Reconstruction of Postinfarcted Cardiac Functions Through Injection of Tanshinone ⅡA@Reactive Oxygen Species-Sensitive Microspheres Encapsulated in a Thermoreversible Hydrogel

Myocardial damage resulting from acute myocardial infarction often leads to progressive heart failure and sudden death,highlighting the urgent clinical need for effective therapies.Recently,tanshinoneⅡA has been identified as a promising therapeutic agent for myocardial infarction.However,efficient delivery remains a major issue that limits clinical translation.To address this problem,an injectable thermosensitive poly(lactic acid-co-glycolic acid)-block-poly(ethylene glycol)-block-poly(lactic acid-co-glycolic acid)gel(PLGA-PEG-PLGA)system encapsulating tanshinoneⅡA-loaded reactive oxygen species-sensitive microspheres(Gel-MS/tanshinoneⅡA)has been designed and synthesized in this study.The thermosensitive hydrogel exhibits good mechanical properties after reaching body temperature.Microspheres initially immobilized by the gel exhibit excellent reactive oxygen species-triggered release properties in a high-reactive oxygen species environment after myocardial infarction onset.As a result,encapsulated tanshinoneⅡA is effectively released into the infarcted myocardium,where it exerts local anti-pyroptotic and anti-inflammatory effects.Importantly,the combined advantages of this technique contribute to the mitigation of left ventricular remodeling and the restoration of cardiac function following tanshinoneⅡA.Therefore,this novel,precision-guided intra-tissue therapeutic system allows for customized local release of tanshinoneⅡA,presenting a promising alternative treatment strategy aimed at inducing beneficial ventricular remodeling in the post-infarct heart.

Tanshinone ⅡA improves Alzheimer’s disease via RNA nuclearenriched abundant transcript 1/microRNA-291a-3p/member RAS oncogene family Rab22a axis

BACKGROUND Alzheimer’s disease(AD)is a neurodegenerative condition characterized by oxidative stress and neuroinflammation.Tanshinone ⅡA(Tan-ⅡA),a bioactive compound isolated from Salvia miltiorrhiza plants,has shown potential neuroprotective effects;however,the mechanisms underlying such a function remain unclear.AIM To investigate potential Tan-ⅡA neuroprotective effects in AD and to elucidate their underlying mechanisms.METHODS Hematoxylin and eosin staining was utilized to analyze structural brain tissue morphology.To assess changes in oxidative stress and neuroinflammation,we performed enzyme-linked immunosorbent assay and western blotting.Additionally,the effect of Tan-ⅡA on AD cell models was evaluated in vitro using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.Genetic changes related to the long non-coding RNA(lncRNA)nuclear-enriched abundant transcript 1(NEAT1)/microRNA(miRNA,miR)-291a-3p/member RAS oncogene family Rab22a axis were assessed through reverse transcription quantitative polymerase chain reaction.RESULTS In vivo,Tan-ⅡA treatment improved neuronal morphology and attenuated oxidative stress and neuroinflammation in the brain tissue of AD mice.In vitro experiments showed that Tan-ⅡA dose-dependently ameliorated the amyloid-beta 1-42-induced reduction of neural stem cell viability,apoptosis,oxidative stress,and neuroinflammation.In this process,the lncRNA NEAT1-a potential therapeutic target-is highly expressed in AD mice and downregulated via Tan-ⅡA treatment.Mechanistically,NEAT1 promotes the transcription and translation of Rab22a via miR-291a-3p,which activates nuclear factor kappa-B(NF-κB)signaling,leading to activation of the pro-apoptotic B-cell lymphoma 2-associated X protein and inhibition of the anti-apoptotic B-cell lymphoma 2 protein,which exacerbates AD.Tan-ⅡA intervention effectively blocked this process by inhibiting the NEAT1/miR-291a-3p/Rab22a axis and NF-κB signaling.CONCLUSION This study demonstrates that Tan-ⅡA exerts neuroprotective effects in AD by modulating the NEAT1/miR-291a-3p/Rab22a/NF-κB signaling pathway,serving as a foundation for the development of innovative approaches for AD therapy.

Protective Effect and Mechanism of Sodium Tanshinone ⅡA Sulfonate on Microcirculatory Disturbance of Small Intestine in Rats with Sepsis

To explore the protective effect of sodium tanshinone ⅡA sulfonate（STS） on microcirculatory disturbance of small intestine in rats with sepsis,and the possible mechanism,a rat model of sepsis was induced by cecal ligation and puncture（CLP）.Rats were randomly divided into 3 groups：sham operated group（S）,sepsis group（CLP） and STS treatment group（STS）.STS（1 mg/kg） was slowly injected through the right external jugular vein after CLP.The histopathologic changes in the intestinal tissue and changes of mesenteric microcirculation were observed.The levels of tumor necrosis factor-α（TNF-α） in the intestinal tissue were determined by using enzyme-linked immunoabsorbent assay（ELISA）.The expression of intercellular adhesion molecule-1（ICAM-1） in the intestinal tissue was detected by using immunohistochemisty and Western blot,that of nuclear factor κB（NF-κB） and tissue factor（TF） by using Western blot,and the levels of NF-κB mRNA expression by using RT-PCR respectively.The microcirculatory disturbance of the intestine was aggravated after CLP.The injury of the intestinal tissues was obviously aggravated in CLP group as compared with S group.The expression levels of NF-κB p65,ICAM-1,TF and TNF-α were upregulaed after CLP（P0.01）.STS post-treatment could ameliorate the microcirculatory disturbance,attenuate the injury of the intestinal tissues induced by CLP,and decrease the levels of NF-κB,ICAM-1,TF and TNF-α（P0.01）.It is suggested that STS can ameliorate the microcirculatory disturbance of the small intestine in rats with sepsis,and the mechanism may be associated with the inhibition of inflammatory responses and amelioration of coagulation abnormality.

Changes of c-fos and c-jun mRNA Expression in Angiotensin Ⅱ-induced Cardiomyocyte Hypertrophy and Effects of Sodium Tanshinone ⅡA Sulfonate

The changes of proto-oncogene c-fos and c-jun mRNA expression in angiotensin Ⅱ （AngⅡ）-induced hypertrophy and effects of sodium tanshinone ⅡA sulfonate （STS） in the primary culture of neonatal rat cardiomyocytes were investigated. Twelve neonatal clean grade Wistar rats were selected. The cardiomyocytes were isolated, cultured and divided according to different treatments in the medium. The cardiomyocyte size was determined by phase contrast microscope, and the rate of protein synthesis was measured by [3H]-Leucine incorporation. The c-fos and c-jun mRNA expression in cardiomyocytes was detected by reverse transcription polymerase chain reaction （RT-PCR）. It was found after cardiomyocytes were treated with AngⅡ for 30 min, the c-fos and c-jun mRNA expression in cardiomyocytes was increased significantly （P〈0.01）. After treatment with AngⅡ for 24 h, the rate of protein synthesis in AngⅡ group was significantly increased as compared with control group （P〈0.01）. After treatment with AngⅡ for 7 days, the size of cardiomyocytes in AngⅡ group was increased obviously as compared with control group （P〈0.05）. After pretreatment with STS or Valsartan before AngⅡ treatment, both of them could inhibit the above effects of AngⅡ （P〈0.05 or P〈0.01）. It was suggested that STS could ameliorate AngⅡ-induced cardiomyocyte hy- pertrophy by inhibiting c-fos and c-jun mRNA expression and reducing protein synthesis rate of cardiomyocytes.

Resonance Rayleigh scattering spectrum for the chelate of lanthanum(Ⅲ) with sodium tanshinon ⅡA silate and its analytical application

In a pH 3.6―5.0 HAc-NaAc buffer solution, when sodium tanshinon ⅡA silate (STSⅡA) reacts with La(Ⅲ) to form a chelate, the resonance Rayleigh scattering (RRS) intensity can be en-hanced greatly and a new RRS spectrum will appear. The maximum RRS peak is located at 306 nm and the RRS intensity is proportional to the concentration of STSⅡA in a certain range. The method is very sensitive and the detection limit for STSⅡA (3σ/K) is 82.12 ng·mL?1. The optimum reaction condi-tions and the effect of coexisting substances have been investigated. A new, simple and fast method for the determination of STSⅡA based on RRS method is developed. It can be applied to the deter-mination of STSⅡA in the synthesis samples and Nuoxinkang injection. Combined with infrared ab-sorption and NMR spectra, the structure of the chelate and the reasons of RRS enhancement are also discussed.

Growth Inhibition and Apoptosis Induction in Human Hepatoma Cells by Tanshinone Ⅱ_A

In order to .study the effect of tanshinone ⅡA on growth and apoptosis in human hepatoma cell line BEL-7402 in vitro, the human hepatoma cell line BEL-7402 was treated with tanshinone ⅡA at various concentrations for 72 h. Growth suppression was evaluated by MTT assay; apoptosis-relat-ed alterations in morphology and biochemistry were ascertained under cytochemical staining (Hoechst 33258), transmission electron microscopy (TEM), and DNA agarose gel electrophoresis. Apoptotic rate was quantified by flow cytometry (FCM). The results showed that Tanshinone ⅡA could inhibit the growth of hepatoma cells in a dose-dependent manner, with IC50 value being 6. 28μg/ml. After treatment with 1-10μg/ml tanshinone ⅡA for 72 h, BEL-7402 cells apoptosis with nuclear chro-matin condensation and fragmentation as well as cell shrinkage and the formation of apoptotic bodies were observed. DNA ladder could be demonstrated on DNA electrophoresis. FCM analysis showed hypodiploid peaks on histogram, and the apoptotic rates at μg/ml concentration for 12 h> 24 h, 36 h, 48 h and 72 h were (2. 32±0. 16)%, (3. 01±0. 35) %, (3. 87±0. 43)%, (6. 73±0. 58)% and (20. 85 ± 1. 74) % respectively, which were all significantly higher than those in the control group (1. 07±0. 13) %. It is concluded that Tanshinone ⅡA could induce human hepatoma cell line BEL-7402 apoptosis, which may be related to the mechanism of growth inhibition.

Altered Erythrocyte Membrane Calcium Binding in Hypertensive Rats and the Effects of Sodium Tanshinone Ⅱ-A Sulphonate on It

The calcium binding of erythrocyte membrane was determined in spontaneous hypertensiverats (SHR)and renovascular hypertensive rats (RVHR two-kidney, one-clip model) and the effect ofsodium tanshinone Ⅱ-A sulfonate(DS-201)on the calcium binding in SHRs was investigated. Ourresults show that the basal calcium binding was reduced in SHRs (P<0.01 vs WKY),while the maximalcalcium binding was not,but both typies calcium bindings had no significant change in RVHRs.Sodiumtanshinone Ⅱ-A sulfonate (125μ mol/L)have no effect on the calcium binding of ecythrocyte membraneof SHR in vitro.These data further support the hypothesis that there is a cell membrane abnormalitypresent in SHRs which may possibly serve as a marker genetics of in hypertension.

改性壳聚糖对Ni(Ⅱ)的吸附性能研究

为研究改性壳聚糖对水中Ni(Ⅱ)的吸附性能,以三聚磷酸钠为交联剂,对经过乙酸-双氧水体系氧化后的壳聚糖进行一步离子交联,制备改性壳聚糖吸附材料。通过扫描电子显微镜、傅里叶变换红外光谱仪、X射线衍射仪等对材料的微观形貌、分子结构及物相进行表征;采用条件实验探究改性壳聚糖吸附性能的影响因素,并对其吸附热力学进行分析。结果显示:改性后的壳聚糖呈纳米片状结构,成功实现了三聚磷酸钠中P—O与壳聚糖中—NH_(2)之间的交联;在三聚磷酸钠浓度为10 g/L、双氧水用量为5 mL、交联温度为40℃条件下制备的改性壳聚糖表现出较好的吸附性能,当pH为7、吸附时间为120 min、三聚磷酸钠改性壳聚糖投加量为50 mg时,其对Ni(Ⅱ)的去除率达到8371%;改性壳聚糖对Ni(Ⅱ)的吸附行为符合Langmuir等温吸附模型,吸附过程为自发吸热过程。

硝酸异山梨酯氯化钠注射液联合酒石酸美托洛尔缓释片(Ⅱ)治疗缺血性心肌病的临床效果

目的观察硝酸异山梨酯氯化钠注射液联合酒石酸美托洛尔缓释片(Ⅱ)治疗缺血性心肌病的临床效果。方法选取2023年4—12月黔东南州人民医院收治的缺血性心肌病患者540例,按照入院顺序分为观察组和对照组各270例。在常规治疗基础上,对照组应用酒石酸美托洛尔缓释片(Ⅱ)治疗,观察组在对照组基础上加用硝酸异山梨酯氯化钠注射液治疗,2组疗程均为1个月。比较2组治疗前后心功能指标[左室射血分数(LVEF)、心输出量(CO)、左室舒张末期内径(LVEDD)、左室收缩末期内径(LVESD)]、心肌标志物[脑钠肽(BNP)、胰岛素样生长因子-1(IGF-1)、肌钙蛋白T(cTnT)],不良反应及不良心血管事件。结果观察组治疗总有效率为98.52%,高于对照组的92.59%(χ^(2)=11.163,P=0.001)。治疗1个月后,2组LVEF、CO高于治疗前,LVEDD、LVESD短于治疗前,且观察组高/短于对照组(P<0.01);2组BNP、cTnT水平低于治疗前,IGF-1水平高于治疗前,且观察组低/高于对照组(P<0.01)。观察组与对照组不良反应总发生率比较差异无统计学意义(1.85%vs.3.33%,χ^(2)=1.173,P=0.279)。观察组不良心血管事件总发生率为2.96%,低于对照组的7.78%(χ^(2)=6.158,P=0.013)。结论硝酸异山梨酯氯化钠注射液联合酒石酸美托洛尔缓释片(Ⅱ)治疗缺血性心肌病效果显著,可明显改善患者心功能及实验室指标,安全性高,且可降低不良心血管事件发生风险。

不同吸附材料对废水中Cd(Ⅱ)的吸附动力学及机理

选择稻壳生物炭、钠基膨润土和天然硅藻土3种常见吸附材料,进行了系列吸附试验,并采用扫描电镜(SEM)和傅里叶红外光谱(FTIR)分析对吸附材料进行了表征,研究3种吸附材料对污水中Cd(Ⅱ)的吸附动力学及吸附机理,结果表明:3种吸附材料对Cd(Ⅱ)的吸附都符合准二级动力学模型,对溶液中Cd(Ⅱ)的吸附均为物理-化学复合过程。生物炭对溶液中Cd(Ⅱ)的吸附机制主要是其孔道内的钙氧化物以及表面的含氧官能团,膨润土和硅藻土则主要依赖于比表面积、表面微孔和双键官能团作用。

丹参酮Ⅱ_A磺酸钠注射液的安全性评价

目的丹参酮ⅡA磺酸钠临床用于抗肿瘤、治疗心脑血管疾病以及抗菌消炎等,文中评价丹参酮ⅡA磺酸钠注射液的安全性。方法以等渗氯化钠溶液为阴性对照进行体外溶血试验,兔耳缘静脉血管刺激试验,肌肉注射刺激试验和豚鼠全身过敏性试验。结果丹参酮ⅡA磺酸钠注射液(临床使用浓度1mg/m l)3 h内不引起溶血或红细胞凝集反应。丹参酮ⅡA磺酸钠注射液(4mg/kg)对兔耳缘静脉和股四头肌无刺激作用,不引起豚鼠全身过敏反应。结论丹参酮ⅡA磺酸钠注射液在本实验条件下安全性较好,可供临床注射使用。

丹参酮Ⅱ_A与丹参酮Ⅱ_A磺酸钠在小鼠体内的分布

目的考察静脉注射丹参酮ⅡA与丹参酮ⅡA磺酸钠后,二者在小鼠体内的分布行为,证实两者穿透血脑屏障的差异。方法小鼠分别静脉给予丹参酮ⅡA乳剂与丹参酮ⅡA磺酸钠注射液,以HPLC法测定各主要脏器组织中的药物含量。结果丹参酮ⅡA乳剂与丹参酮ⅡA磺酸钠静脉给药后均快速分布至各主要脏器组织,其中以肝脏的药物分布量最高;前者在脑组织中的分布明显高于后者。结论丹参酮Ⅱ比丹参酮ⅡA磺酸钠更易进入血脑屏障,提示丹参酮ⅡA乳剂有望用于脑血管病的预防和治疗。

RP-HPLC法测定注射用丹参酮Ⅱ_A磺酸钠含量和有关物质

目的:建立丹参酮Ⅱ_A 磺酸钠制剂的高效液相色谱含量测定方法和有关物质检查方法。方法:采用 C_(18)柱(6.0mm×150mm,5μm),流动相 A 相为20mmol·L^(-1)磷酸二氢钾(含0.5%三乙胺,磷酸调节 pH 至4.0)-甲醇(20:80),B 相为20mmol·L^(-1)磷酸二氢钾(含0.5%三乙胺,磷酸调节 pH 至4.0)-甲醇(80:20),梯度洗脱,流速1.0mL·min^(-1),检测波长为271nm。结果:丹参酮Ⅱ_A 磺酸钠与有关物质分离良好,辅料不干扰测定,方法线性范围1.6～39.2μg·mL^(-1)(r=0.9999),最低检测限10ng·mL^(-1),回收率99.1%(n=9),精密度(RSD)为0.44%(n=6)。结论:方法操作简便准确,灵敏度高,适用于丹参酮Ⅱ_A 磺酸钠制剂的含量测定和有关物质检查。

丹参酮Ⅱ_A磺酸钠注射液治疗急性脑梗死的临床研究

目的:探讨丹参酮Ⅱ_A磺酸钠注射液对急性脑梗死患者血清P-选择素、胶质纤维酸性蛋白(GFAP)和血管内皮生长因子(VEGF)及神经功能的影响。方法:选择2013年4月-2016年4月连云港市第一人民医院收治的急性脑梗死患者114例,按随机数字表法分为对照组与观察组,各57例。对照组患者给予常规治疗;观察组患者在对照组基础上加用丹参酮Ⅱ_A磺酸钠注射液40mg加入0.9%氯化钠注射液250 mL中,ivgtt,qd。7 d为1个疗程,两组均治疗2个疗程。比较两组患者治疗前和治疗7、14 d时的美国国立卫生院卒中量表(NIHSS)评分,血清P-选择素、GFAP和VEGF水平,以及不良反应发生情况。结果:治疗前,两组患者上述各项指标比较,差异均无统计学意义(P>0.05);与治疗前比较,两组患者治疗7、14 d时的NIHSS评分、血清P-选择素和GFAP水平均明显下降,血清VEGF水平明显上升,且治疗14 d时指标水平(NIHSS评分除外)均明显优于同组治疗7 d时,观察组指标水平均明显优于同期对照组,差异均有统计学意义(P<0.05)。两组患者均未见明显不良反应发生。结论:丹参酮Ⅱ_A磺酸钠注射液能显著降低急性脑梗死患者血清P-选择素和GFAP水平,提高VEGF水平,促进神经缺损功能恢复,且安全性较高。

丹参酮Ⅱ_A对AngⅡ诱导的心肌成纤维细胞增殖及Ⅰ型胶原合成的影响

目的:通过观察丹参酮ⅡA(TSN)对AngⅡ诱导的心肌成纤维细胞(CFs)增殖及Ⅰ型胶原合成的影响,探讨其抗心肌纤维化的作用机制。方法:差速贴壁法提取原代CFs,采用四氮唑盐(MTT)比色法测定细胞数目,ELISA法检测Ⅰ型胶原合成,RT-PCR法半定量检测Ⅰ胶原mRNA表达。结果:①AngⅡ组OD值高于空白对照组,两者比较有显著性差异(P<0.01);AngⅡ+TSN组OD值低于AngⅡ组,两者比较有显著性差异(P<0.01)。②AngⅡ组有促进心肌成纤维细胞分泌Ⅰ型胶原的作用,与空白对照组比较,有显著性差异(P<0.01);AngⅡ+TSN组Ⅰ型胶原含量低于AngⅡ组,两者比较,有显著性差异(P<0.01)。③AngⅡ组Ⅰ型胶原mRNA表达高于空白对照组,两者比较有显著性差异(P<0.05);AngⅡ+TSN组Ⅰ型胶原mRNA表达低于AngⅡ组,两者比较有显著性差异(P<0.05)。结论:AngⅡ可直接诱导CFs的增殖,促进其分泌Ⅰ型胶原,并能显著增加Ⅰ型胶原mRNA的表达;TSN对AngⅡ诱导的CFs增殖及Ⅰ型胶原分泌增加,及Ⅰ型胶原mRNA表达增强均有抑制作用。提示:TSN抗心肌纤维化作用的产生可能与丹参酮ⅡA抑制心脏局部的RAS系统有关。

丹参酮Ⅱ_A诱导白血病NB4细胞分化分子机制研究

目的:探讨丹参酮ⅡA诱导白血病NB4细胞分化的分子机制。方法:0.5 mg.L-1丹参酮ⅡA体外处理NB4细胞72 h后,分别采用显微镜观察细胞形态分化;MTT检测细胞增殖抑制作用;收集细胞并提取总RNA,反转录获得cDNA,再转录并标记成cRNA(Cy3荧光标记),与Express ChipTMH04芯片杂交,最后对芯片进行扫描和数据分析,检测丹参酮ⅡA诱导NB4细胞分化前后相关基因谱表达的变化。结果:0.5 mg.L-1丹参酮ⅡA可诱导92.8%NB4细胞向终末细胞分化。其中,中、晚幼粒细胞占27.0%;杆状及分叶核粒细胞占68.2%;细胞生长被明显抑制。基因芯片检测发现:3 360条基因中有183条基因差异表达,其中包括23条(5条上调和18条上调)分化相关基因和与细胞凋亡、周期调控、DNA转录、DNA损伤/修复、蛋白转运、信号传导、核受体、细胞因子和生长因子、癌基因和抑癌基因等相关基因。结论:丹参酮ⅡA可能通过调控多种相关基因、特别是分化相关基因的表达诱导白血病细胞分化,本研究有助于阐明丹参酮ⅡA诱导分化抗肿瘤的分子机制。

丹参酮Ⅱ_A对肝纤维化大鼠肝组织胶原表达的影响

目的探讨丹参酮ⅡA(TanshinoneⅡA,TSN)对肝纤维化大鼠肝组织胶原纤维表达的作用。方法采用四氯化碳(CCl4)诱导大鼠肝纤维化动物模型。将Wistar大鼠随机分为空白对照组,CCl4模型组,阳性对照联苯双酯组(100mg/kg),TSN高、中、低(21.3,14.2,7.1 mg/kg)剂量组,均以灌胃的方式给药。治疗结束后,动物采血处死,分离血清进行血清总蛋白(TP)和白蛋白(ALb)含量检测,以及肝组织匀浆羟脯氨酸(Hyp)的含量检测,观察TSN对慢性肝纤维化大鼠的肝纤维生化指标的影响;取固定部位肝组织做HE染色和Masson胶原纤维特殊染色病理组织学检查,观察肝组织中胶原纤维表达的情况。结果TSN可以恢复肝纤维化大鼠血清中已降低的TP和ALb含量,并下调肝组织Hyp的含量(P<0.05或P<0.01);HE染色显示TSN可以明显改善肝纤维化的病理损伤;Masson胶原纤维特殊染色发现TSN可以显著降低肝纤维化大鼠肝组织中的胶原纤维的表达。结论TSN对肝组织中胶原纤维的的合成过程具有显著的抑制作用,从而能阻断肝纤维化的病理过程。

丹参酮Ⅱ_A磺酸钠注射液与4种输液配伍的稳定性考察

目的考察丹参酮ⅡA磺酸钠与4种输液配伍后的稳定性。方法常温下将丹参酮ⅡA磺酸钠注射液分别与0.9%氯化钠注射液、10%葡萄糖注射液、葡萄糖氯化钠注射液、乳酸钠林格注射液配伍,分别在0,1,2,4,8,12 h时观察配伍溶液的外观、pH、不溶性微粒,应用高效液相色谱法测定丹参酮ⅡA磺酸钠的含量。结果丹参酮ⅡA磺酸钠注射液与4种输液配伍12 h内溶液澄明,颜色无变化,无气泡产生,pH无明显变化,不溶性微粒检测符合中国药典要求。含量测定4 h后溶液主药浓度有所下降,但均大于95%,符合质量要求。结论丹参酮ⅡA磺酸钠注射液与4种输液在常温下、12 h内配伍稳定。

丹参酮Ⅱ_A对四氯化碳损伤原代培养大鼠肝细胞的影响

目的 :研究丹参酮ⅡA 对四氯化碳 (CCl4)损伤原代培养大鼠肝细胞的保护作用。方法 :原位灌流分离大鼠肝细胞培养 36h后加入丹参酮ⅡA,同时造成CCl4损伤 ,于损伤 3h测培养液中丙二醛 (MDA)、一氧化氮 (NO)的含量 ,谷丙转氨酶 (ALT)、乳酸脱氢酶 (LDH)、超氧化物歧化酶 (SOD)的活性 ,并用MTT法测肝细胞存活率。结果 :丹参酮ⅡA 明显改善细胞存活率 ,抑制CCl4引起的ALT、LDH活力的升高 ,同时抑制MDA、NO的产生及提高SOD活力。结论 :丹参酮ⅡA 能有效抑制CCl4造成的原代培养大鼠肝细胞损伤。

RP-HPLC法同时测定丹参中丹参酮Ⅱ_A和隐丹参酮的含量

目的 研究丹参药材中新的质控指标。方法 采用细胞膜色谱法对丹参中的有效成分进行筛选 ,在此基础上建立 RP-HPLC法同时测定丹参中丹参酮 A和隐丹参酮含量的方法。色谱条件为 L ichrosorb C1 8色谱柱 ,流动相为甲醇 -水 (75∶ 2 5 ) ;2 70 nm下检测 ;流速 1.0 m L/min,室温。药材用甲醇超声处理 ,过滤后直接进样分析。结果丹参酮 A和隐丹参酮的回收率分别为 10 1.74%和 99.2 8% ,RSD分别为 3 .68%和 1.78%。重现性的 RSD分别为 1.88%和 1.3 5 %。所收集的 12份丹参药材中丹参酮 A含量为 0 .60 7%～ 0 .14 8% ,隐丹参酮为 0 .0 73 %～0 .0 2 1%。结论 该方法快速、简便、准确 ,当丹参用于治疗心血管疾病时 ,可以同时将丹参酮