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.

Two-step continuous flow process of sodium tanshinone ⅡA sulfonate using a 3D circular cyclone-type microreactor

A sustainable and practical process is presented for the direct synthesis of sodium tanshinone IIA sulfonate(STS).Our approach was inspired by the well-established and industrially applied batch synthetic route for STS production.We constructed a telescoped two-step continuous flow platform.This involved a continuous tanshinone IIA sulfonation and in-line salt formation.For the setup,we constructed a 3D circular cyclone-type microreactor using femtosecond laser micromachining.Compared to the 68%yield for 2 h in batch,the two-step continuous flow had an STS yield of 90%,achieved for a total residence time of<3.0 min under optimal conditions.The proposed continuous flow method vastly simplified the operation and improved procedural safety,while significantly reducing the required acid content and wastewater production.

Effect of Sodium Tanshinone ⅡA Sulfonate on Phosphorylation of Extracellular Signal-regulated Kinasel/2 in Angiotensin Ⅱ-induced Hypertrophy of Myocardial Cells

Objective： To observe the effects of sodium tanshinone ⅡA sulfonate （STS） on angiotensin Ⅱ （Ang Ⅱ）-induced hypertrophy of myocardial cells through the expression of phosphorylated extracellular signal-regulated kinase （p-ERK1/2）. Methods： In the primary culture of neonatal rat myocardial cells, the total protein content in myocardial cells was determined by coomassie brilliant blue and the protein synthesis rate was measured by [3H]-Leucine incorporation as indexes for hypertrophy of myocardial cells. The expression of p-ERK1/2 was determined using Western blot and immunofluorescence labeling. Results： （1） The total protein and protein synthesis rate increased significantly in contrast to the control group after the myocardial cells were stimulated by Ang Ⅱ （1 μ mol/L） for 24 h; STS markedly inhibited the increment of the total protein level induced by Ang Ⅱ and the syntheses of protein. （2） After pretreatment of myocardial cells with Ang Ⅱ （1 μmol/L） for 5 min, the p-ERK1/2 protein expression was increased, with the most obvious effect shown at about 10 min; pretreatment of myocardial cells with STS at different doses （2, 10, 50μmol/L） for 30 min resulted in obvious inhibition of the expression of p-ERK1/2 stimulated by Ang Ⅱ in a dose-dependent manner. （3） After the myocardial cells were stimulated by AngⅡ （1 μ mol/L）, the immunofluorescence of ERK1/2 rapidly appeared in the nucleus. The activation and translocation process of ERK1/2 induced by Ang Ⅱ was blocked distinctly by STS. （Conclusion： STS inhibited the myocardial cell hypertrophy induced by Ang Ⅱ, and the mechanism may be associated with the inhibition of p-ERK1/2 expression.

Effect of Sodium Tanshinone ⅡA Sulfonate on Cardiac Myocyte Hypertrophy and Its Underlying Mechanism

Objective： To investigate the effects of sodium tanshinone Ⅱ A sulfonate （STS） on the hypertrophy induced by angiotensin Ⅱ（Ang Ⅱ） in primary cultured neonatal rat cardiac myocytes. Methods： The effect of STS on cytotoxicity was evaluated using the 3-（4,5-dimethylthiazol-2-yl）-3,5- phenytetrazoliumromide （MTT） assay. As indexes for cardiocyte hypertrophy, cell size was determined by phase contrast microscopy and protein synthesis rate was measured by 3H-leucine incorporation. The proto-oncogene c-fos mRNA expression of cardiocytes was assessed using reverse transcription polymerase chain reaction （RT-PCR）. Results： STS could inhibit cardiocyte hypertrophy, increase the protein synthesis rate and enhance proto-oncogene c-fos mRNA expression in cardiocytes induced by Ang Ⅱ（P〈0.01）, with an effect similar to that of Valsartan, the Ang Ⅱ receptor antagonist. Conclusion： STS can prevent the hypertrophy of cardiac myocytes induced by Ang Ⅱ, which may be related to its inhibition of the expression of proto-oncogene c-fos mRNA.

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

Objective： To explore the protective effect of sodium tanshinone ⅡA sulfonate （STS） on small intestine injury in rats with sepsis and its possible mechanism. Methods： According to a random number table, 24 Tats were randomly divided into 3 groups： sham operation group （sham group）, sepsis model group （model group） and STS treatment group （STS group）, with 8 Tats in each group. A rat model of sepsis was induced by cecal ligation and puncture （CLP） for 5 h. STS （1 mg/kg） was slowly injected through the right external jugular vein after CLP. The histopathologic changes in the intestine tissue were observed under a light microscope, and the intestinal epithelial cell apoptosis was evaluated by terminal deoxynucleoddyl transferase （TdT）-mediated dUTP nick-end labeling （TUNEL） method. The expressions of Bcl-2, Bax and nuclear factor κB （NF- κ B） p65 in the intestinal tissue was determined by Western blot. The levels of tumor necrosis factor α （TNF-α） and interleukin 6 （IL-6） in the intestinal tissue were determined using enzyme-linked immuno-sorbent assay （ELISA）. Results： Obvious injuries were observed in the intestinal tissue in the CLP group compared with the sham group. The expression of NF- K B p65 and the levels of TNF- α and IL-6 were up-regulated after CLP, the apoptosis of intestinal epithelial cells was increased after CLP, and the ratio of Bcl-2 to Bax was decreased. STS post- treatment could attenuate the injury on the intestinal tissue induced by CLP, decrease the apoptosis of intestinal epithelial cells and the levels of NF- κ B p65, TNF-α and IL-6, and increase the ratio of Bcl-2 to Bax. Conclusion： STS can protect the small intestine in rats with sepsis, and the mechanism may be associated with the inhibition of intestinal epithelial apoptosis and the reduction of activation of inflammatory cytokines.

Sodium tanshinone ⅡA sulfonate prevents radiation-induced damage in primary rat cardiac fibroblasts

This study investigated the effects of X-ray irradiation on primary rat cardiac fibroblasts(CFs) and its potential mechanism, as well as whether sodium tanshinone ⅡA sulfonate(STS) has protective effect on CFs and its possible mechanism. Our data demonstrated that X-rays inhibited cell growth and increased oxidative stress in CFs, and STS mitigated X-ray-induced injury. Enzyme-linked immuno-sorbent assay showed that X-rays increased the levels of secreted angiotensin Ⅱ(Ang Ⅱ) and brain natriuretic peptide(BNP). STS inhibited the X-ray-induced increases in Ang Ⅱ and BNP release. Apoptosis and cell cycle of CFs were analyzed using flow cytometry. X-rays induced apoptosis in CFs, whereas STS inhibited apoptosis in CFs after X-ray irradiation. X-rays induced S-phase cell cycle arrest in CFs, which could be reversed by STS. X-rays increased the expression of phosphorylated-P38/P38,cleaved caspase-3 and caspase-3 as well as decreased the expression of phosphorylated extracellular signal-regulated kinase 1/2(ERK1/2)/ERK 1/2 and B cell lymphoma 2(Bcl-2)/Bcl-2 associated X protein(BAX) in CFs, as shown by Western blotting. STS mitigated the X-ray radiation-induced expression changes of these proteins. In conclusion, our results demonstrated that STS may potentially be developed as a medical countermeasure to mitigate radiation-induced cardiac damage.

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.

Tanshinone ⅡA： an overview of its biological activity and the molecular mechanism

Danshen, the rhizome of Salvia miltiorrhiza Bunge, has been used in traditional Chinese medicine （TCM） for treatment of various diseases. Tanshinone IIA （TSA） is one of the main active components of Danshen, which has multiple bioactivities. This article reviews the research progress of TSA in the treatment of cardiovascular disease, anti-inflammatory and immune, anti-tumor, liver protection, neuroprotection. It provides more ideas for the clinical application of TSA and the development of drug resistance.

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。

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。

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。

基于Meta分析的丹参酮Ⅱ_A磺酸钠注射液治疗急性脑梗死临床评价研究

目的:采用Meta分析方法评价丹参酮Ⅱ_A磺酸钠注射液治疗急性脑梗死的有效性及安全性。方法:计算机检索the Cochrane library、PubMed、Embase、SinoMed、中国知网、维普期刊数据库和万方数据库有关丹参酮Ⅱ_A磺酸钠注射液治疗急性脑梗死的随机对照试验,检索时限为各数据库建库至2016年10月。采用Cochrane风险评价表进行偏倚风险评价,提取资料通过Stata 13.1进行Meta分析。结果:最终共纳入13个随机对照试验,累计1 273名患者。Meta分析结果显示,对比西医常规治疗,丹参酮Ⅱ_A磺酸钠注射液辅助西医常规治疗急性脑梗死可提高临床总有效率(RR=1.22,95%CI:1.16~1.28,P<0.01),改善神经功能缺损(MD=-5.08,95%CI:-7.40^-2.77,P<0.01),降低炎性指标。在减少恶化情况方面,差异无统计学意义。有7篇文献明确无不良反应,2篇研究报道了共11例不良反应,其他文献均未对安全性做出说明,无严重不良反应。敏感性分析显示结果稳定性较好。结论:现有证据表明,丹参酮Ⅱ_A磺酸钠注射液治疗急性脑梗死在临床疗效、神经功能缺损改善及炎性指标减少等方面比单用西医常规疗效较好。但基于现有研究缺陷,所获得的支持证据强度有待提高,尚需要更多设计严谨、随访时间更长的临床研究予以证实。

丹参酮Ⅱ_A磺酸钠联合吲哚布芬对心源性脑栓塞血液流变学的影响

目的观察丹参酮Ⅱ_A磺酸钠联合吲哚布芬治疗心源性脑栓塞的临床疗效,探讨该联合治疗方案对血液流变学改变的作用机制,为临床治疗心源性脑栓塞提供理论依据。方法按入院先后顺序将我院康复中心2014年1月至2015年4月收治的224例脑栓塞住院患者,随机分为对照组与观察组。对照组对症治疗(如脱水及口服吲哚布芬+舒降之),观察组在此基础上静脉滴注丹参酮Ⅱ_A磺酸钠注射液,检测治疗前及治疗21 d后血液流变学指标,记录脑电图(Electroencephalogram,EEG)病理性棘波振幅及局部脑血流量(Regional cerebral blood flow,rCBF),计算治疗前、后患者卒中量表神经缺损(ESS)评分、日常生活能力(ADL)评分及总有效率,比较两组临床疗效。结果丹参酮Ⅱ_A磺酸钠联合吲哚布芬能显著降低脑栓塞患者脑电图病理性棘波振幅、ESS评分及血液流变学指标,显著提高脑栓塞患者局部脑血流量、ADL评分及总有效率,与对照组比较,差异均有统计学意义(P<0.05)。结论丹参酮Ⅱ_A磺酸钠联合吲哚布芬能明显改善患者血液流变学效应,松弛脑栓塞区血管平滑肌以增加局部脑血流量,降低脑栓塞患者脑电图病理性棘波振幅,有效改善脑栓塞患者神经功能缺损及临床症状,提高患者日常生活能力,对脑栓塞有理想的治疗作用,有一定的临床推广价值。

注射用丹参酮Ⅱ_A磺酸钠细菌内毒素检查法

目的建立检测注射用丹参酮ⅡA磺酸钠中内毒素的试验方法。方法运用干扰初筛法对供试品进行干扰试验,采用鲎试剂法对样品中的内毒素进行检测。结果注射用丹参酮ⅡA磺酸钠在药液稀释浓度为0.016 8 mg.m l-1以下时,与鲎试剂反应无干扰。结论所采用的细菌内毒素检查法可用于注射用丹参酮ⅡA磺酸钠的内毒素检查。

丹参酮Ⅱ_A磺酸钠联合前列地尔对椎动脉型颈椎病血液流变学及血清炎性因子的影响

目的:探讨丹参酮Ⅱ_A磺酸钠联合前列地尔对椎动脉型颈椎病血液流变学及血清炎性因子的影响。方法:选取90例椎动脉型颈椎病患者,随机分为观察组和对照组,每组各45例。对照组注射前列地尔干乳剂,观察组在对照组的基础上给予丹参酮Ⅱ_A磺酸钠注射液,评定两组患者的治疗效果及血液流变学指标的变化。结果:观察组的总有效率显著高于对照组(P<0.05);治疗后,两组患者炎性因子水平、血液流变学指标水平均显著低于治疗前(P<0.05);治疗后观察组的炎性因子水平、血液流变学指标水平均显著低于对照组(P<0.05)。结论:丹参酮Ⅱ_A磺酸钠联合前列地尔治疗椎动脉型颈椎病,能显著提高治疗效果,降低炎症因子水平,降低血液黏度和血小板聚集率。

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。

银丹心脑通软胶囊联合丹参酮Ⅱ_A磺酸钠治疗冠状动脉粥样硬化性心脏病不稳定型心绞痛临床研究

目的探讨银丹心脑通软胶囊联合丹参酮Ⅱ_A磺酸钠对冠状动脉粥样硬化性心脏病(简称冠心病)不稳定型心绞痛患者炎症因子和斑块的影响。方法选择2014年1月至2017年1月在医院就诊的冠心病不稳定型心绞痛患者179例,随机分为对照组(90例)和观察组(89例)。对照组患者给予基础治疗,同时给予丹参酮Ⅱ_A磺酸钠注射液50 mg,加入0.9%氯化钠注射液250 mL,每日1次,静脉滴注。观察组患者在对照组基础上加用银丹心脑通软胶囊(3粒/次,每日3次)口服。均治疗2周。结果观察组总有效率为83.15%,高于对照组的66.67%(P<0.05);治疗后,两组患者颈动脉内-中膜厚度、颈动脉粥样硬化斑块最大长度、颈动脉粥样硬化斑块最大厚度、白细胞介素6、肿瘤坏死因子α、C反应蛋白及转化生长因子β_1均较治疗前显著降低(P<0.05),且观察组均较对照组降低明显(P<0.05);两组患者不良反应发生率比较无明显差异(P>0.05)。结论银丹心脑通软胶囊联合丹参酮Ⅱ_A磺酸钠治疗冠心病不稳定型心绞痛疗效显著,能显著改善动脉粥样硬化程度,减轻因粥样硬化导致的炎症状态,不良反应少。

丹参酮Ⅱ_A磺酸钠注射液致变态反应的自动监测研究

目的:利用"医疗机构ADE主动监测与智能评估警示系统"分析丹参酮Ⅱ_A磺酸钠注射液致变态反应的发生率及相关影响因素。方法:借助系统回顾性调取我院2014~2016年使用丹参酮Ⅱ_A磺酸钠注射液住院患者的病历,设置"变态反应"与"过敏性休克"模块的事件配置器参数,分析系统阳性报警病例及各ADR发生率,并利用巢式病例对照研究设计,对丹参酮Ⅱ_A磺酸钠注射液致皮肤类变态反应的影响因素进行分析。结果:借助系统自动监测11 969例丹参酮Ⅱ_A磺酸钠注射液用药患者,用时约2 h;经临床药师再评估,皮肤类变态反应的发生率分别为0.15%,过敏样反应0.01%,无过敏性休克。丹参酮Ⅱ_A磺酸钠注射液致皮肤类变态反应在年龄、性别、过敏史、溶媒、BMI等方面差异无统计学意义。结论:专项软件系统可以高效快速进行丹参酮Ⅱ_A磺酸钠注射液致变态反应的自动监测,且能够初步预测其ADR相关影响因素,是中药注射剂上市后安全性再评价的好工具。