期和凋亡对食管癌Eca9706细胞增殖起抑制作用。

Two Minor Saponins from Leaves of Panax ginseng C. A.Meyer

Two minor saponins were isolated from the leaves of P. ginseng and their struc-tures were elucidated as 3β,12β, 20(S)-trihydroxyl-dammar-24(25)-ene-(20-O-α-L-arabinofurano-syl(1→6)-β-D-glucopyranosyl)-3-O-β-D-glucopyranoside (1),and 3β,12β, 20(S)-trihydroxyl-dam-mar-24(25)-ene-(20-O-α-L-arabinopyranosyl(1→6)-β-D-glucopyranosyl)-3-O-β-glucopyranoside(2),respectively The fonner corresponds to notoginsenoside-Fe which is isolated for the first time from the title plant The latter is a new natural product and named as ginsenoside-Rd2.

Activation of Plasma Membrane NADPH Oxidase and Generation of H_2O_2 Mediate the Induction of PAL Activity and Saponin Synthesis byEndogenous Elicitor in Suspension-Cultured Cells of Panax ginseng

Endogenous elicitor, termed cellulase-degraded cell wall (CDW), was prepared from the cell wall of suspension-cultured ginseng (Panax ginseng C.A. Meyer) cells via cellulase degradation. CDW activated the NADPH oxidase activity of isolated plasma membranes and stimulated in vivo H2O2 generation in ginseng cell suspensions. CDW also increased the activity of phenylalanine ammonia lyase (PAL), expression of a P. ginseng squalene epoxidase (sqe) gene and saponin synthesis. NADPH oxidase inhibitors inhibited both in vitro NADPH oxidase activity and in vivo H2O2 generation. Induction of PAL activity, saponin synthesis and sqe gene expression were all inhibited by such inhibitor treatments and reduced by incubation with catalase and HA scavengers. These data indicate that activation of NADPH oxidase and generation of H2O2 are essential signalling events mediating defence responses induced by the endogenous elicitor(s) present in CDW.

Modulatory Effect of Rg_1 on the Activity of ProteinTyrosine Kinase of Lymphocytes in the Elderly

The effect of Rg1,a saponin extracted froin Panax ginseng, on the phenotype,receptor and the activity of protein tyrosine kinase (PTK) of lymphocytes isolated from 7 healthy oldpersons were studied. The CD25, CD45RA and CD45RO phenotypes of lymphocytes were 4eter-mined by indirect immunofluorescence technique. The percentage of CD25, CD45RA and CD45ROpositive lymphocytes was 38.3%±17.3%, 46.0% 15.1%, and 52.6%±14.1% respectively after incu-bation with PHA (5 μ±/ml) for 72 hours. However, there were 58.0%±12.5%, CD25, 64.1% ± 12.4%,CD45RA, and 74.0%±8.0%, CD45RO positive cells in the presence of Rg, ( 1μg/ml) along with PHA(5 μg/ml) over the sanie period of incubation. A significant increase was induced by Rgi (P<0.05).The activities of PTK in the cytoplasm and membrane of lymphocytes were measured by ELISAmcthod after incubation with PHA or PHA+Rg1. The absorbance value of PTK activity in cytoplasmafter 72 hr incubation was 0. 120±0.020 in PHA group, but 0. 1 38±0.015 in PHA+Rg1 group. In thelymphocyte membrane, it was 0.374± 0.060 in PHA group and 0.403 ± 0.008 in PHA+Rg1 group(P<0.001). These results showed that Rgi significantly arid simultaneously increased both the PT Kactivity and the expression of phenotype of lymphocytes.

Pharmacokinetics of 20(R)-Ginsenoside Rg3 in Human Volunteers

Objective: To study the pharmacokinetics of 20(R)-Ginsenoside Rg3 in the human body. Methods: High-performance liquid chromatography-ultraviolet detection method was used in this study. Results: The pharmacokinetics of Ginsenoside Rg3 in 14 healthy volunteers were investigated. After a single oral dose of 3.2 mg.g-1 Ginsenoside Rg3 in 8 male volunteers, the plasma concentration-time course fitted in well with a two-compartment open model, with the following pharmacokinetic parameters: Tmax 0.660.10 h, Cmax 166 ngmL-1, T1/2a 0.460.12 h, T1/2b 4.91.1 h, T1/2(Ka) 0.280.04 h, AUC0-∞ 7726 ngmL-1h, respectively. No kinetic analysis was made after an oral dose of 0.8 mg.g-1 Rg3 in other 6 volunteers because of the low concentration, but there was a good correlation between Cmax and dosage of the two groups. Conclusion: The absorption of Rg3 was rapid in the human body, and its elimination was rapid too after oral administration of Ginsenoside Rg3. The pharmacokinetic results shows that it exhibited the first-order kinetic characteristics.

人参皂苷Rg1对异丙肾上腺素致乳鼠心肌细胞肥大及过氧化物酶体增殖活化受体γ辅助活化因子1α的影响

目的:探讨人参皂苷Rg1对异丙肾上腺素致乳鼠心肌细胞肥大的抑制作用及过氧化物酶体增殖活化受体γ辅助活化因子1α(PGC-1α)的影响。方法:原代培养SD乳鼠心肌细胞,用异丙肾上腺素(10μmol/L)诱导心肌细胞肥大,观察核因子-кB(NF-кB)特异性抑制剂BAY11-7082(5μmol/L)及不同浓度人参皂苷Rg1(12.5、25、50μmol/L)对肥大心肌细胞的影响。消化分离法及计算机图像分析系统检测细胞体积;考马斯亮蓝法检测细胞中蛋白的量;RT-PCR法检测心肌细胞心房钠尿肽(ANP)mRNA的表达;Western blotting法检测心肌细胞p65、PGC-1α蛋白的表达;酶联免疫吸附测定(Elisa)法检测细胞外液中三磷酸腺苷(ATP)、单磷酸腺苷(AMP)及游离脂肪酸(FFA)的含量。结果:与正常对照组相比,模型组心肌细胞体积明显增大,总蛋白的量增加,ANP mRNA、p65蛋白表达上调,PGC-1α蛋白表达下调,心肌细胞中FFA含量及ATP/AMP比值减少。人参皂苷Rg1(25、50μmol/L)、BAY11-7082(5μmol/L)均能有效抑制异丙肾上腺素诱导的心肌细胞肥大,使心肌细胞体积减小,总蛋白的量降低,ANP mRNA、p65蛋白表达下调,PGC-1α蛋白表达上调,且上述作用呈一定的剂量相关性。结论:人参皂苷Rg1对异丙肾上腺素诱导乳鼠心肌细胞肥大有保护作用,改善肥大心肌细胞的能量代谢表达水平,其机制可能与抑制NF-кB/PGC-1α信号通路有关。

High-Performance Liquid Chromatographical Analysis of Ginsenosides in Panax ginseng,P.quinquef(?)lium and P.notoginseng

The compositions and contents of ginsenbsides in Panax ginseng,P.quinquefolium and P.notoginseng were determined and compared by reversed-phase High-Performance Liquid Chro- matography(HPLC).The method was performed on an Alltech Adsorbosphere HS C_(18) column,using 5×10^(-3)M NaH_2PO_4-H_3PO_4 buffer solution(pH 3.0)and acetonitrile-water(50:50)as gradient eluents. The baseline separation of ginsenosides Rb_1,Rb_2,Rb_1,Rc,Rd,Rf,Ro,and Re+Rg_1 was obtained in one analytical run.The ginsenosides are directly detected at 203 nm.The detection limit is 40μg at a signal to noise ratio of 3:1.The improved sample preparation and clean-up prior to injection with SEP-PAK C_(18)cartridge strongly reduced the front peaks caused by the impurities in the methanolic extracts of samples to afford a smooth baseline and clear background.The HPLC patterns of methanolic extracts mainly including the ginsenosides were found capable of serving as chemical fingerprints to differentiate the three species from each other.It was also found that there are no significant diffe- rences of the HPLC patterns between the wild Panax ginseng and the cultivated,the white and the red ginsengs,Chinese and Korean red ginsengs,and the tap roots of Panax ginseng collected in four consecutive months,only certain differences in contents of ginsenosides do exist.The contents of the nine major ginsenosides present in the rhizome,tap root and rootlet as well as the leaf of Panax quinquefolium were also determined and compared.

Ginsenoside Rg_3 inhibit hepatocellular carcinoma growth via intrinsic apoptotic pathway

AIM:To investigate the anti-tumor function of ginsenoside Rg3 on hepatocellular carcinoma(HCC) in vitro and in vivo,and its mechanism.METHODS:Hep1-6 and HepG2 cells were treated by Rg3 in different concentrations(0,50,100 and 200 μg/mL) in vitro.After incubation for 0,6,12,24 and 48 h,cell viability was measured by 3-(4,5-dimethylthiazol-2yl)-2,5-diphenyltetrazolium bromide assay.Apoptosis was identified by terminal deoxynucleotidyl transferasemediated dUTP-biotin nick end labeling.Caspase-3 activity was measured by chromophore p-nitroanilide and flow cytometry.Bcl-2 family proteins were ascertained by Western-blotting.Mitochondria membrane potentialwas detected by 5,5',6' 6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolylcarbocyanine iodide.Forty liver tumor-bearing C57Bl6 mice were divided randomly into 4 groups for intra-tumor injection of saline,ginsenoside Rg3,cyclophosphamide(CTX) and ginsenoside Rg3 + CTX combination.RESULTS:The survival time was followed up to 102 d.The mice in the Rg3 + CTX group showed significant increased survival time compared with those in the control group(P < 0.05).Rg3 could inhibit HCC cell proliferation and induce cell apoptosis in vitro in the concentration and time dependent manner.It also induced mitochondria membrane potential to decrease.Caspase-3 activation can be blocked by the inhibitor z-DEVD-FMK.Bax was up-regulated while Bcl-2 and Bcl-XL were down-regulated after Rg3 treatment.CONCLUSION:Our data suggested that Rg3 alone or combined with CTX inhibited tumor growth in vivo and prolonged mouse survival time by inducing HCC cell apoptosis via intrinsic pathway by expression alterations of Bcl-2 family proteins.

High efficiency production of ginsenoside compound K by catalyzing ginsenoside Rb1 using snailase

The rare ginsenoside Compound K （C-K） is attracting more attention because of its good physiological activity and urgent need. There are many pathways to obtain ginsenoside C-K, including chemical and biological methods. Among these, the conversion of PPD-type ginsenosides by enzymatic hydrolysis is a trend due to its high efficiency and mild conditions. For effectively extracting from the other panaxadiol saponins, the conversion process for ginsenoside C-K was investigated using snailases in this study. The univariate experimental design and response surface methodology were used to determine the optimal hydrolysis conditions for the conversion of ginsenoside Rbl into ginsenoside C-K by snailases. The optimum conditions were as follows： pH 5,12, temperature 51 ℃, ratio of snailase/substrate 0.21, and reaction time 48 h. On the basis of these parameters, the addition of 1.0 mmol· L- 1 ferric ion was found to significantly improve the enzymolysis ofsnailases for the first time. With the above conditions, the maximum conversion rate reached 89.7%, suggesting that the process can obviously increase the yield of ginsenoside C-K. The bioassay tests indicated that the ginsenoside C-K showed anti-tumor activity in a series of tumor cell lines. Based on these results, we can conclude that the process of rare ginsenoside C- K production by enzymolysis with snailase is feasible, efficient, and suitable for the industrial production and application.

Inhibitory Effects of Ginsenoside Rb1 on Apoptosis Caused by HSV-1 in Human Glioma Cells

To investigate the inhibitory effects of Ginsenoside Rbl （GRbl） on apoptosis caused by Herpes Simplex Virus-1 （HSV-1） in Human Glioma Cells （U251）, U251 cells were infected by HSV-1 at a multiplicity of infection of 5 and GRbl, GRbl＋HSV-1, HSV-1 and control groups. MTT and cell apoptosis assays were used to detect the inhibitory effects of GRbl on the apoptosis of U251 cells that caused by HSV-1 infection for various concentrations of drug and virus treatments by MTT assay. We found that in the 400 μg/mL GRb 1 and 400 μg/mL GRbl＋HSV-1 groups, MTT values were higher than control group at all times （P〈0.05）. Moreover, the apoptosis rate in the 400 μg/mL GRbl＋HSV-1 group was lower than the HSV-1 group （P〈0. 05）. These results confirmed that, at appropriate concentrations, GRbl could inhibit nerve cell apoptosis in HSV-1 infections.

Effect of the ginsenoside Rb1 on the spontaneous contraction of intestinal smooth muscle in mice

AIM: To investigate the effect and the possible mechanism of ginsenoside Rb1 on small intestinal smooth muscle motility in mice. METHODS: Intestinal smooth muscle strips were isolated from male ICR mice (5 wk old), and the effect of ginsenoside Rb1 on spontaneous contraction was recorded with an electrophysiolograph. The effect of ginsenoside Rb1 on ion channel currents, including the voltage-gated K + channel current (IK V ), calcium-activated potassium channel currents (IK Ca ), spontaneous transient outward currents and ATP-sensitive potassium channel current (IK ATP ), was recorded on freshly isolated single cells using the whole-cell patch clamp technique. RESULTS: Ginsenoside Rb1 dose-dependently inhibited the spontaneous contraction of intestinal smooth muscle by 21.15% ± 3.31%, 42.03% ± 8.23% and 67.23% ± 5.63% at concentrations of 25 μmol/L, 50 μmol/L and 100 μmol/L, respectively (n=5,P<0.05). The inhibitory effect of ginsenoside Rb1 on spontaneous contraction was significantly but incompletely blocked by 10 mmol/L tetraethylammonium or 0.5 mmol/L 4-aminopyridine, respectively (n=5, P<0.05). However, the inhibitory effect of ginsenoside Rb1 on spontaneous contraction was not affected by 10 μmol/L glibenclamide or 0.4 μmol/L tetrodotoxin. At the cell level, ginsenoside Rb1 increased outward potassium currents, and IK V was enhanced from 1137.71 ± 171.62 pA to 1449.73 ± 162.39 pA by 50 μmol/L Rb1 at +60 mV (n=6, P<0.05). Ginsenoside Rb1 increased IK Ca and enhanced the amplitudes of spontaneous transient outward currents from 582.77 ± 179.09 mV to 788.12 ± 278.34 mV (n=5, P<0.05). However, ginsenoside Rb1 (50 μmol/L) had no significant effect on IK ATP (n=3, P<0.05). CONCLUSION: These results suggest that ginsenoside Rb1 has an inhibitory effect on the spontaneous contraction of mouse intestinal smooth muscle mediated by the activation of IK V and IK Ca , but the K ATP channel was not involved in this effect.

The impact on secreted VEGF of Hep-2 human laryngeal cancer cell induced by Rg3

Objective：The aim of this study was to investigate the af ecting of Rg3 to secreted VEGF of human laryngeal carcinoma Hep-2 cells and its mechanism of inhibition to tumor angiogenesis. Methods：Cultured human laryngeal cancer cellline Hep-2 and human vascular endothelial cells in vitro, cells got into the period of exponential phase of growth, was diviced into 3 groups：group I （control group）, group II （DDP group）, group III （Rg3 group）. Added to the Hep-2 cells Rg3 and DDP, made Rg3 final concentration was 300μg/mL, and DDP was 3μg/mL. 48 h later, specimens from sample to be done immunocytochemistry, and the protein of VEGF in Hep-2 cells to be detected. Col ecting Hep-2 cells supernatant, some was used to measure the protein level of VEGF in Hep-2 cells supernatant by ELISA. Some was used to culture HVEC. 24 h later, cellgrowth inhibition rate of human vascular endothelial was determined by MTT. Results：The protein level of VEGF was evi-dently higher in group I compared to group II and group III, it was not only in Hep-2 cells, but also in supernatant of Hep-2 cells. There was no significantly dif erent between group II and group III. MTT results showed that, the human vascular endothelial cellgrowth inhibition rate of group I was significantly lower than that of group II and group III （P〈0.05）. At the same time the HVEC growth inhibition rate of group II was significantly lower than that of group III （P〈0.05）. Conclusion：The inhibition to tumor angiogenesis of Rg3 is stronger than traditional chemotherapy drug cisplatin. It worke by reducing the biological ef ects of secreted VEGF, But the ef ecting worke by reducing the activity of secreted VEGF itself or af ecting endothelial function of VEGF receptor or some other ways to be further studied.

A Meta-analysis of Ginsenoside Rg3 for Non-small Cell Lung Cancer

OBJECTIVE Ginsenoside Rg3 （Rg3） has shown anti-tumor effects on various tumor cells. It has been widely used in China for non-small cell lung cancer （NSCLC）. However, there are only a few clinical trials to study the effectiveness of Rg3 on NSCLC, and almost them are small- samples, so we performed a meta-analysis on the results of the studies we collected in order to investigate the effectiveness of Rg3 on NSCLC. METHODS A meta-analysis was conducted in all the selected randomized controlled trials evaluating the effectiveness of Rg3 on NSCLC patients. All on-line databases regarding Rg3 from 1950 to 2011 were searched. Supplemental hand searching of the references of retrieved articles was performed. RESULTS Six trials met the inclusion criteria. Four of them compared chemotherapy plus Rg3 with chemotherapy alone, and the other 2 compared chemotherapy plus Rg3 with chemotherapy plus placebo. These trials are homogeneous. Two of the trials report overall survival, but the data are not suitable for a meta-analysis. After meta-analysis was conducted in the included studies comparing the effects of chemotherapy plus Rg3 with that of chemotherapy alone or chemotherapy plus placebo, it was suggested that chemotherapy plus Rg3 increased the response rate [odds ratio： 2.64 （95% Ch 1.70-4.11）, fixed effects model] and disease control rate [odds ratio： 3.34 （95% CI： 1.92-5.81）; fixed effects model] of the patients at stage II-IV, especially for the patients at stage Ill-IV. CONCLUSION Meta-analysis of the available evidence suggests that Rg3 plus chemotherapy improves the response rate of NSCLC patients, and well-designed RCTs with large sample size are needed.

Roles and mechanisms of ginsenoside in cardiovascular diseases: progress and perspectives

Ginseng is among the oldest traditional Chinese medicinal herbs and is widely used in China and Southeast Asia. Over the past 50 years, considerable research has focused on the chemical constituents, pharmacological action, and clinical applications of ginseng. In this review, we examine the current state of research on ginseng, including the main active ingredient ginsenoside, its pharmacological effects on the cardiovascular system, and mechanisms of action. We focus on what is known of the effects of ginseng against atherosclerosis, arrhythmia, myocardial ischemia, and its inhibition of ventricular remodeling, providing a basis for expanding the clinical applications of ginseng.

Qualitative detection of ginsenosides in brain tissues after oral administration of high-purity ginseng total saponins by using polyclonal antibody against ginsenosides

Given the limited studies and conflicting findings, the transport character of ginsenosides crossing the blood-brain barrier （BBB） remains unclear. The present study was designed to qualitatively determine the distribution of ginsenosides in brain tissues after oral administration of ginseng total saponins, using high-performance liquid chromatography-tandem mass spectrometry （HPLC-MS/MS） combined with immunohistochemistry. In brain tissue homogenates, ginsenoside Rgl was detectable and no other ginsenosides or their metabolites were found. No ginsenosides were detected in cerebrospinal fluid. Immunohistochemistry staining of brain tissue sections by using anti-ginsenoside polyclonal antibodies revealed the localization of ginsenosides in brain tissues. Furthermore, immunofluorescence double staining revealed that ginsenosides widely existed in vascular endotheliocytes and astrocytes, and in few neurons. These results indicated that Rgl was the main component that entered the brain after oral administration of ginseng total saponins and that ginsenosides could cross the BBB, although the transport capability ofginsenosides through the BBB may be poor.

Ginsenosides stimulated the proliferation of mouse spermatogonia involving activation of protein kinase C

The effect of ginsenosides on proliferation of type A spermatogonia was investigated in 7-day-old mice. Spermatogonia were characterized by c-kit expression and cell proliferation was assessed by immunocytochemical demonstration of proliferating cell nuclear antigen (PCNA). After 72-h culture, Sertoli cells formed a confluent monolayer to which numerous spermatogonial colonies attached. Spermatogonia were positive for c-kit staining and showed high proliferating activity by PCNA expression. Ginsenosides (1.0～10 μg/ml) significantly stimulated proliferation of spermatogonia. Activation of protein kinase C (PKC) elicited proliferation of spermatogonia at 10-8 to 10-7 mol/L and the PKC inhibitor H7 inhibited this effect. Likewise, ginsenosides-stimulated spermatogonial proliferation was suppressed by combined treatment of H7. These results indicate that the proliferating effect of ginsenosides on mouse type A spermatogonia might be mediated by a mechanism involving the PKC signal transduction pathway.