Effects of plumbagin on migration and invasion of human hepatoma cell line via JAK2/STAT3 signaling pathway

Objective:To study the effect of plumbagin(PL)on the migration and invasion of human hepatocellular carcinoma(HCC)cells and its possible mechanism.Methods:The cell counting kit(CCK-8)was used to detect the effects of different concentrations of plumbagin on the proliferation of human hepatocellular carcinoma Huh-7 and LM3 cells.The effect of plumbagin on the migration ability of Huh-7 and LM3 cells was detected by scratch test and Transwell migration test,and the effect of on the invasion ability of Huh-7 and LM3 cells was detected by Transwell invasion test.Western Blot was used to detect the expression of E-cadherin,N-cadherin,matrix metalloproteinase-2 and related proteins in JAK2/STAT3 signaling pathway in Huh-7 and LM3 cells.Results:Plumbagin could inhibit the proliferation of Huh-7 and LM3 cells in a time-and concentration-dependent manner.Plumbagin inhibited the migration and invasion of Huh-7 and LM3 cells in a concentration dependent manner,and it can down-regulate the expression of N-cadherin and MMP-2 protein,up-regulate the expression of E-cadherin protein,and inhibit the activation of JAK2/STAT3 signaling pathway.Conclusion:Plumbagin can inhibit the migration and invasion of human hepatocellular carcinoma Huh-7 and LM3 cells,and the molecular mechanism of this process may be related to the inhibition of JAK2/STAT3 signaling pathway activation.

Research Progress and Ideas on the Anti-liver Fibrosis Effect of Ethnic Medicine Plumbagin Based on microRNAs/TLR4/NF-κB and NLRP3 Inflammasome Activation

The core of hepatic fibrosis is the activation of hepatic stellate cells.Through the lipopolysaccharide/TLR4/MyD88/NF-κB signal transduction pathway,the inflammatory response in the liver is directly enhanced,and then returns to promote the activation of hepatic stellate cells.And TLR4/MyD88/NF-κB signaling pathway can directly regulate the activation of NLRP3 inflammasome and is an important pathway for activating hepatic stellate cells.TLR4/MyD88/NF-κB/NLRP3 inflammasome pathway is regulated by upstream microRNAs.These miRNAs can significantly regulate the inflammatory response of the liver and the activation behavior of hepatic stellate cells,affecting the formation of liver fibrosis.Previous studies have found that the active ingredient of Guangxi specialty ethnic medicine,plumbagin,has a definite anti liver fibrosis effect,but its mechanism of action is not clear.This paper provides a review of the research progress on the above issues,and further research ideas have been derived from this,stating that"the anti liver fibrosis effect of plumbagin is achieved by regulating miRNA/TLR4/MyD88/NF-κB inflammatory pathway and activating downstream NLRP3 inflammasome".

Preparation Process of Plumbagin Nanomicelle In-situ Gel

[Objectives]To prepare plumbagin nanomicelle(PLB-N)in-situ gel,and optimize the formulation and process.[Methods]PLB-N was prepared by self-assembly method,and the optimal formulation of PLB-N in-situ gel was determined by orthogonal experiment design and single factor method.[Results]The optimal preparation process for PLB-N was a drug to lipid ratio of 1:3,a Tween 80 content of 5%,an ethanol content of 7.5%of the hydration medium,a magnetic stirring speed of 2200 rpm,a stirring time of 30 min,and an ultrasound time of 10 min.The optimal formulation of PLB-N in-situ gel was 22%of poloxamer 407,6%of poloxamer 188,and 1:1 of PLB-N to water.The encapsulation efficiency of PLB-N prepared with the optimal formula was(95.8%±0.4%),and the average particle size was(75.19±1.14)nm,and the Zeta potential was(-20.73±1.19)mv.[Conclusions]PLB-N in-situ gel had stable and reliable preparation process,uniform content,and broad application prospects.

Suppressive Effects of Plumbagin on Invasion and Migration of Breast Cancer Cells via the Inhibition of STAT3 Signaling and Down-regulation of Inflammatory Cytokine Expressions

Objective： The aim of this study was to investigate the effects of plumbagin （PL）, a naphthoquinone derived from the medicinal plant plumbago zeylanica, on the invasion and migration of human breast cancer cells. Methods： Human breast cancer MDA-MB-231SArfp cells were treated with different concentrations of plum- bagin for 24 h. The effects of plumbagin on the migration and invasion were observed by a transwell method. The expressions of IL-1α, IL-1β, IL-6, IL-8, TGF-β, TNFα, MMP-2 and MMP-9 mRNA in MDA-MB-231SArfp cells were detected using Real-Time PCR. MDA-MB-231SArfp cells were treated with plumbagin at different concentrations for 45 minutes. The activation of STAT3 was detected by western blot. Following this analysis, STAT3 in MDA-MB-231SArfp cells was knocked out using specific siRNA, mRNA levels of IL-1α, TGF-β, MMP-2 and MMP-9 were then detected. Consequently, MDA-MB-231SArfp cells were injected intracardially into BALB/c nude mice to construct a breast cancer bone metastatic model. The mice were injected intra- peritoneally with plumbagin. Non-invasive in vivo monitoring, X-ray imaging and histological staining were performed to investigate the effects of plumbagin on the invasion and migration of breast cancer cells in vivo. Results： The in vitro results showed that plumbagin could suppress the migration and invasion of breast cancer cells and down-regulate mRNA expressions of IL-1α TGF-β, MMP-2 and MMP-9. Western blotting demonstrated that plumbagin inhibited the activation of STAT3 signaling in MDA-MB-231SArfp cells. The inactivation of STAT3 was found to have an inhibitory effect on the expressions of IL-1α, TGF-β, MMP-2 and MMP-9. In vivo studies showed that plumbagin inhibited the metastasis of breast cancer cells and decreased osteolytic bone metastases, as well as the secretion of MMP-2 and MMP-9 by tumor cells at metastatic lesions. Conclusions： Plumbagin can suppress the invasion and migration of breast cancer cells via the inhibition of STAT3 signaling and by downregulation of IL-1α, TGF-β, MMP-2 and MMP-9.

Plumbagin Enhances TRAIL-mediated Apoptosis through Up-regulation of Death Receptor in Human Melanoma A375 Cells

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a promising anti-cancer agent. However, emergence of drug resistance limits its potential use. Plumbagin is a natural quinonoid compound isolated from plant. In this study, induced apoptosis effect of the combined treatment with plumbagin and TRAIL on human melanoma A375 cell line was examined and possible mechanism was investigated. The cells were divided into four groups: control group, plumbagin group (plumbagin, 5 or 10 μmol/L), TRAIL group (TRAIL, 30 ng/mL) and plumbagin+TRAIL group (combined treatment group). The apoptosis, and the expression of DR4 and DR5 were detected by flow cytometry. The activities of caspase-8 and caspase-3 were determined by colorimetric assay. The results showed that the apoptosis rate was 8.3% in TRAIL group, 10.35%–16.94% in plumbagin group and 52.39%–65.39% in combined treatment group, respectively, with the difference being significant between combined treatment group and plumbagin or TRAIL group (P<0.05 for each). Moreover, plumbagin alone could markedly up-regulate DR5 mRNA and protein expression, and slightly increase DR4 mRNA and protein expression. Treatment of human melanoma A375 cells with plumbagin resulted in the activation of Caspase-3, but not Caspase-8. These results suggest that plumbagin might be useful for TRAIL-based treatment for melanoma.

In vitro inhibitory effects of plumbagin,the promising antimalarial candidate,on human cytochrome P450 enzymes

Objective:To investigate the propensity of plumbagin to inhibit the three isoforms of human cytochrome P450(CYP),ie.,CYP1A2,CYP2C19,and CYP3A4 using human liver microsomes in ritro.Methods:Inhibitory effects of plumbagin on the three human CYP isoformswere investigated using pooled human liver microsomes.Phenacetin O-deethylation,omeprazole hydroxylation and nifedipine oxidation were used as selective substrates for CYP1A2,CYP2C19 and CYP3A4 activities,respectively.Concentrations of paracetamol,5-hydroxyomeprazole,and oxidized nifedipine were determined in microsomal incubation mixture using high performance liquid chromatography.Results:Plumbagin showed significantinhibitory effects on all CYP isoforms.but with the most potent activity on CYP2C19-mediated omeprazole hydroxylation.The IC50(concentration that inhibits enzyme activity by 50%) values of plumbagin and nootkatone(selective inhibitor) for CYP2C19 were(0.78±0.01) and(27.31±0.66) μM,respectively.The inhibitory activities on CYP1 A2-mediated phenacetin O-deethylation and CYP3A4-mediated nifedipine oxidation were moderate.The IC_(50) values of plumbagin and-naphthoflavone(selective inhibitor) for CYP1A2 were(1.39±0.01) and(0.02±.0.36) μM,respectively.The corresponding IC_(50) values of plumbagin and ketoconazole(selective inhibitor) for CYP3A4 were(2.37+0.10) and(0.18±0.06) μM,respectively.Conclusions:Clinical relevance of the interference of human drug metabolizing enzymes should be aware of for further development scheme of plumbagin as antimalarial drug when used in combination with other antimalarial drugs which are metabolized by these CYP isoforms.

Inhibitory activities of plumbagin on cell migration and invasion and inducing activity on cholangiocarcinoma cell apoptosis

Objective: To investigate the cytotoxic, apoptotic and inhibitory activities on cell migration and invasion of plumbagin in the human cholangiocarcinoma(CCA) cell line(CL-6) in comparison with human embryonic fibroblast cell line(OUMS). Methods: Cytotoxicity activity was evaluated using MTT assay. Inhibitory effect on cell migration and invasion were investigated using label-free real-time cell analysis and QCM ECMatrix cell invasion chamber, respectively. Apoptotic activity was evaluated using flow cytometry and Cell Event? Caspase 3/7 assay. Results: Based on results of the cytotoxicity test in CL-6 cells, 50% inhibitory concentration(IC_(50), Mean±SD) values of plumbagin and the standard drug 5-fluorouracil were(24.00±3.33) and(1 036.00±137.77) μmol/L, respectively. The corresponding values for OUMS cells were(57.00±5.23) and(2 147.00±209.98) μmol/L, respectively. The selectivity index was 2.28. The inhibitory activities of plumbagin on cell migration and invasion were potent and concentration-dependent with IC_(50) of 25.0 μmol/L and complete inhibition at 25.0 μmol/L. Flow cytometry analysis showed that plumbagin at 12.5 μmol/L(half IC_(50)) induced CL-6 cell apoptosis(43.24% of control) through stimulation of caspase 3/7 activities. Complete cell apoptosis was observed at 12.5 μmol/L. Conclusions: The cytotoxic activity and inhibition of migration and invasion including apoptosis induction in the human CCA cell line(CL-6) suggest that plumbagin could be a promising candidate for CCA chemotherapeutics. However, its relatively low selective cytotoxic effect on CCA cells is a major concern.

Inhibitory effect of plumbagin,a potential anticancer natural compound,on cytochrome P450 2J2 in humans

OBJECTIVE Cytochrome P450(CYP)2J2 is highly expressed in many kinds of human tumors and promotes tumor cell growth via regulating the metabolism of arachidonic acids.The purposes of this study were toidentify the new inhibitor of CYP2J2 from natural compounds and evaluate its potential to inhibit hepatoma carcinoma cells.METHODS Total fifty natural products were screened for the inhibitory potency against the activity of CYP2J2-mediated astemizole O-demethylation via LCMS/MS analysis.Enzyme kinetic and molecular docking studies were also carried out.RESULTS Our data found that plumbagin potently inhibited CYP2J2 with IC50value at 3.42,3.37 and 1.17μmol·L-1in rat liver microsomes,human liver microsomes(HLMs)and recombinant CYP2J2(rC YP2J2),respectively.Further enzyme kinetic studies showed that plumbagin was a mixed-type inhibitor of CYP2J2 in HLMs and r CYP2J2 with Kivalues of 1.88and 0.92μmol·L-1,respectively.Docking data presented that plumbagin interacted with CYP2J2 mainly through GLU222 and ALA223,which were crucial residues for substrates binding.At the same time,plumbagin showed cytotoxicity effects on hepatic carcinoma cell lines,such as HepG 2 and SMMC-7721,with IC50values at 11.55±1.06and(13.15±1.11)μmol·L-1,respectively.CONCLUSION These results indicated that plumbagin was a potent CYP2J2 inhibitor and potential anticancer agent.Further studies are needed to cover the mechanism of its antitumor activity.

Research on the Antitumor Effect of Plumbagin by Inhibiting IL-6/STAT3 Pathway in Large Cell Lung Cancer

Background and Objective Lung cancer, which has become the leading cause of tumor mortality in many countries, appears to be one of the most dangerous malignant tumors that

Plumbagin对人高转移大细胞肺癌细胞系抑制作用的研究

目的:研究Plumbagin对人高转移大细胞肺癌L9981细胞系的体外抗肿瘤作用,并初步探讨其机制。方法:不同浓度Plumbagin处理L9981细胞系,采用MTT法观察对肿瘤细胞增殖的影响,确定药物IC50;采用流式细胞术检测对细胞系诱导凋亡的作用;采用Boyden小室侵袭实验检测对体外侵袭力的抑制作用。以IC50Plumbagin处理L9981细胞系,于处理后6、24、48h收获细胞,以实时定量PCR方法检测Bcl-2、Bax、VEGF和CYCD1等基因的mRNA表达变化。结果:MTT法显示,Plumbagin明显抑制L9981细胞系的细胞增殖(F=39.535,P=0.000),IC50为9.0μmol/L;Plum-bagin对L9981细胞系具有体外诱导凋亡作用(F=23.671,P=0.000),且明显抑制其体外侵袭能力。Bodyen小室侵袭实验检测对照组和Plumbagin组平均穿膜细胞数分别为228.17±55.12和9.83±3.87,差异有统计学意义,t=13.598,P=0.000。Plumbagin处理L9981细胞系后不同时间点检测结果显示,Bcl-2、VEGF和CYCD1基因表达均逐渐降低,bax基因表达逐渐增高,组间差异有统计学意义(F=13.520,P=0.000;F=15.778,P=0.000;F=10.163,P=0.000;F=18.635,P=0.000)。结论:Plumbagin对大细胞肺癌L9981细胞系具有明确的抗肿瘤作用。Plumbagin通过多种作用机制发挥其抑癌作用,显示了其成为抗大细胞肺癌药物的前景。

Plumbagin对人类大细胞肺癌NL9980细胞系抑癌作用的研究

目的研究Plumbagin对人类大细胞肺癌NL9980细胞系的抗肿瘤作用并探索其机制。方法不同浓度Plumbagin处理NL9980细胞系，采用MTT法观察其对肿瘤细胞增殖的影响，确定药物IC50，采用流式细胞术检测对细胞系诱导凋亡的作用，采用Boyden小室侵袭实验检测对体外侵袭力的抑制作用；以IC50 Plumbagin处理NL9980细胞系，于处理后6、24及48h收获细胞，以实时定量PCR方法检测bcl-2、bax、VEGF和CYCD1等基因的mRNA表达变化。结果MTT法显示Plumbagin明显抑制NL9980细胞系的细胞增殖，IC50为7．5μmol／L；Plumbagin对NL9980细胞系具有体外诱导凋亡作用，且明显抑制其体外侵袭能力，Bodyen小室侵袭实验检测对照组和Plumbagin组平均穿膜细胞数分别为161．59±47．32和26．58±9．07。Plumbagin处理NL9980细胞系后不同时间点检测结果显示，bcl-2、VEGF和CYCD1基因表达均逐渐减低，bax基因表达逐渐增高，组间差异有统计学意义（均P〈0．05）。结论Plumbagin对大细胞肺癌NL9980细胞系具有明确的抗肿瘤作用。Plumbagin可能通过多种作用机制发挥其抑癌作用，显示了其成为抗大细胞肺癌药物的前景。

Self-assembled metal-organic frameworks nanocrystals synthesis and application for plumbagin drug delivery in acute lung injury therapy

Metal-organic frameworks(MOFs)have recently allured a variety of concern in the fields of nanotechnology.However,exploring their biomedical applications is still a relatively new field.In this work,zeolite imidazole skeleton-8(ZIF-8)was reported for the first time as a drug carrier for the treatment of lung injury.Uniform ZIF-8 nanoparticles encapsulating plumbagin(PLB)are achieved by a facile physical adsorption process.Scanning electron microscopy(SEM),powder X-ray diffraction(PXRD)and UV–vis absorption spectrum were conducted to investigate the physical properties of ZIF-8 and PLB@ZIF-8.In animal model,the collagen fibers deposition produced by severe lung injury is significantly decreased.The secretion of inflammatory factor TGF-βand IL-6 were efficiently dropped by the combination of plumbagin and ZIF-8.At the same time,the expressions of collagen I,α-SMA and TNF-αwere also suppressed.This strategy puts forth a promising blueprint in the application of MOF materials,especially in biomedical fields.

基于JAK2/STAT3信号通路探讨白花丹醌对人肝癌细胞迁移和侵袭的影响

目的:探讨中药单体白花丹醌(plumbagin,PL)对人肝癌细胞迁移与侵袭的影响及其可能的机制。方法:以人肝癌Huh-7和LM3细胞为研究对象,采用细胞计数试剂盒(CCK-8)法检测不同浓度的PL对Huh-7和LM3细胞增殖的影响,通过划痕实验和Transwell迁移实验检测PL对Huh-7和LM3细胞迁移能力的影响,Transwell侵袭实验检测PL对Huh-7和LM3细胞侵袭能力的影响,Western Blot检测Huh-7和LM3细胞中E-钙黏蛋白(E-cadherin)、N-钙黏蛋白(N-cadherin)和基质金属蛋白酶-2(MMP-2)及酪氨酸蛋白激酶2(Janus kinase 2,JAK2)/信号传导及转录激活因子3(signal transducer and activator of transcription3,STAT3)信号通路中相关蛋白的表达情况。结果:PL可抑制Huh-7和LM3细胞增殖,且呈现出时间和浓度依赖性;PL以浓度依赖性方式抑制Huh-7和LM3细胞迁移和侵袭;PL可下调N-cadherin、MMP-2蛋白表达,上调E-cadherin蛋白表达,且能够抑制JAK2/STAT3信号通路的激活。结论:PL可抑制人肝癌Huh-7和LM3细胞迁移和侵袭,该过程的分子机制可能与抑制JAK2/STAT3信号通路的激活有关。

白花丹素抗肿瘤基础作用机制研究进展

恶性肿瘤严重威胁人类生命健康。通过检索白花丹素抗肿瘤相关研究,发现白花丹素具有良好的抗肿瘤活性,对各种类型的恶性肿瘤都表现出良好的抑制效果。其抗肿瘤的作用机制主要是通过激活线粒体凋亡途径,破坏肿瘤细胞内氧化还原平衡状态;降低周期蛋白表达水平,紊乱肿瘤细胞周期;降低细胞侵袭、迁移能力和诱导肿瘤细胞发生自噬等实现。其分子机制与抑制Akt激活,调节PI3K/Akt/mTOR、PI3K/Akt/GLUT等多条信号通路有关。此外,白花丹素还可联合其他治疗手段,逆转肿瘤细胞多药耐药反应,增强肿瘤细胞对放疗的敏感性。然而现阶段对白花丹素主要集中于体外的基础研究,关于白花丹素对同种肿瘤不同表型细胞的机制差异性尚不清晰,且白花丹素具有一定细胞毒性,开发更多安全高效的载体系统,明确临床给药剂量也是广大学者的研究重点。故该文对近5年有关白花丹素抗肿瘤作用的相关文献进行归纳总结,为白花丹素抗肿瘤的进一步开发利用提供一定参考。

白花丹醌通过CXCL8/PI3K/AKT糖酵解通路抑制结肠癌细胞增殖、促进凋亡

目的:观察白花丹醌对结肠癌细胞Caco-2增殖、凋亡的影响,探究其潜在的作用机制。方法:运用CCK8法、流式细胞术检测不同浓度白花丹醌(4、8、12μmol/L)处理的Caco-2细胞的增殖抑制率、凋亡率。不做任何处理的Caco-2细胞设为Control;脂质体法将si-NC组(转染si-NC)、si-CXCL8组(转染si-CXCL8)转染至Caco-2细胞;8μmol/L的白花丹醌与0.5%DMSO处理的Caco-2细胞设为8μmol/L+DMSO组;8μmol/L的白花丹醌分别与z-VAD-FMK、740Y-P处理的Caco-2细胞设为8μmol/L+z-VAD-FMK组、8μmol/L+740Y-P组。RT-qPCR、Western blot实验检测细胞中CXCL8的mRNA、蛋白表达,CXCL8、M2-型丙酮酸激酶(M2 pyruvate kinase,PKM2)、L-乳酸脱氢酶A(lactate dehydrogenase A,LDHA)、人α-烯醇化酶(apha-enolase,ENO1)、葡萄糖磷酸异构酶(glucose phosphate isomerase,GPI)、磷酸化磷脂酰肌醇3激酶(phosphorylated phosphatidylinositol 3 kinase,p-PI3K)、磷酸化蛋白激酶B(phosphorylated protein kinase B,p-AKT)的蛋白表达。结果:与Control组相比,白花丹醌(4、8、12μmol/L)呈浓度依赖性促进Caco-2细胞增殖抑制率、凋亡率升高,抑制CXCL8的mRNA和蛋白表达。与8μmol/L+DMSO组相比,8μmol/L+z-VAD-FMK组细胞的增殖抑制率、凋亡率明显降低,CXCL8的mRNA和蛋白表达明显升高(P<0.05)。白花丹醌(4、8、12μmol/L)呈浓度依赖性抑制PKM2、LDHA、p-PI3K、p-AKT的蛋白表达。si-CXCL8组PKM2、LDHA、p-PI3K、p-AKT的蛋白表达明显低于si-NC组。740Y-P明显减弱白花丹醌对Caco-2细胞增殖抑制率和凋亡率的促进作用。结论:白花丹醌抑制结肠癌细胞增殖,促进凋亡,其潜在的作用机制与CXCL8/PI3K/AKT糖酵解通路有关。

白花丹素缓解眼小梁网细胞氧化应激损伤的作用

目的探讨白花丹素缓解眼小梁网细胞氧化应激损伤的作用。方法取人眼小梁细胞系iHTM进行培养、传代,建立小梁网细胞氧化应激损伤模型,分为对照组、模型组、抑制剂组、白花丹素联合抑制剂组和白花丹素组。检测各组丙二醛(malondialdehyde,MDA)、超氧化物歧化酶(superoxide dismutase,SOD)、谷胱甘肽过氧化物酶(glutathione peroxidase,GPX 1)、细胞增殖活性、细胞凋亡率和活性氧水平;检测各组Kelch样ECH关联蛋白1(Kelch like ECH associated protein 1,Keap1)、核因子相关因子2(nuclear factor erythroid 2-related factor 2,Nrf2)和抗氧化反应元件(antioxidant response element,ARE)蛋白的相对表达量。结果与对照组比较,其他4组的MDA均升高,SOD、GPX 1均降低,且比较MDA,白花丹素组<白花丹素联合抑制剂组<模型组<抑制剂组,比较SOD、GPX 1,抑制剂组<模型组<白花丹素联合抑制剂组<白花丹素组(P<0.05);与对照组比较,其他4组的细胞增殖活性、细胞凋亡率、活性氧和Keap1蛋白的相对表达量均升高,Nrf2、ARE蛋白的相对表达量均降低,且比较细胞增殖活性、细胞凋亡率、活性氧和Keap1蛋白的相对表达量,白花丹素组<白花丹素联合抑制剂组<模型组<抑制剂组,而比较Nrf2、ARE蛋白的相对表达量,抑制剂组<模型组<白花丹素联合抑制剂组<白花丹素组(P<0.05)。结论白花丹素可缓解小梁网细胞氧化应激损伤,作用机制可能与激活Keap1/Nrf2信号通路有关。

白花丹素对涎腺腺样囊性癌细胞增殖、迁移、凋亡的干预作用及其机制

目的观察白花丹素(PLB)对涎腺腺样囊性癌细胞增殖、迁移、凋亡的干预作用,并探讨其作用机制。方法取涎腺腺样囊性癌SACC-83细胞进行体外培养,将细胞分为0、12.5、25、50μmol/L PLB组,分别加入含0、12.5、25、50μmol/L PLB的DMSO培养基培养24 h。采用乳酸脱氢酶(LDH)释放法检测细胞毒性;CCK-8实验观察细胞增殖能力;Transwell试验观察细胞迁移能力;TUNEL染色法观察细胞凋亡情况;荧光探针法检测活性氧(ROS)水平,微量法检测丙二醛(MDA)含量;荧光探针法检测线粒体膜电位;Western blotting法检测细胞凋亡相关蛋白Bcl-2、Bax、Cleaved Caspase-3、Caspase-3表达,计算Bcl-2/Bax、Cleaved Caspase-3/Caspase-3。结果12.5、25、50μmol/L PLB组细胞LDH释放量均高于对照组,其中25、50μmol/L PLB组高于12.5μmol/L PLB组,50μmol/L PLB组高于25μmol/L PLB组(P均<0.05)。不同浓度PLB组细胞增殖能力、细胞迁移率均较对照组下降,其中25、50μmol/L PLB组低于12.5μmol/L PLB组(P均<0.05),25μmol/L PLB组与50μmol/L PLB组比较无统计学差异(P>0.05)。不同浓度PLB组细胞凋亡率均高于对照组,其中25、50μmol/L PLB组高于12.5μmol/L PLB组,50μmol/L PLB组高于25μmol/L PLB组(P均<0.05)。25、50μmol/L PLB组细胞内ROS水平均高于对照组和12.5μmol/L PLB组,且50μmol/L PLB组高于25μmol/L PLB组(P均<0.05);25、50μmol/L PLB组细胞内MDA水平均高于对照组,且50μmol/L PLB组高于12.5、25μmol/L PLB组(P均<0.05)。25、50μmol/L PLB组线粒体膜电位低于对照组,50μmol/L PLB组低于12.5μmol/L PLB组(P均<0.05)。不同浓度PLB组细胞Bcl-2/Bax均低于对照组,Cleaved Caspase-3/Caspase-3均高于对照组(P均<0.05),不同浓度PLB组间比较差异无统计学意义(P均>0.05)。结论PLB可抑制涎腺腺样囊性癌细胞增殖和迁移,促进其凋亡;PLB可能是通过诱导线粒体氧化应激以及ROS介导的细胞凋亡发挥抗肿瘤作用。

白花丹素对金黄色葡萄球菌的体外抑菌效果

文章通过研究白花丹素对金黄色葡萄球菌(MSSA)与耐甲氧西林金黄色葡萄球菌(MRSA)的生长和对MSSA、MRSA生物被膜的抑制效果,为治疗金黄色葡萄球菌感染提供了新的研究方向。研究采用微量稀释法测定白花丹素对MRSA与MSSA的最低抑菌浓度(MIC)和最小杀菌浓度(MBC);用微孔板建立金黄色葡萄球菌的生物被膜体外模型,采用结晶紫染色法测定生物被膜的形成量。研究结果表明:白花丹素对MRSA和MSSA的生长均有抑制效果,且对两种细菌生物被膜的清除效果显著,MRSA形成的生物被膜更难被清除。

RP-HPLC测定民族药材白花丹不同药用部位中白花丹醌的含量

目的：建立白花丹药材中白花丹醌的含量测定方法并考察白花丹不同药用部位中的含量。方法：色谱条件：KromasilCi8柱（4．6mm×200mm，5μm），柱温30℃。流动相甲醇．水（65：35），检测波长213nm，流速1mL·min^-1。结果：白花丹醌在0．0208—0．104μg，峰面积与进样量具有良好的线性关系，回归方程y=-14．29＋9138．9X，r=0．9999，平均回收率为98．7％。白花丹各部位中白花丹醌的含量分别为：根0．394％，茎0．050％，叶0．031％。结论：本法简便、准确、重复性好，可用于控制白花丹药材质量。

中药单体白花丹醌对鲍曼不动杆菌的耐药逆转作用

目的:探索中药单体白花丹醌对临床分离的鲍曼不动杆菌耐药性的逆转作用。方法:取临床分离的鲍曼不动杆菌53株,检测其对临床常用的14种抗菌药物的敏感性。观察中药单体白花丹醌对标准菌株的直接作用。在确定白花丹醌以及羰基氰化氯苯腙(CCCP)的工作浓度以后,观察对比白花丹醌与阳性药CCCP的外排抑制试验结果。结果:临床分离的53株鲍曼不动杆菌对临床常用的14种抗菌药物耐药率较高,其中氨苄西林、头孢唑啉、头孢呋辛、头孢西丁耐药率最高,分别为100%、100%、98.1%、98.1%。其余药物耐药率也均在50%以上。白花丹醌对标准质控菌的直接抗菌作用较弱。而白花丹醌与CCCP均显示了对庆大霉素、诺氟沙星、米诺环素和氯霉素的增敏作用,其外排阳性率分别达11.3%和18.9%,3.8%和7.5%,13.2%和17.0%,28.3%和20.8%,两组之间无统计学差异(P>0.05)。结论:鲍曼不动杆菌临床耐药情况严重,而白花丹醌作为一种中药单体可能具有一定的耐药逆转作用。