一年生桔梗质量研究初探

为了促进中药材GAP的发展，本文采用中国药典法测定了不同产地一年生桔梗的总皂苷含量。结果表明，某些地区的一年生桔梗达到中国药典标准，可以人药，因而各产地应根据实际情况来决定桔梗的采收。     

桔梗皂苷D对MG-63细胞的凋亡作用

目的 研究桔梗皂苷D对MG-63细胞的促凋亡作用.方法 MTT法测定桔梗皂苷D对MG-63细胞增殖抑制情况及其IC50值,利用流式细胞仪检测加入桔梗皂苷D作用24 h后的MG-63细胞的凋亡情况、凋亡类型.使用二氯荧光黄二乙酸酯(DCFH-DA)检测加入桔梗皂苷D后肿瘤细胞内活性氧水平,加入JC-1线粒体染料试剂盒检测被桔梗皂苷D孵育24 h后肿瘤细胞线粒体膜电位的变化.结果 MTT数据表明桔梗皂苷D对细胞的生长半数抑制浓度IC50为11.80μmol/L.MG-63细胞被桔梗皂苷D作用24 h后,通过JC-1和DCFH-DA染色的实验结果表明桔梗皂苷D作用后的MG-63细胞内的活性氧水平上升,细胞线粒体膜电位下降.结论 桔梗皂苷D可能通过增加细胞内活性氧水平破坏线粒体从而导致细胞发生凋亡.     

正交设计考察不同干燥方法对桔梗质量的影响

目的确立桔梗的产地加工的干燥工艺。方法以药典方法并结合其他方法测定桔梗的出干率、总皂苷与水溶性浸出物的含量。结果桔梗采集后,洗净,以微波3min或80℃烘干较好,尤以微波干燥其出干率、桔梗总皂苷、水浸出物含量最高。结论通过微波干燥所得的桔梗饮片其桔梗总皂苷的含量明显高于晒干法,降低劳动强度,是一种值得研究和推广的干燥方法。     

桔梗总皂苷的制备工艺研究

目的研究桔梗总皂苷的制备工艺。方法桔梗粉末 (84 0 μm)共加 2 0倍量水提取 3次 ,0 5h/次 ,滤液行大孔吸附树脂柱 ,用水 乙醇溶剂系统洗脱 ,分离得到桔梗总皂苷。结果平均得率为 1 6 0 3%。结论该法适于工业化生产     

UPLC-Q-TOF-MS测定治咳川贝枇杷滴丸中6种有效成分的含量

 目的 建立同时测定治咳川贝枇杷滴丸中6种有效成分（鸟苷、贝母素乙、桔梗皂苷D、桔梗皂苷D₃、齐墩果酸和熊果酸）含量的超高压液相色谱串联四级杆飞行时间质谱联用（UPLC-Q-TOF-MS）的检测方法。方法 采用Waters Acquity BEH C₁₈色谱柱（2.1 mm×100 mm,1.7 μm),流动相为乙腈-甲酸-水体系梯度洗脱,流速为0.4 mL·min^-1,PDA检测190~400 nm扫描;进样量：2.0 μL。结果 6种成分在一定范围内均呈现良好线性,r均大于0.999 6;精密度、重复性和稳定性良好;加样回收率在99%~101%之间。 结论 所建立的方法简便、准确、快速、重复性好,可用于治咳川贝枇杷滴丸中鸟苷、贝母素乙、桔梗皂苷D、桔梗皂苷D₃、齐墩果酸和熊果酸6个有效成分的含量测定。     

反相高效液相色谱法测定桔梗中3种三萜皂苷类化合物的含量

目的建立RP-HPLC法同时测定桔梗中去芹糖桔梗皂苷E、桔梗皂苷E和桔梗皂苷D3的含量。方法以Hypersil-ODS(4.6 mm×250 mm,5μm)为色谱柱,流动相为乙腈(A)-水(B),梯度洗脱,流速为0.8 mL.min-1,检测波长210 nm,温度为室温。结果去芹糖桔梗皂苷E、桔梗皂苷E和桔梗皂苷D3分别在4.160~83.2、10.75~215.0、4.080~81.6μg.mL-1与峰面积线性关系良好,平均回收率分别为96.5%、97.0%和97.3%,RSD分别为1.2%、1.0%和1.3%。结论该方法快速稳定且分离度好,为桔梗的质量控制提供可借鉴的分析方法。     

比色法测定桔梗中桔梗总皂苷的含量

目的建立桔梗中桔梗总皂苷的含量测定方法。方法以香草醛．高氯酸为显色剂,桔梗皂苷D为对照品,采用比色法测定。结果比色法测定的线性范围为0．096～0．672mg,相关系数为0．99997,平均加样回收率为96．8％（RSD=3．87％,n=9）。结论本法测定准确,重复性好,可用于桔梗药材中桔梗总皂苷的含量测定。     

桔梗烘法炮制初探

目的:探讨桔梗烘法最佳炮制条件.方法:采用正交试验法,对桔梗在不同炮制条件下,其有效成分桔梗总皂甙的浸出率进行测定,并测定桔梗的各炮制品的收得率.结果:温度90℃下烘45 min为桔梗烘法的最佳炮制条件.此条件所得桔梗总皂甙含量稍高于炒品,明显高于生品.结论:炮制条件与桔梗总皂甙含量有密切关系,为优选桔梗最佳炮制工艺提供参考.     

Proposed mechanisms for the extracellular release of PD-L1 by the anticancer saponin platycodin D

Platycodin D (PTD) is an oleanane-type terpenoid saponin, isolated from the plant Platycodon grandiflorus. PTD displays multiple pharmacological effects, notably significant anticancer activities in vitro and in vivo. Recently, PTD was shown to trigger the extracellular release of the immunologic checkpoint glycoprotein PD-L1. The reduction of PD-L1 expression at the surface of cancer cells leads to interleukin-2 secretion and T cells activation. In the present review, we have analyzed the potential origin of this atypical PTD-induced PD-L1 release to propose a mechanistic explanation. For that, we considered all published scientific information, as well as the physicochemical characteristics of the natural product (a modeling analysis of PTD and the related saponin β -escin is provided). On this basis, we raise the hypothesis that the capacity of PTD to induce PD-L1 extracellular release derives from two main mechanisms: (i) a drug-promoted shedding of membrane PD-L1 by metalloproteases or more likely, (ii) a cholesterol binding-related effect, that would lead to perturbation of membrane raft domains, limiting the recruitment of proteins like TLR4. The drug-induced membrane effects (frequently observed with saponin drugs), associated with a production of interferon-γ,can favor the release of proteins like PD-L1 into membrane vesicles. Our analysis supports the hypothesis that PTD is a cholesterol-dependent lipid raft-modulating agent able to promote the formation of PD-L1 containing extracellular vesicles. The anticancer potential of PTD and its capacity to modulate the functioning of the PD-1/PD-L1 checkpoint should be further considered.     

Involvement of intestinal efflux and metabolic instability in the pharmacokinetics of platycodin D in rats

We aimed to investigate the underlying mechanisms for low bioavailability of Platycodin D (PD) in rats. The bioavailability of PD was 1.89% with different half-lives depending on the administration route (2.14 ± 0.18 h for intravenous injection vs 5.42 ± 1.9 h for oral administration). The mean absorption time was 6.3 h calculated from the mean residence time of both administration routes. Consistent with these parameters, rat intestinal permeability using 3 different intestinal segments showed a low but greatest permeability in lower ileum (0.05 × 10⁻⁶ cm/s in jejunum and upper ileum vs 0.13 × 10⁻⁶ cm/s in lower ileum). The involvement of efflux system, probably Mrps, in upper ileum, could be explained from the efflux ratio of 6.4 and reduced efflux ratio by an Mrp inhibitor, MK571. The recovery of unchanged PD after the intravenous and oral administration was 50% and 5.2%, respectively, suggesting the contribution of gastrointestinal metabolism. In the gastrointestinal content, 4 metabolites of PD were identified: acetylated PD (m/z 1265.6), deglucose PD (m/z 1061.5), deapiose PD (m/z 1091.5), and deapiose-dexylose-derhamnose PD (m/z 813.4). In conclusion, the intestinal first-pass effect such as the presence of efflux functions in the upper ileum, limited but steady intestinal permeability, and gastrointestinal metabolism could explain the low bioavailability and prolonged absorption time of orally administered PD.