Ginsenoside Rg1 protects against ischemia-induced neuron damage by regulating the rno-miRNA-27a-3p/PPARγaxis

A preliminary miRNA screening showed that expression levels of rno-miRNA-27a-3p were significantly increased in the serum and brain tissues of rats undergoing cerebral ischemia.In recent years,there is evidence of the protective capacity of the saponins extracted from panax ginseng and its primary active ingredient ginsenosideRg1oncerebral ischemic injury.Methods:Fetal rat neurons(FRNs)were cultured in glucose-and-serumfree medium and exposed to hypoxia to establish a cerebral ischemia model in vitro(oxygen and glucose deprivation model,OGD).Antioxidant indexes(CAT,SOD),inflammatory markers(MPO,TNF-αand IL-6),and the expression of apoptosis and proliferation associated proteins(NF kB-p65,Caspase 3-cleaved,BCL-2)were examined.Results:Pre-treatment of Rg1(30–100μg/mL)could effectively inhibit the decline of antioxidant indexes(CAT,SOD)and increase in inflammatory markers(MPO,TNF-αand IL-6),and effectively inhibited the apoptosis in FRNs induced by OGD in a gradient-dependent manner.The mechanism analysis showed that the role of Rg1 in protecting against ischemia-induced neuron damage depends on its indirect up-regulation of PPAR protein via suppression of rnomiRNA-27a-3p.Moreover,these effects of Rg1 could be reversed by exogenous rno-miRNA-27a-3p and PPAR gene silencing in FRNs exposed to OGD.Conclusion:To summarize,our study demonstrates that Rg1 could effectively attenuate neuronal damage caused by cerebral ischemia via the rno-miRNA-27a-3p/PPARγpathway.Further,clarification of the novel mechanism will certainly improve our previous understanding of the role of Rg1 and enhancing its level in treatments for alleviating ischemic brain injury.

基于DLL4/Notch1信号通路探讨人参皂苷Rg-3对AOM/DSS诱导的炎症相关性结直肠癌小鼠血管形成机制

目的基于Delta样配体4(delta-like ligand 4,DLL4)/Notch1信号通路探究人参皂苷Rg-3对氧化偶氮甲烷/葡聚糖硫酸钠(azoxymethane/dextran sulphate sodium,AOM/DSS)诱导的炎症相关性结直肠癌小鼠血管形成机制。方法48只C57BL/6J APCMin/+小鼠随机分为对照组、模型组、人参皂苷Rg-3组(10 mg/kg),每组16只。建立AOM/DSS诱导的结直肠癌模型,采集腹主动脉血与完整结直肠组织,检测血常规与炎症指标,HE染色观察肠组织形态,免疫组化、Western blotting检测肠组织DLL4、Notch1表达。肿瘤细胞、人脐静脉内皮细胞(human umbilical vascular endothelial cells,HUVECs)分为对照组、人参皂苷Rg-3组、人参皂苷Rg-3+DLL4组,通过MTT、克隆形成、划痕、Transwell与血管形成实验检测细胞增殖、迁移、血管形成能力,Western blotting检测DLL4/Notch信号通路、血管形成相关分子表达情况。结果与对照组相比,模型组、人参皂苷Rg-3组RBC、Hct、Hb水平降低(P<0.05),IL-1β、IL-6、TNF-α、DLL4、Notch1表达水平升高(P<0.05);与模型组相比,人参皂苷Rg-3组RBC、Hct、Hb水平提高(P<0.05),IL-1β、IL-6、TNF-α、DLL4、Notch1表达水平下降(P<0.05),肿瘤数量、2~3.5 mm及>3.5 mm的肿瘤数量减少(P<0.05)。细胞实验结果显示,与对照组相比,人参皂苷Rg-3组肿瘤细胞、HUVECs增殖、克隆形成、迁移、血管形成能力下降(P<0.05),DLL4、Notch1、VEGF、VEGFR2、转录因子重组信号结合蛋白Jκ(recombination signal binding protein-Jκ,RBP-Jκ)、Hes1表达水平降低(P<0.05)。结论人参皂苷Rg-3通过抑制DLL4/Notch1信号通路促进血管形成,抑制AOM/DSS诱导结直肠癌进展。

Inhibiting effect of Endostar combined with ginsenoside Rg3 on breast cancer tumor growth in tumor-bearing mice

Objective: To study the inhibiting effect of Endostar combined with ginsenoside Rg3 on breast cancer tumor growth in tumor-bearing mice. Methods: Female mice were selected as experimental animals, and breast cancer tumor-bearing mouse models were established and then divided into group A, B, C and D that respectively received saline, recombinant human endostatin, ginsenosides Rg3 and recombinant human endostatin combined with Rg3 intervention; 7 d, 14 d and 21 d after intervention, tumor tissue volume was measured; 21 d after intervention, mice were killed, tumor tissue was collected, and m RNA contents of angiogenesis molecules, invasion molecules, autophagy marker molecules and autophagy signaling pathway molecules were detected. Results: At 7 d, 14 d and 21 d after intervention, tumor tissue volume of group B, C and D was lower than that of group A, and tumor tissue volume of group D was lower than that of group B and C; m RNA contents of VEGFA, VEGFB, VEGFC, MMP2, MMP9, p62, m TOR, PI3 K, Akt, JNK and Beclin-1 in tumor tissue of group B, C and D were significantly lower than those of group A, and LC3-II/LC3-I was significantly higher than that of group A; m RNA contents of VEGFA, VEGFB, VEGFC, MMP2, MMP9, p62, m TOR, PI3 K, Akt, JNK and Beclin-1 in tumor tissue of group D were significantly lower than those of group B and C, and LC3-II/LC3-I was higher than that of group B and C. Conclusions: Endostar combined with ginsenoside Rg3 has stronger inhibiting effect on breast cancer tumor growth in tumor-bearing mice than single drug, and it can inhibit angiogenesis and cell invasion, and enhance cell autophagy.

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.

Preparation and Characterization of Biodegradable Polylactide(PLA) Microspheres Encapsulating Ginsenoside Rg3

In this study, the process of a biodegradable polylactide（PLA） microsphere encapsulating ginsenoside Rg3 was first studied by the emulsion solvent evaporation method, for enhancing solubility and stability of ginsenoside Rg3. Alabum was also first used as a modifier in this method. The mean diameter of the prepared PLA microspheres containing Rg3 was 40 μm. Ginsenoside Rg3 released from the microspheres was studied by HPLC and detected by UV. It was found that the drug release curve fitted the Model Heller-Baker best.

Enrichment of the less polar ginsenoside (Rg3) from ginseng grown in New Zealand by post-harvest processing and extraction

Background:Previous studies showed that New Zealand-grown ginseng contains an abundance of ginsenosides and that rare less polar ginsenosides,such as Rg3,exhibit more pharmacological activities than polar ginsenosides,which are the major components of ginseng.Methods:The ginsenoside profile of New Zealand-grown Panax ginseng was manipulated by treatment with acetic acid,sodium hydroxide,pH,and high temperature.The abundance of 23 ginsenosides extracted by different treatments was quantified using high-performance liquid chromatography.Results:Treatment with 0.5 mol/L acetic acid can stimulate the degradation of polar ginsenosides to less polar ginsenosides(5.6%Rg3 was accumulated,P<0.0001).Furthermore,when ginseng root was treated at 121℃ for 100 min in a pH 3.0 acetic acid aqueous solution,the majority of the polar ginsenosides were converted into less polar ginsenosides.Specifically,83.46±3.69%(P=0.0360)of the less polar ginsenosides and 41.01±2.39%(P=0.0412)of Rg3 were enriched.In contrast,alkali treatment did not convert the polar ginsenosides into less polar ginsenosides at mild temperature and less conversion was observed compared with acid treatment at high temperature.Conclusion:This is the first attempt to manipulate the ginsenoside profile of New Zealand-grown ginseng.The conditions(high temperature with low pH)may be modified to produce and enrich the less polar ginsenoside fraction(especially Rg3)from the total ginseng extract.

THE CLINICAL EVALUATION OF ANGIOGENESIS INHIBITOR-20(R)-GINSENOSIDE RG_3 IN LUNG CANCER

Objective The aim of the study was to make a further evaluation of Ginsenoside Rg3. Methods The clinical effects of the drug on moderate and advanced lung cancer, including side effects, were observed. Results Ginsenoside Rg3 improved chemotherapy significantly. The clinical relief rate of patients treated with antiangiogenic agent 20 (R) Ginsenoside Rg3 was 36.6%, which was higher than that of the patients not treated with it (16.7%)( P <0.05). It had no significantly different effects on lung cancers of different types of tissues ( P >0.05). It provided better treatment on the cancer at early stage than that at advanced stage ( P <0.05). Moreover the living qualities of the patients were improved notably ( P <0.05). Conclusion Combined with chemotherapy, angiogenesis inhibitor 20(R) Ginsenoside Rg3 can improve clinical therapeutic efficacy and the living qualities of patients significantly.

Ginsenoside rg3 reduces body weight by regulating fat content and browning in obese mice

Objective:To determine the effects of ginsenoside rg3 on the body weight of C57BL/6J obese mice and to investigate its underlying weight loss mechanisms with a focus on white fat browning-related factors.Methods:Eight-week-old C57BL/6J male mice were fed a high-fat diet for 12 successive weeks to construct the obese model.C57BL/6J male mice were fed a standard chow diet to construct normal control group.After 8 weeks of intervention with ginsenoside rg3,the food intake,body weight,body fat mass,blood sugar,and lipid profiles of the mice in each group were detected.Hematoxylin and eosin(HE)staining was used to observe the histological morphology of the adipose tissues.Real-time polymerase chain reaction(RT-PCR)and Western blotting(WB)were applied to detect the gene and protein expression levels of peroxisome proliferators-activated receptor gama(PPARg),Peroxisome proliferatoractivated receptor-gamma coactivator-1alpha(PGC-1a),PR domain containing 16(PRDM16),and uncoupling protein 1(UCP-1).Results:Compared to normal control group mice,the body weight,food intake,body fat composition,and blood lipid levels of model group mice increased significantly.After 8 weeks of intervention with ginsenoside rg3,body weight,body fat composition,food intake,and blood lipid profiles decreased.HE staining showed that ginsenoside rg3 can improve white adipocyte hypertrophy to a certain extent.RTPCR and WB demonstrated that ginsenoside rg3 can increase the mRNA and protein expression levels of PPARg,PGC-1a,PRDM16,and UCP-1 in the adipose tissues of obese mice.Conclusion:The weight reduction effect of ginsenoside rg3 may be related to the promotion of white fat browning.

Apoptosis Induced by Ginsenoside Rg3 in a Human Bladder Carcinoma Cell Line

OBJECTIVE This study was conducted to explore the effect of Rg3 on inhibition of proliferation and induction of apoptosis in bladder cancer cells. METHODS The EJ bladder cancer cell line was treated with Rg3 at various concentrations. Cell proliferation was measured by the MTT assay. Morphological changes in the cells were observed by fluorescent staining using Hoechst 33258. The cell cycle and apoptotic rate were analyzed by flow cytometry （FCM） and the expression of caspase-3 in cells was detected by immunocytochemistry. DNA ladder analysis was conducted by agarose gel electrophoresis. RESULTS Rg3 inhibited proliferation of EJ cells in a concentration-dependent manner, resulting in an IC50 for Rg3 at 48 h of 125.5 μg/ml. When treated with 150 μg/ml of Rg3 for 24 h and 48 h, the cells showed apoptotic morphological characteristics including condensed chromatin, nuclear fragmentation, apoptotic bodies and bright fluorescent granules as well as a higher caspase-3 expression. The FCM assay indicated that Rg3 altered the cell cycle and induced apoptosis of the EJ cells, when treated for 24 h and 48 h with 75 μg/ml of Rg3 as well as for 48 h with 150 μg/ml. The percentages of cells in the S phase and the GJM transition were increased, whereas the percentages of cells in the G0-G1 transition were decreased. The apoptotic rates were increased from （1.05±0.17）% in the control group cells to （8.41 ±0.98）%, （18.57±2.20）% and （33.98±1,64）% respectively. Significant changes in the DNA ladders, showed that the effects of Rg3 were displayed in a dose and time dependent manner. CONCLUSION The results suggest that Ginsenoside Rg3 exerts an inhibitory effect on proliferation of EJ cells by inducing apoptosis.

Ginsenoside Rg3 Promotes the Survival and Migration of Trophoblast Cells in a Rat Model of Gestational Hypertension by Regulating miR-100a/Insulin Growth Factor-2 Axis

Objective:Preeclampsia(PE)is a common complication during pregnancy.miR-100a is expressed in the placenta and regulates the survival and development of placental cells.Insulin growth factor-2(IGF-2)may serve as its downstream target.This study investigated the protective mechanisms of ginsenoside Rg3 against PE in rat model.Materials and Methods:LPS-induced rat PE models were suitable for intravenous administration of the highly expressed miR-100a ginsenoside Rg3 lentiviral vector.Human trophoblasts were cultured in vitro for JEG-3,and PE cell models were constructed.In vivo effects on tumor growth and apoptosis were observed.Ginsenoside Rg3 was treated with different concentrations of shRNA,miR-100a analogs,inhibitors,or IGF-2.Autophagy and the expression of autophagy-related proteins were examined.Trophoblast activity and migration were determined using Cell Counting Kit-8 and Transwell assays.Both drugs strongly inhibited trophoblasts under normal conditions with some synergy between them.Double-luciferase return assay confirmed the binding affinity of miR-100a for IGF-2.Results:In response to Rg3,autophagy and the expression of autophagy-related proteins LC3-I/II,Beclin1,and SQSTM1 were reduced in PE rat placental trophoblasts.Rg3 inhibited autophagy in JEG-3 cells and promoted JEG-3 survival and migration in a concentration-dependent manner.miR-100a upregulated PE expression.These results suggested that autophagy was a vital signaling system.Rg3 intervention inhibited miR-100a expression and miR-100a downregulated IGF-2 expression in placental tissues and promoted autophagy,thereby inhibiting JEG-3cell survival and migration.In rats,Rg3 inhibited PE development by regulating the activity of the miR-100a-IGF-2 signaling axis.Conclusion:Ginsenoside Rg3 positively regulates the miR-100a-IGF-2 axis and protects PE rats by inhibiting trophoblastic autophagy and promoting trophoblastic cell survival and migration.

人参皂甙Rg_3对免疫功能的影响

对人参皂甙Ｒｇ３的免疫功能进行了实验研究，结果表明：人参皂甙Ｒｇ３能明显提高小鼠碳粒廓清速率、免疫器官重量、血清溶血素含量、脾淋巴细胞转化和ＮＫ活性，其结果均具有显著性差异（Ｐ＜０．０５），表明人参皂甙Ｒｇ３具有提高免疫功能的作用。

20(S/R)-人参皂苷Rg_3的制备及调节Th1/Th2免疫失衡活性

采用醋酸溶液作为提取溶剂,使西洋参叶中的二醇组人参皂苷在提取过程中发生降解,从而直接获得20(S)-人参皂苷Rg_3和20(R)-人参皂苷Rg_3,并对其调节Th1/Th2免疫失衡活性进行了研究.正交实验结果表明,当醋酸浓度为50%(体积分数),提取温度为80℃,提取时间为1 h时,20(S)-人参皂苷Rg_3和20(R)-人参皂苷Rg_3的转化率最高,分别为12. 30%和14. 80%.将20(S)-人参皂苷Rg_3和20(R)-人参皂苷Rg_3处理后的朗格汉斯状树突细胞(LDCs)分别作用于小鼠抗原诱导的Th1/Th2免疫失衡模型,发现细胞上层清液中IL-4的水平均显著降低,说明20(S)-人参皂苷Rg_3和20(R)-人参皂苷Rg_3对小鼠Th1/Th2免疫失衡具有调节作用.本文不仅建立了一种制备20(S)-人参皂苷Rg_3和20(R)-人参皂苷Rg_3的新方法,也为人参皂苷Rg_3在免疫系统疾病中的应用提供了新的科学依据.

人参皂苷Rg3联合顺铂对高转移人卵巢癌细胞系H0-8910PM增殖的抑制作用

背景与目的:人参皂苷(Rg3)有抑制肿瘤细胞生长的作用,顺铂为诱导肿瘤凋亡的化疗药物,中西医结合治疗肿瘤日益受到重视。本研究探讨Rg3联合顺铂对高转移人卵巢癌细胞系H0-8910PM增殖的抑制作用。方法:采用我院自建的高转移人卵巢癌细胞系H0-8910PM进行实验研究。实验分成6组:①空白对照组:只加新鲜的全培养液;②Rg3低浓度组:10μg/mlRg3培养液;③Rg3中浓度组:20μg/mlRg3培养液;④Rg3高浓度组:40μg/mlRg3培养液;⑤顺铂单药对照组:含10μg/ml顺铂的培养液;⑥顺铂+Rg3(中浓度)联合用药组:含10μg/ml顺铂+20μg/mlRg3培养液。分别观察各组对细胞核分裂指数、细胞集落形成率的影响。结果:随着Rg3浓度增高及Rg3和DDP的联合应用细胞核分裂指数下降,以联合用药组下降最明显(F=5.498,P=0.011)。空白对照组和Rg3高浓度组,顺铂单药组及顺铂+Rg3(中浓度)联合用药组相比,差异有非常显著性(P=0.011,0.007和0.001);Rg3低、中浓度组分别与顺铂+Rg3(中浓度)联合用药组相比,差异有显著性(P=0.010和0.015)。细胞集落形成率随着Rg3浓度增高而下降(F=100.69,P=0.000),高浓度的Rg3、DDP和联合用药组三者结果相近(P=0.887)。Rg3高浓度组、顺铂单药组合顺铂+Rg3(中浓度)组与空白对照组、Rg3低浓度组和Rg3中浓度组相比,及Rg3高浓度组与其他各组相比,差异均有显著性(P<0.05)。结论:Rg3对高转移人卵巢癌细胞有一定的杀伤作用,能有效抑制细胞核分裂、细胞集落形成,但未发现Rg3和顺铂联合用药会相加或协同作用。

基体辅助激光解吸电离飞行时间质谱用于人参皂甙Rg_3的定量分析

考察了基体辅助激光解吸电离时间飞行质谱用于人参皂甙Rg3 定量分析时内标的选择。加入棉子糖作为内标时 ,Rg3 的定量标准曲线的回归系数R2 =0 .938,平均相对误差为 2 8 6 % ;加入性质相近的芦丁后 ,Rg3 的定量标准曲线的回归系数R2 =0 993,平均相对误差为 7 5 %。分辨率的提高以及采用Rg3 和内标物的质谱峰的相对面积来代表Rg3

人参皂苷Rg_3对培养人视网膜色素上皮细胞增生的抑制作用

目的 研究人参皂苷Rg3(Ginsenoside Rg3)对体外培养视网膜色素上皮 (RPE)细胞增生的直接抑制作用及可能机制。方法 通过活细胞计数法与MTT比色法分别检测不同浓度 (10、2 0、5 0、80、10 0、15 0mg L)Rg3和Rg380mg L在不同作用时间 (6～ 12 0h)对RPE细胞增生及代谢的影响。结果 Rg3组细胞增殖受到抑制并出现细胞脱落 ,Rg310 0mg L具有最强的抑制效应 ,其明显抑制效应在 6h即出现 ,96h达高峰。Rg3组A值明显低于对照组 ,RPE细胞生存率下降。结论 Rg3可能通过抑制钙内流促进钾外流改变细胞膜电位、干扰RPE细胞代谢 。

人参皂苷Rg3与顺铂对高转移人卵巢癌细胞系HO-8910PM细胞周期和转移抑制的影响

目的探讨人参皂苷（Rg3）对高转移人卵巢癌细胞系HO-8910PM的体外抑制杀伤作用。方法用流式细胞仪和基底膜侵袭实验观察不同浓度的Rg3和／或顺铂（DDP）对高转移人卵巢癌细胞系HO-8910PM细胞的DNA含量、细胞转移抑制和细胞形态的影响。结果细胞DNA含量分析示：在G0／G1期HO-8910PM对照组与Rg3组、DDP组、Rg3＋DDP组比较差异均有统计学意义（F=54．416，P〈001），低浓度与高浓度组差异有统计学意义（P〈0．05）；S期对照组除与低浓度Rg3组外其余各组比较差异均有统计学意义（F=67810，P〈0．01），低浓度Rg3组与高浓度Rg3组比较差异有统计学意义（P〈005），G0／G1期和G2／M期DDP组与Rg3＋DDP组比较差异均统计学意义（均P〈005）。基底膜侵袭实验结果示：对照组分别与中浓度Rg3组、高浓度Rg3组、DDP组、Rg3＋DDP组比较差异均有统计学意义（F=15．052，P〈001）；低浓度与中、高浓度Rg3组比较差异有统计学意义（均P〈0.01）。结论中、高浓度的Rg3和Rg3＋DDP联合用药可以产生较好的抑制肿瘤细胞分化和转移作用并呈一定的剂量依赖性，Rg3与DDP的联合用药可能会产生药效增强作用。

20(R)-人参皂苷Rg3对人乳腺癌细胞自噬作用的影响

目的 观察20(R)-人参皂苷Rg 3 对人乳腺癌细胞（MCF-7）自噬作用的影响，并探讨20(R)-人参皂苷Rg 3 诱导MCF-7 自噬作用的最佳剂量。方法 人乳腺癌细胞株分为20(R)-人参皂苷Rg 3 实验组及空白对照组。采用MTT 法观察20(R)-人参皂苷Rg 3 对MCF-7 细胞生长的抑制作用，并依据计算出的IC 50 值确定20(R)-人参皂苷Rg 3 的有效浓度。结果 当20(R)-人参皂苷Rg 3 浓度在37.5～600.0 mg/L 时，MCF-7 细胞的生长抑制率最高，并随其浓度的增加而增大，与对照组比较差异有统计学意义（P＜0.05）。在荧光显微镜下观察到细胞所含自噬泡明显增多，说明20(R)-人参皂苷Rg 3 可诱导乳腺癌细胞自噬。蛋白质印迹法检测结果显示：LC 3 蛋白，特别是LC 3-II 的表达量与细胞自噬程度呈正相关，随着20(R)-人参皂苷Rg 3 干预浓度的增大，LC 3-I 和LC 3-II 蛋白表达量亦明显升高，与对照组比较差异有统计学意义（P＜0.05）。结论 20(R)-人参皂苷Rg 3 能显著抑制MCF-7细胞的增殖，且呈现良好的剂量、时间依赖性；20(R)-人参皂苷Rg 3 有诱导MCF-7 细胞自噬作用。

人参皂苷Rh2和Rg3抗肿瘤作用研究进展

人参皂苷是人参抗肿瘤的有效成分,其中人参皂苷Rh2（ginsenoside Rh2,GRh2）和人参皂苷Rg3（ginsenoside Rg3,GRg3）是人参抗肿瘤的主要活性成分。研究表明,二者可阻滞细胞周期,诱导分化,抑制转移,调节免疫功能,逆转多药耐药性,诱导凋亡等（[1]）,综术如下。1人参皂苷Rh2和Rg3药理作用抑制肿瘤细胞的增殖。洪新雨等（[2]）用聚合酶链反应检测到GRh2可使人脑胶质瘤SHG44中PCNA表达与转录产物明显下降。游智梅等（[3]）研究发现。

Effect of the structure of ginsenosides on the in vivo fate of their liposomes

To utilize themultiple functions and give full play of ginsenosides,a variety of ginsenosides with different structures were prepared into liposomes and evaluated for their effect on the stability,pharmacokinetics and tumor targeting capability of liposomes.The results showed that the position and number of glycosyl groups of ginsenosides have significant effect on the in vitro and in vivo properties of their liposomes.The pharmacokinetics of ginsenosides liposomes indicated that the C-3 sugar group of ginsenosides is beneficial to their liposomes for longer circulation in vivo.The C-3 and C-6 glycosyls can enhance the uptake of their liposomes by 4T1 cells,and the glycosyls at C-3 position can enhance the tumor active targeting ability significantly,based on the specific binding capacity to Glut 1 expressed on the surface of 4T1 cells.According to the results in the study,ginsenoside Rg3 and ginsenoside Rh2 are potential for exploiting novel liposomes because of their cholesterol substitution,long blood circulation and tumor targeting capabilities.The results provide a theoretical basis for further development of ginsenoside based liposome delivery systems.

Preparation, Release-control and Cell Apoptosis of C_6 Glioma Cells in PEG-PLGA-Rg3 Nanoparticles

With biodegradable material poly（ethylene glycol）-poly（lactide-co-glycolide） （PEG-PLGA） as substrate, the size distribution of Rg3-NPs was approved by the scanning electron microscopy. MTT assay was used to detect the effects of Rg3-NPs on the growth rate of C6 cells at various concentrations and flow cytometry（FCM） was applied to assay the cell cycle and cell apoptosis of C6 glioma cells. Western blot analysis was used to measure the protein level of PCNA. The results show that Rg3-NPs are slick and uniformity, the average diameter of the nanoparticles is about 75-90 nm, entrapment efficiency is （89.7±1.7）%. MTT assay shows the growth of C6 Glioma Cells can be significantly inhibited by Rg3-NPs in a dose-dependence manner. FCM and Western blot analysis show Rg3 can be released from the conjugated nanoparticles to function in the cell nuclei so as to lead to the changes in the growth cycle of the cells, which results in the arrest of G0-G1 cell cycle and induces the apoptosis of C6 cells. Therefore, Rg3-NPs may be used for the auxiliary therapy of brain glioma.