绞股蓝皂甙

摘要： 绞股蓝为临床常见中药制剂,其为除却五加科药物之外唯一一类含有和人参皂甙类似结构的皂甙植物,其应用以及药理作用引起了广大学者的重视.结合实际情况,本文全面分析了绞股蓝药理研究进展情况,旨在为相关学者的研究工作提供参考建议.

摘要： 目的观察绞股蓝皂甙对暴露于脂多糖中的小胶质细胞活化水平的影响.方法：采用脂多糖刺激N9 小胶质细胞系,诱导其活化.通过专用试剂盒检测炎症因子水平、Western blot 检测诱导型-氧化氮合酶和TOLR4 受体蛋白表达和免疫荧光染色观察iNOS 表达水平,评价细胞活化水平.结果：与对照组相比,LPS 可显著增加（Interleukin-6, IL-6）和肿瘤坏死因子-α 的释放量,并增加iNOS 和TOLR4 受体表达水平,而绞股蓝皂甙显著降低了LPS 对小胶质细胞产生的上述作用.此外,蛋白激酶C 抑制剂显著逆转了绞股蓝皂甙对TNF-α 和IL-6 释放量的增加作用.结论：绞股蓝皂甙可抑制小胶质细胞的活化,上述作用可能通过蛋白激酶C 介导.

摘要： Objective To investigate the effect and mechanism of gypenoside (GP) in improving the learning and memory ability of rats with mild cognitive impairment (MCI). Methods SD rats aged 12-15 months were randomly divided into 5 groups:sham surgery control (SSC), mild cognitive impairment model control (MCI), and low-, medium-and high-GP groups (LGP, MGP, HGP), each with 20 rats. The rat model of MCI was constructed by ligating bilateral internal carotid arteries (ICA) to induce severe stenosis, followed by persistent cerebral hypoperfusion for 2 months. Gastric lavage was performed for 2 months using GP in MCI group. The behaviors of rats, the changes of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity and the concentrations of malondialdehyde (MDA), nitric oxide synthase (NoS) and nitric oxide (No) in the cerebral cortex and hippocampus were observed. Results (1) Compared with MCI group, the latency stage in the groups LGP, MGP and HGP was shortened (P0.05);(2) compared with MCI group, the number of crossings of the original platform was increased from LGP, MGP to HGP (P0.05); (3) compared with MCI, the activities of SOD and GSH-Px were increased successively from LGP, to MGP and to HGP (P0.05). Conclusion Gypenoside improves the learning and memory ability of MCI rats by promoting the activities of SOD and GSH-Px, inhibiting the activity of NOS and reducing the contents of MDA and NO contents.%目的：探讨绞股蓝皂甙（GP）改善轻度认知功能障碍（MCI）大鼠学习记忆能力的作用及其机制。方法将12~15个月龄SD健康大鼠随机分为5组：假手术对照组（SSC组）、MCI模型对照组（MCI组）和GP低、中、高剂量组（LGP组、MGP组、HGP组），每组20只。通过结扎双侧颈内动脉（ICA）致其重度狭窄并大脑持续低灌注2个月，建立MCI大鼠模型。采用GP连续灌胃2个月作用于MCI大鼠，观察各组大鼠行为学、大脑皮层和海马超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活性和丙二醛（MDA）、一氧化氮合酶（NOS）、一氧化氮（NO）含量的变化。结果（1）与MCI组比较，LGP组、MGP组、HGP组的潜伏期依次变短（P0.05）。（2）与MCI组比较，LGP组、MGP组、HGP组穿过原平台位置的次数依次增多（P0.05）。（3）与MCI组比较，LGP组、MGP组、HGP组的SOD、GSH-Px活性依次升高（P0.05）。结论绞股蓝皂甙可能通过提高脑组织SOD、GSH-Px活性、抑制NOS活性以及降低MDA、NO含量，改善MCI大鼠学习记忆能力。

摘要： 目的：研究绞股蓝皂甙对人衰老皮肤成纤维细胞增殖的影响及机制。方法原代培养并建立人衰老皮肤成纤维细胞系，0、5、10、15μg/mL绞股蓝皂甙处理细胞，24、72、96 h后MTT检测细胞增殖；72h后流式细胞仪检测细胞周期。结果10、15μg/mL绞股蓝皂甙可以促进人衰老成纤维细胞增殖，使 S期细胞数增多且呈浓度依赖。结论绞股蓝皂甙可以使S期细胞数增多且成纤维细胞增殖能力增强，具有延缓细胞衰老的作用。%Objective To study the ef ect of Gypenosides on the proliferation of aged fibroblasts. Methods Fibroblasts were cultured and fed by Gypenosides with 0μg/ml,5μg/ml,10μg/ml and 15μg/ml for 24h,72h and 96h. cellproliferation and cellcycle were tested by MTT method and flow cytometer. Results Gypenosides could promote aged fibroblasts proliferation. At the same time,increased the number of cells in S stage. Conclusions Gypenosides can promote the proliferation of the aged fibroblasts and therefore could delay the cells ageing.

摘要： Objective To study the antioxidative damage ef ect and mechanism of Gypenosides at the cellular level. Methods Fibroblasts were cultured and fed by 0μg/ml,5μg/ ml,10μg/ ml and 15μg/ ml Gypenosides for 24h,72h and 96h. MTT method tested the cellproliferation. Relative level of MDA and activity of SOD in cells were measured. Results Gypenosides could promote aged fibroblasts proliferation. At the same time, decreased MDA volume and increased the activity of SOD. Conclusions Gypenosides protected the aged fibroblasts in oxidative stress and therefore could delay the cells ageing.%目的：在细胞水平研究绞股蓝皂甙抗氧化损伤的影响及机制。方法原代培养并建立人衰老皮肤成纤维细胞系，0、5、10、15μg/ml绞股蓝皂甙处理细胞，24、72、96h后，MTT检测细胞增殖；72h后检测SOD 活性、MDA 含量。结果绞股蓝皂甙可以促进人衰老成纤维细胞增殖，增强细胞SOD活性，降低MDA含量，且呈浓度依赖。结论绞股蓝皂甙可以通过提高SOD活性，降低MDA含量，削弱氧化应激反应对细胞的损伤，使细胞增殖能力增强，延缓细胞衰老。

摘要： 目的 探讨绞股蓝皂甙对Aβ诱导AD细胞模型的影响.方法 原代培养胎鼠基底前脑胆碱能神经元,实验细胞分为6组:空白对照组、BDNF组、SLs组、β淀粉样蛋白1-40(Aβ1-40)组、Aβ1-40+BDNF组和Aβ1-40+SLs组.应用MTT比色试验检测SLs对细胞活性的影响,免疫细胞化学染色检测胆碱乙酰转移酶(ChAT)的表达；采用Aβ1-40诱导AD细胞模型,运用免疫细胞化学染色和流式细胞仪分别检测诱导型一氧化氮合酶(iNOS)的表达和凋亡.结果 空白对照组、BMDF组、SLs组、Aβ1-40组、Aβ1-40+BNDF组、Aβ1-40+SLS组实验细胞MTT检测细胞积分吸光度(IA)值分别为0.61±0.04、0.91±0.07、0.92±0.07、0.36±0.02、0.56±0.04、0.55±0.04,ChAT免疫阳性细胞数分别为43.00士2.73、64.00±4.57、61.00±4.62、21.00±1.92、41.00±2.69、40.00±2.54,iNOS免疫阳性细胞数分别为41.00±2.92、40.00±2.89、40.00±2.96、67.00±5.26、46.00±2.78、45.00±2.97,细胞凋亡数分别为30.00±2.31、29.00±2.12、28.00±2.49、57.00±3.83、33.00±1.75、34.00±3.46.Aβ1-40+SLs组细胞活性与ChAT阳性细胞数均高于Aβ1-40组(P＜0.05),Aβ1-40+SLs组iNOS阳性细胞数与细胞凋亡数均低于Aβ1-40组(P＜0.05).结论SLs可促进体外培养的胆碱能神经元及其突起生长,可提高神经元的活性和ChAT表达,并可有效抑制Aβ1-40诱导的神经元iNOS表达和细胞凋亡.绞股蓝皂甙对Aβ诱导的AD细胞模型具有保护作用.%Objective To explore the effects of stevenleafs (SLs) on the cells model of Alzheimer's disease inducted by amyloid beta peptide 1 -40(A(3i-4o). Methods Basal forebrain cholinergic neurons from fetal rats were primarily cultured. The experimentation cells were divided into the blank cpntrol group,brain derived neurotrophic factor (BDNF) group.SLs group, A(3no group, Afjuo + BD-NF group,and the A￡ii-4o + SLs gfoup at random. The cells were observed under inverted microscope and the cells viability was assessed using MTT assay. The expression of choline acetyltransferase (ChAT)- positive neurons was detected by immunocytochemical staining. Afj,-l0 was added. The expression of inducible nitric oxide synthase (iNOS) in the cells with or without SLs pretreatment was observed by immunocytochemical staining. The cells apoptosis was detected by flow cytomertry. Results MTT assay showed that incubation of the cells with SLs resulted in the highest cell viability, which was incomparable with that cell incubated in the presence of BDNF (P>0. 05). A significant increase of ChAT - positive neurons in SLs and BDNF groups was demonstrated by immunocyto-chemistry as compared with those in the blank control group(P<0. 05). In the cells with SLs pretreatment,iNOS expression and cell apoptosis rates were significantly higher than those in the blank control group by immunocytochemistry and flowcytomertry, but it was obviously lower than those in A]3i-ir - treated cells without SLs pretreatment(P<0. 05). Conclusion SLs may offer protection effects on the cells model of Alzheimer's disease inducted by amyloid beta peptide 1 -40.

摘要： 目的 探讨绞股蓝皂甙对D-半乳糖(D-gal)所致阿尔茨海默病(AD)模型小鼠海马胆碱能系统功能的影响.方法 昆明小鼠颈背部皮下注射10％ D-gal,连续6 w造模.同时,各组分别灌胃生理盐水(正常对照组、模型组)、绞股蓝(高、低剂量组).给药结束后进行水迷宫训练,24h后进行学习记忆功能测试和海马胆碱乙酰基转移酶(ChAT)与乙酰胆碱酯酶(AchE)活性测定以及Western印迹检测ChAT表达.结果 与正常对照组相比,D-gal模型组小鼠学习记忆能力,模型组ChAT活性和ChaT表达明显下降(P ＜0.05,P＜0.01)；模型组AchE活性明显升高(P＜0.01).给予绞股蓝皂甙可明显改善AD模型小鼠的学习记忆功能(P＜0.05,P＜0.01),增强海马ChAT活性(P＜0.01)和降低AchE活性(P＜0.01),上调ChAT的表达(P＜0.01).结论 绞股蓝皂甙可明显提高模型小鼠的学习记忆能力,改善海马胆碱能系统功能.%Objective To investigate the effects of gypenosides on the hippocampal cholinergic system in D-galactose induced Alzheimer's disease (AD) in mice. Methods The mice were given subcutaneous injection of 10% D-galactose for 6 weeks (125 ml · kg · d-1 ). Normal saline, gypenosides respectively were given by intragastric administration in different study groups. The mice were trained to find the platform in the water maze on the 43th day. After 24 hours, learning and memory ability was tested, choline acetyltransferase (chAT) activity, acetylcholinesterase (AchE) activity, the expression of ChAT in hippocampus was observed by Western blotting after treatment. Results Compared with the normal control group, the learning and memory dysfunction, the decreases of ChAT activity and expression of ChAT were found in model group, AchE activity was increased in model group (P < 0. 05, P < 0. 01). The gypenosides could markedly attenuate cognitive dysfunction, elevate ChAT and expression of ChAT, decrease AchE activity in the hippocampi of mice treated with D-galactose (P <0. 05, P <0. 01). Conclusions The gypenosides can significantly improve the hippocampal cholinergic system function, and thus enhance the learning and memory ability in D-galactose induced AD model mice model.

摘要： 目的 观察绞股蓝皂苷(GP)对光损伤Balb/C小鼠皮肤中核转录因子kappa-B(NF-κB)、p38丝裂原活化蛋白激酶(p38MAPK)的影响,进一步探讨GP抗皮肤光损伤的可能机制.方法 将80只雌性Balb/C小鼠随机分为8组,每组10只.①空白对照组:不做任何处理；②UVB模型组:UVB照射60 s；③GP乳膏Ⅰ组；④GP乳膏Ⅱ组；⑤维生素E乳膏Ⅰ组；⑥维生素E乳膏Ⅱ组；⑦基质Ⅰ组；⑧基质Ⅱ组.Ⅰ组均先外涂相应的乳膏或基质,30 min后照射UVB 60 s；Ⅱ组均先用UVB照射60 s,30 min后外涂相应的乳膏或基质.采用隔日UVB照射7次Balb/C小鼠建立皮肤光损伤动物模型,应用Western印迹法检测小鼠皮肤中NF-κB抑制蛋白(IκB蛋白)、κB抑制蛋白激酶(IKK蛋白)及p38MAPK、磷酸化p38MAPK(pp38)的表达.结果 空白对照组小鼠表皮中IκB、IKK蛋白未见表达.UVB模型组小鼠表皮中IκB蛋白水平为0.40±0.07,IKK蛋白为2.01±1.75.GP乳膏Ⅰ组与Ⅱ组IκB蛋白表达(分别为1.63±0.85和0.90±0.40)明显高于UVB模型组(P值均＜0.05),IKK蛋白表达(分别为0.23±0.12和0.45±0.29)明显低于UVB模型组(P值均＜0.05),与维生素E组小鼠皮肤中IκB蛋白、IKK蛋白的表达结果相似.各组p38MAPK表达量没有明显差异.GP乳膏Ⅰ组与Ⅱ组磷酸化p38MAPK表达水平(分别为0.425±0.054和0.571±0.090)明显低于UVB模型组(0.835±0.049),与维生素E组相似.结论 UVB照射能促使NF-κB活化,激活磷酸化p38MAPK; 1.5％GP乳膏能抑制UVB诱导的NF-κB通路及p38MAPK的激活,可能是其抗炎、抗光损伤的作用机理之一.%Objective To observe the effects of gypenosides (GP) on nuclear factor κB (NF-κB) and p38 mitogen activated protein kinase (p38MAPK) signaling pathways in photodamaged skin of mice,and to explore the mechanisms underlying the protective effects of GP against photodamage.Methods Eighty Balb/C female mice were randomly divided into 8 groups: blank control group receiving no treatment,ultraviolet B (UVB) model group receiving UVB irradiation for 60 seconds,GP group Ⅰ receiving topical GP treatment followed by UVB irradiation,GP group Ⅱ receiving UVB irradiation followed by topical GP treatment,VitE group Ⅰ receiving topical VitE treatment followed by UVB irradiation,VitE group Ⅱ receiving UVB irradiation followed by topical VitE treatment,matrix group Ⅰ receiving topical matrix treatment followed by UVB irradiation,matrix group Ⅱ receiving UVB irradiation followed by topical matrix treatment.UVB irradiation lasted 60 seconds at one time,and was given once every other day for 7 times to establish a skin model of photodamage.The interval between irradiation and topical treatment was 30 minutes in all the groups except the control group and UVB model group.After the last treatment,mice were sacrificed.Western blot was performed to measure the protein expressions of inhibitor of NF-κB(IκB),inhibitor of NF-κB kinase (IKK),p38MAPK as well as phosphorylated p38MAPK (pp38) in skin tissue from the mice.Results No expressions of IκB or IKK were observed in the blank control group.The expression level of IκB was 0.40 ± 0.07 in UVB model group,significantly lower than that in GP group Ⅰ (1.63 ± 0.85,P ＜ 0.05) and GP group Ⅱ (0.90 ± 0.40,P ＜ 0.05),whereas the level of IKK protein was higher in UVB model group than in the GP group Ⅰ and Ⅱ (2.01 ± 1.75vs.0.23 ± 0.12 and 0.45 ± 0.29,both P ＜ 0.05).No significant difference was observed in the expression of IκB or IKK proteins between the GP group Ⅰ,Ⅱ,VitE group Ⅰ and Ⅱ or in the expression of p38MAPK between the 8 groups.The phosphorylated p38MAPK expression in UVB model group was significantly higher than that in GP group Ⅰ and Ⅱ (0.835 ± 0.049 vs.0.425 ± 0.054 and 0.571 ± 0.090,both P＜ 0.05),but similar to that in VitE groups.Conclusions UVB can activate NF-κB and phosphorylated p38MAPK signaling pathways; GP 1.5％ cream can inhibit UVB-induced activation of NF-κB and p38MAPK pathways,which may be one of the mechanisms underlying its protective effects against inflammation and photodamage.

摘要： 目的:观察绞股蓝皂甙(GPS)对2型糖尿病(T2DM)并非酒精性脂肪性肝病(NAFLD)大鼠肝组织肝细胞核因子-1α(HNF-1α)的影响.方法:65只SPF级雄性SD大鼠(SD)，体质量220～2508，随机分为空白对照组(7只，N组)，NAFLD模型组(NM组，7只)，T2DM并NAFLD模型组(模型组，51只)。N组给予普通饲料喂养。NM组给予高脂饲料喂养。模型组先给予高糖高脂饲料喂养4周;隔夜空腹腹腔注射链尿佐菌素(STZ) 40mg/kg，继续给予高糖高脂饲料喂养至8周，建立T2DM并NAFLD大鼠模型;将大鼠模型分为GPS大剂量干预组((9只，JH组)，给予GPS lg/kg.d灌胃;GPS小剂量千预组(9只，JL组)，给予GPS 0.5g/kg.d灌胃;T2DM并NAFLD模型对照组(9只，M组)，同等体积纯净水灌胃;.继续给予高糖高脂饲料;治疗周期为6周。实验周期14周。定量PCR技术检测肝组织HNF-1α，肝脏病理学。结果:(1)肝组织HNF-1α:以N组扩增倍数为1计算，NM组肝细胞核因子表达为0.85，与N组比较有显著差异(P<0.05);M组为0.62，与N组比较有非常显著差异(P<0.01);治疗后，JH组HNF-1α升至0.80，与M组比较有非常显著差异(P<0.01);JL组HNF升至0.68，与M组比较有非常显著差异(P<0.05)。(2)肝脏病理学:NM组、M组重度NAFLD, JH组、JL组中度至重度NAFLD.结论:GPS能够抑制T2DM并NAFLD大鼠肝脏HNF-1α表达的下降。

摘要： 利用体外产气量法研究绞股蓝皂甙对瘤胃微生物甲烷产量及体外发酵的影响.试验以0.42g羊草+0.126g玉米+0.054g豆粕为发酵底物,在60ml培养基中绞股蓝皂甙添加量分别为0(对照)、5、10、20和40mg,发酵24h.结果显示,与对照组比较,各处理组甲烷摩尔产量显著下降(P＜0.05),甲烷产量与皂甙之间有显著的线性效应.10mg绞股蓝皂甙水平与对照组比较,显著提高了总的挥发性脂肪酸(TVFA)产量及乙酸、丙酸和丁酸的比例(P＜0.05),乙丙比无显著变化,乙酸,丁酸,异丁酸,戊酸,异戊酸,支链脂肪酸百分比及乙丙比和TVFA浓度随着皂甙剂量增加呈现显著的二次方效应,丁酸同时具有显著的线性效应.处理组原虫数量显著下降(P＜0.05),有着显著的线性和二次方效应(P＜0.05),而微生物蛋白含量没有显著变化,但呈现上升趋势.高剂量皂甙组的氨态氮浓度显著高于对照组(P＜0.05),与绞股蓝皂甙之间有显著的线性效应.以上结果表明,绞股蓝皂甙能抑杀瘤胃原虫,显著减少甲烷产量,提高挥发性脂肪酸(VFA)的生成.

摘要： 本发明公开了一种绞股蓝总皂甙酸水解产物中分离的化合物，该化合物的结构式为：

摘要： 本发明提供了一种快速培养绞股蓝总皂甙的方法，包括以下步骤：S1.取绞股蓝幼茎，在MS半固体培养基上避光继代培养，选取连续继代培养4次且生长旺盛、质地疏松、珊瑚状细胞团的愈伤组织；S2.将步骤S1得到的愈伤组织接种至MS液体培养基中进行摇床培养，培养至4~5d时加入柠檬酸、酵母提取物，培养至12~15d时加入苹果酸、茉莉酸甲酯，第20~26天收获绞股蓝悬浮细胞。本发明通过细胞悬浮培养方法可快速培养绞股蓝总皂甙，且能进一步提高绞股蓝总皂甙的含量。

摘要： 本发明公开了一种从绞股蓝中提取绞股蓝皂甙的方法，包括下述步骤:原料处理、高压提取、双水相萃取、脱盐、浓缩干燥，得到绞股蓝皂甙。具有含量高，提取率高，工艺简单，适合生产，生产成本低等优点。

摘要： 本发明提供了一种从绞股蓝中提取含量≥99%的绞股蓝皂甙的工艺，包括提取和纯化，提取步骤为：原料加水加热煮沸，然后用乙醇回流提取，浓缩的滤饼用6号提取脱脂，得到60%以上的总皂甙；纯化步骤为：总皂甙用乙醇加热溶解，上大孔树脂柱，用盐酸洗脱，氢氧化钠中和得浸膏，经结晶和重结晶纯化得到含量99%的皂甙。本发明的优点是：工艺简便、环境友好、提取的绞股蓝甙含量≥99%，而且提取量稳定。

摘要： 本发明一种绞股蓝总皂甙的制取方法，属于化工技术，提出一种工艺流程短、皂甙得率高、纯度高的绞股蓝皂甙制取方法。该绞股蓝总皂甙的制取方法以绞股蓝为原料，将绞股蓝加入50－95%乙醇或甲醇，提取1－3次，过滤，取滤液回收至无醇味，再加盐酸调PH值＝3.5－4.5，加热煮沸后过滤，取滤渣加水重结晶再过滤，浓缩，真空干燥粉碎，得股蓝总皂甙制品。该方法所制取的绞股蓝总皂甙口感好、吸收快、有效的提高了生物利用度，疗效显著。

摘要： 本发明提供了一种从绞股蓝中提取含量≥99%的绞股蓝皂甙的工艺，包括提取和纯化，提取步骤为：原料加水加热煮沸，然后用乙醇回流提取，浓缩的滤饼用6号提取脱脂，得到60%以上的总皂甙；纯化步骤为：总皂甙用乙醇加热溶解，上大孔树脂柱，用盐酸洗脱，氢氧化钠中和得浸膏，经结晶和重结晶纯化得到含量99%的皂甙。本发明的优点是：工艺简便、环境友好、提取的绞股蓝甙含量≥99%，而且提取量稳定。

摘要： 本发明公开了一种从绞股蓝中提取绞股蓝皂甙的方法，包括下述步骤：原料处理、高压提取、双水相萃取、脱盐、浓缩干燥，得到绞股蓝皂甙。具有含量高，提取率高，工艺简单，适合生产，生产成本低等优点。

摘要： 本发明属于中药材分离提取领域，尤其是一种绞股蓝皂甙B在拮抗放化疗和糖皮质类激素药物副作用新药的发明和应用和制备，针对现有的以糖皮质激素类药物为代表的药品在众多疾病中显示出抗炎、抗休克、抗病毒和免疫抑制等治疗作用，但同时给患者造成的副作用也是很大的，主要是长期服用糖皮激素造成肾上腺萎缩，糖盐代谢失调以及对心、肝、肺和肾脏的损害的问题，现提出如下方案，其制备方法包括以下步骤：S1、取绞股蓝总皂苷20kg，以甲醇溶解，与40kg硅胶混合拌样，挥干溶剂；S2、上100kg干法硅胶层析柱，以氯仿‑甲醇梯度洗脱，本发明提取的绞股蓝皂苷B的药物，用于拮抗糖皮质激素类药物副作用及放化疗所产生的副作用，疗效确切，安全无毒付作用。

摘要： 本发明公开了一种绞股蓝皂甙的提取方法，属于植物提取技术领域，所述的方法包括粉碎、超声波辅助热水浸提、大孔树脂富集和萃取等步骤。本发明的方法对生产设备要求较低，对绞股蓝皂甙的破坏小、提取率高，所用试剂污染小，能够实现工业化生产。

摘要： 本发明一种绞股蓝总皂甙的制取方法，属于化工技术，提出一种工艺流程短、皂甙得率高、纯度高的绞股蓝皂甙制取方法。该绞股蓝总皂甙的制取方法以绞股蓝为原料，将绞股蓝加入50－95%乙醇或甲醇，提取1－3次，过滤，取滤液回收至无醇味，再加盐酸调PH值＝3.5－4.5，加热煮沸后过滤，取滤渣加水重结晶再过滤，浓缩，真空干燥粉碎，得股蓝总皂甙制品。该方法所制取的绞股蓝总皂甙口感好、吸收快、有效的提高了生物利用度，疗效显著。