丹参酮ⅡA对大鼠移植性肝癌的抑制作用

目的:观察丹参酮Ⅱ A对大鼠移植性肝癌的抑制作用.方法:将SD大鼠随机分为假手术组、模型组、丹参酮ⅡA高、低剂量组.各组动物于移植术后12d处死.分离肿瘤测量其体积,realtime RT-PCR法和western blot法检测肿瘤组织中HMGB1、VEGFmRNA和蛋白的表达.结果:丹参酮ⅡA能明显降低肿瘤体积,降低肿瘤组织中HMGB1、VEGFmRNA和蛋白的表达.结论:丹参酮ⅡA能抑制大鼠移植性肝癌的生长,其机制可能与抑制HMGB1、VEGF表达有关.     

丹参酮IIA磺酸钠对烧伤植皮创面愈合及瘢痕形成的影响

目的:探讨丹参酮IIA磺酸钠注射液对烧伤患者植皮创面愈合及瘢痕形成情况的影响。方法:选取2014年3月至2014年12月我院收治的烧伤植皮患者62例,根据临床用药分为试验组(使用丹参酮IIA磺酸钠注射组)与对照组(未使用丹参酮IIA磺酸钠注射液)。比较两组创面愈合情况,术后植皮成活率及愈合后瘢痕形成情况。结果:1经治疗,两组创面均愈合,试验组患者植皮成活率为(97.12±1.89)%,高于对照组(89.96±1.86)%,差异具有统计学意义(P0.01);试验组愈合时间较对照组短,试验组创面愈合时间为10.1±1.9天,对照组为14.3±2.3天,两组比较差异具有统计学意义(P0.001);瘢痕形成评价试验组均优于对照组,差异具有统计学意义,其中血肿面积(1.50±0.03 vs.3.04±0.08,P0.01)、畸形率[2(6.45)vs.8(25.81),P0.05]、感染率[2(6.45)vs.9(29.03),P0.05]。结论:丹参酮IIA磺酸钠注射液对于烧伤植皮创面的患者,能够提高植皮成活率,促进创面愈合,减轻瘢痕形成,改善创面愈合质量。     

丹参酮IIA缓解大鼠心肌梗死后左心室重构的作用及其机制研究

摘要 目的：探讨丹参酮IIA（T-IIA）对于缓解大鼠心肌梗死（MI）后左心室重构（LVR）的作用及其机制。方法：选取SD雄性大鼠80只,通过结扎左前降支（LAD）建立MI大鼠模型。将大鼠随机分为8组,假手术组未结扎LAD,其余各组均结扎LAD;除假手术组和MI组腹腔注射生理盐水外,其余各组分别给予T-IIA、脂多糖（LPS）和TAK-242治疗。HE和马松（Masson）三色染色评估MI大小、组织病理改变和纤维化程度。末端dUTP镍末端标记（TUNEL）染色观察心肌细胞凋亡情况。采用反转录定量聚合酶链反应(RT-qPCR)和蛋白免疫印迹试验检测Toll样受体4（TLR4）、髓样分化蛋白88（MyD88）和核因子κB（NF-κB）的表达水平。结果：T-IIA能改善MI大鼠心功能,可降低MI大鼠心脏体积,改善心脏形态,减轻MI大鼠的组织病理学改变,并有效减轻MI和心肌纤维化。T-IIA抑制MI大鼠的TLR4/MyD88/NF-κB信号通路,且能有效减少MI大鼠梗死边缘区心肌细胞凋亡。结论：T-IIA通过抑制TLR4/MyD88/NF-κB信号通路的激活,改善心脏形态、功能和病理组织学变化,有效减轻MI的严重程度,预防LVR。     

丹参酮IIA衍生物的合成

目的:丹参酮IIA是中药丹参的脂溶性成分,具有抗肿瘤、抗氧化、抗心脑血管疾病等多种生理活性。本文拟对其进行结构改造以获得活性更好的丹参酮IIA衍生物。方法:首先,以丹参酮IIA为原料,通过Vilsmeier反应在其16-位引入醛基,再与醋酸胺进行还原胺化反应,以较高收率得到16-位胺甲基取代的丹参酮IIA衍生物。接着,对其氨基进行修饰,得到10个不同N-取代的丹参酮IIA衍生物。同时考察反应温度、反应溶剂和反应时间等条件对还原胺化反应的影响,确定最佳反应条件。结果:通过1H-NMR、13C-NMR以及LC-MS对所有产物结构进行了确认。还原胺化反应的最佳反应条件为:以1,2-二氯乙烷为溶剂,温度保持40℃,反应时间为2h。结论:反应步骤简单、条件温和、产率较高,是合成16-位取代的丹参酮IIA衍生物的理想方法。     

丹参酮IIA磺酸钠注射液佐治蝮蛇咬伤35例疗效观察

毒蛇咬伤是夏秋季节农村地区常见急诊病种之一.被毒蛇咬伤后除应用抗蛇毒血清外,强调的是综合整体治疗尤其是蛇伤引起的肢体肿胀常成为临床后期治疗的主要问题.我院于2007年5～10月采用丹参酮IIA磺酸钠注射液治疗蝮蛇咬伤35例,取得满意疗效,现报告如下.     

丹参酮IIA 磺酸钠在创伤失血性休克过程中的保护作用研究

目的:研究中药提取物丹参酮IIA磺酸钠在创伤失血性休克中的作用。方法:复制SD大鼠创伤失血性休克模型,即经右侧股动脉插管放血,左侧股静脉建立液体通道,经颈动脉插管至左心室监测创伤失血性休克大鼠平均动脉压;在达到最大放血量后,治疗组大鼠给予丹参酮IIA磺酸(10mg/kg)。按时间点经股静脉取大鼠静脉血,测量血清肌酸激酶(CK)及乳酸脱氢酶(LDH)水平,比较各组心肌酶改变。并以酶联免疫法检测各组大鼠血清促炎因子IL-Iβ、IL-6、IL-10和TNFα的改变。结果:丹参酮IIA磺酸钠在一定程度上改善了创伤失血性休克导致大鼠的血流动力学的改变,显著减轻了炎症反应过程中的各种炎症因子的表达。结论:丹参酮IIA磺酸钠改善了创伤失血性休克导致大鼠的低血压;抑制了大鼠创伤失血性休克过程中炎症因子的表达,可能在创伤失血性休克过程中发挥保护作用,为临床提供了疗创伤失血性休克提供了新的可能的参考。     

丹参酮IIA磺酸钠注射液辅助治疗对突发性耳聋患者血液流变学及临床疗效的影响

目的：探讨丹参酮IIA 磺酸钠注射液辅助治疗对突发性耳聋患者血液流变学及临床疗效的影响。方法：选取我院收治的突发 性耳聋患者78 例,并将其随机分为实验组和对照组,每组39 例。对照组给予三磷酸腺苷二钠、辅酶A、复合维生素、双密达莫片 及高压氧治疗,而实验组在对照组的基础上给予丹参酮IIA 磺酸钠注射液治复合组治疗。观察和比较两组患者治疗后的听力恢复 等级分布以及治疗前后的电测听情况和各项血液流变学指标的变化情况。结果：治疗后,与对照组比较,实验组听力恢复Ⅰ级患 者的比例更高,电听力平均值均显著降低,各项血液流变学指标均明显改善,差异均有统计学意义(P<0.05)。结论：丹参酮IIA 磺酸 钠注射液辅助治疗能够显著提高突发性耳聋的临床疗效,这可能其改善患者的血液流变学有关     

人参皂甙Rg1、肉桂酸和丹参酮IIA组合对成骨肉瘤MG-63细胞增殖与相关基因表达的影响

研究中药有效成分人参皂甙Rg1、肉桂酸和丹参酮IIA组合对人成骨肉瘤MG-63细胞增殖抑制和相关基因表达影响,探索其对肿瘤细胞的生物学效应.以33 μg/ml人参皂甙Rg1、296.32 μgml肉桂酸和0.3 μg/ml丹参酮IIA的组合(简称RCT)处理人成骨肉瘤MG-63细胞,以肿瘤细胞分化诱导物HMBA处理MG-63细胞为平行对照,用流式细胞仪、免疫细胞化学检测及光镜观察系统研究RCT组合对MG-63细胞的作用.生长曲线及细胞周期检测显示RCT组合可显著抑制MG-63细胞的增殖,细胞生长抑制率达72.37%,细胞周期阻滞于G0/G1期;免疫细胞化学检测显示RCT组合处理后MG-63细胞的癌基因c-fos、c-myc表达下调,抑癌基因p27、Rb表达上调.RCT组合对MG-63细胞增殖及相关基因表达的影响与分化诱导物六亚甲基双乙酰胺(HMBA)处理组相似.     

丹参酮IIA对阿尔茨海默症模型小鼠神经保护作用及对PI3K/AKT通路的影响

目的 探究丹参酮IIA(TanⅡA)对阿尔茨海默症(AD)模型小鼠神经保护作用及对磷脂酰肌醇-3-激酶/蛋白激酶B(PI3K/AKT)通路的影响.方法 采用侧脑室注射脂多糖(LPS)法构建AD小鼠模型,随机分为模型组、TanⅡA低、中及高剂量组,另选取未处理小鼠作为空白组;TanⅡA处理组以腹腔注射进行给药,剂量分别为...     

丹参酮ⅡA磺酸钠抗金黄地鼠皮脂腺增生的作用分析

目的:对丹参酮IIA磺酸钠抗金黄地鼠皮脂腺增生的作用进行探讨与分析。方法:依照自身对照的方式,分别对雄性金黄地鼠的两侧皮脂腺斑涂抹丹参酮IIA磺酸钠(STS侧)以及生理氯化钠溶液(生理盐水侧),在各个时间点(用药之前、药后10d、药后20d以及药后30d)对两侧皮脂腺斑的面积利用游标卡尺进行测量。结果:用药之后,在金黄地鼠皮脂腺斑面积的缩小上,STS侧要优于生理盐水侧(P<0.05),皮脂腺排列疏松;在皮脂腺细胞PCNA表达上,STS侧要比生理盐水侧下降的明显(P<0.05);在用药20d之后,STS侧的皮脂腺细胞凋亡最为显著(P<0.05)。结论:在金黄地鼠皮脂腺斑上涂抹丹参酮IIA磺酸钠,可以使其面积得到缩小,使皮脂腺斑显微结构得到明显的改变,能够对皮脂腺增生进行抑制,效果显著。     

Tanshinone IIA, an isolated compound from Salvia miltiorrhiza Bunge, induces apoptosis in HeLa cells through mitotic arrest

AIMS: Tanshinone IIA (Tan IIA) is a compound isolated from Salvia miltiorrhiza Bunge (Danshen). The aim of this study is to investigate the mechanisms of its anti-cancer effect. MAIN METHODS: To clearly delineate the cell cycle-dependent effects of Tan IIA, we used either synchronized cells or single living cell analysis to conduct our studies. Subcellular fractionation, Western blot analysis, immuno-fluorescence staining and FACS analysis were also employed in our study. KEY FINDINGS: We found that Tan IIA could arrest cancer cells in mitosis by disrupting the mitotic spindle and subsequently triggered cells to enter apoptosis through the mitochondria-dependent apoptotic pathway. Thus, Tan IIA could selectively kill mitotic cells over interphase cells. In comparison with other existing anti-cancer drugs that cause mitotic arrest by interfering with the microtubule structure (such as vincristine or taxol), Tan IIA destroyed only the mitotic spindle during the M phase but not the microtubule structure in interphase cells. Furthermore, Tan IIA could trigger the mitotic arrested cells to enter apoptosis faster than vincristine or taxol. SIGNIFICANCE: Since Tan IIA can selectively induce cancer cells to enter apoptosis through mitotic arrest, it has the potential to be developed into an anti-cancer drug.     

Tanshinone IIA isolated from Salvia miltiorrhiza elicits the cell death of human endothelial cells

Summary Tanshinone IIA, a major component extracted from the traditional herbal medicine, Salvia miltiorrhiza Bunge, is known to exhibit potent cytotoxicity against various human carcinoma cells in vitro. However, the mechanism by which tanshinone IIA produces this anti-tumor effect remains unknown. Since anti-neovascularization has generally been regarded as an effective strategy for anti-cancer therapy, we decided to investigate the mechanism underlying tanshinone IIA-mediated death of human endothelial cells. In this study, we demonstrate that tanshinone IIA elicits human endothelial cell death independent of oxidative stress. These events are partially calcium-dependent and actually dependent upon NAD(P)H: quinone oxidoreductase (NQO1) activity. Tanshinone IIA induces an increase in intracellular calcium, which triggers the release of cytochrome c, thus causing loss of the mitochondrial membrane potential (MMP), resulting in the subsequent activation of caspases. Blocking the induction of Ca²⁺ perturbation with BAPTA-AM partially rescued cells from tanshinone IIA-induced cytotoxicity. Additionally, blocking NQO1 activity with dicoumoral or inhibiting caspase activities with the general caspase inhibitor, z-VAD-fmk, prevented cell death induced by tanshinone IIA. Therefore, our results imply that tanshinone IIA-mediated cytotoxicity against human endothelial cells may occur through activation of NQO1, which induces a calcium imbalance and mitochondrial dysfunction, thus stimulating caspase activity.These authors contributed equally to this work.     

The anti-inflammatory activities of Tanshinone IIA, an active component of TCM, are mediated by estrogen receptor activation and inhibition of iNOS

Tanshinone IIA (Tan IIA) is a major compound extracted from a traditional herbal medicine Salvia miltiorrhiza BUNGE, which is used to treat cardiovascular diseases, cerebrovascular diseases and postmenopausal syndrome. It has also been shown to possess anti-inflammatory activity. Since Tan IIA has a similar structure to that of 17β-estradiol (E₂), the present study was undertaken to characterize the estrogenic activity of Tan IIA and to demonstrate a functional role of this activity in RAW 264.7 cells. In transient transfection assay, Tan IIA (10 μM) increases ERE-luciferase activity in an estrogen receptor (ER) subtype-dependent manner when either ERα or ERβ were co-expressed in Hela cells. In LPS-induced RAW 264.7 cells, Tan IIA exerts anti-inflammatory effects by inhibition of iNOS gene expression and NO production, as well as inhibition of inflammatory cytokine (IL-1β, IL-6, and TNF-α) expression via ER-dependent pathway. Therefore, it could serve as a potential selective estrogen receptor modulator (SERM) to treat inflammation-associated neurodegenerative and cardiovascular diseases without increasing the risk of breast cancer.     

丹参酮ⅡA磺酸钠注射液辅助治疗溃疡性结肠炎的临床疗效研究

目的:探究丹参酮ⅡA磺酸钠注射液辅助治疗溃疡性结肠炎的临床疗效及其可能的作用机制。方法:选择2013年1月~2014年10月我院肝脾胃病科收治的住院患者100例并将其随机分为实验组与对照组,每组50例。对照组患者给予美沙拉嗪肠溶片治疗,而实验组在对照组的基础上给予丹参酮ⅡA磺酸钠注射液辅助治疗。治疗后,比较两组患者的临床有效率、结肠镜检查情况,并检测和比较两组患者治疗前后的C反应蛋白水平。结果:经治疗后,两组患者溃疡性结肠炎的症状及结肠镜检查结果均有改善,充血水肿及溃疡处明显减少,脓性分泌物也明显减少或消失,与对照组相比,实验组的总有效率显著升高(P0.05),结肠改善情况更好。两组患者治疗后的CRP水平均较治疗前显著下降,且实验组患者的CRP水平较对照组更低,差异均具有统计学意义(P0.05)。结论:丹参酮ⅡA磺酸钠注射液辅助治疗能够有效提高UC的临床疗效,这可能与其降低UC患者的C反应蛋白水平有关。     

Tanshinone IIA alleviates lipopolysaccharide‐induced acute lung injury by downregulating TRPM7 and pro‐inflammatory factors

The study aimed to investigate the role of Tanshinone IIA (Tan IIA) in lipopolysaccharide (LPS)‐induced acute lung injury (ALI) in its regulation of TRPM7. Wistar male rats were randomly divided into the normal saline (NS), LPS, knockout (KO) + LPS, low‐dose Tan IIA (Tan‐L), middle‐dose Tan IIA (Tan‐M), high‐dose Tan IIA (Tan‐H) and KO + high‐dose Tan IIA (KO + Tan‐H) groups. The level of tumour necrosis factor‐α (TNF‐α), interleukin (IL)‐1β, IL‐6, TRPM7 protein expression, current density‐voltage curve and Ca²⁺ concentration were detected through ELISA, Western blotting, electrophysiological experiment and a calcium‐imaging technique, respectively. The rats in the KO + LPS, Tan‐L, Tan‐M, Tan‐H and KO + Tan‐H groups all displayed lower levels of TNF‐α, IL‐1β and IL‐6 than the LPS group. Rats in the KO + Tan‐H group exhibited lower levels of NF‐α, IL‐1β and IL‐6 than rats in the Tan‐H group. Elevated levels of TRPM7 protein expression in the LPS and Tan groups were detected in comparison with the NS group. However, TRPM7 protein expression in Tan‐M and Tan‐H groups was notably lower than in that of the LPS group. In comparison with the NS group, the LPS and Tan groups had a greater PIMs cell density and a higher concentration of Ca²⁺. Contrary results were observed in the KO + LPS, Tan‐H and KO + Tan‐H groups. Tan IIA decreases calcium influx in PIMs and inhibits pro‐inflammatory factors which provide an alleviatory effect in regards to LPS‐induced ALI by suppressing TRPM7 expression.     

姜黄素抑制大鼠C6 胶质瘤生成及机制初步研究

目的:观察姜黄素对大鼠C6胶质瘤的抑制作用。方法:将SD大鼠随机分为假手术组、模型组、姜黄素高、低剂量组。各组动物于移植术后7天给予干预,姜黄素组给予姜黄素灌胃,14天后处死。分离肿瘤测量其体积,realtime RT-PCR法和western blot法检测肿瘤组织中核转录因子-κ B(nuclear factor-κ B,NF-κB)、EGFR mRNA和蛋白的表达。结果:姜黄素能明显降低肿瘤体积,降低肿瘤组织中NF-κ B、EGFR mRNA和蛋白的表达。结论:姜黄素能抑制大鼠C6胶质瘤的生长,其机制可能与抑制NF-κ B、EGFR表达有关。