Therapeutic effect of Qingyi decoction in severe acute pancreatitis-induced intestinal barrier injury

AIM: To investigate the effect of Qingyi decoction onthe expression of secreted phospholipase A2(s PLA2) in intestinal barrier injury.METHODS: Fifty healthy Sprague-Dawley rats were randomly divided into control, severe acute pancreatitis(SAP), Qingyi decoction-treated(QYT), dexamethasonetreated(DEX), and verapamil-treated(VER) groups. The SAP model was induced by retrograde infusion of 1.5% sodium deoxycholate into the biliopancreatic duct of the rats. All rats were sacrificed 24 h post-SAP induction. Arterial blood, intestine, and pancreas from each rat were harvested for investigations. The levels of serum amylase(AMY) and diamine oxidase(DAO) were determined using biochemical methods, and serum tumor necrosis factor(TNF)-α level was measured by an enzyme linked immunosorbent assay. Pathologic changes in the harvested tissues were investigated by microscopic examination of hematoxylin and eosinstained tissue sections. The expressions of s PLA2 at m RNA and protein levels were detected by reverse transcriptase PCR and Western blot, respectively. A terminal deoxynucleotidyl transferase-mediated d UTP nick-end labeling assay was used to investigate apoptosis of epithelial cells in the intestinal tissues. RESULTS: Compared to the control group, the expression of s PLA2 at both the m RNA and protein levels increased significantly in the SAP group(0.36 ± 0.13 vs 0.90 ± 0.38, and 0.16 ± 0.05 vs 0.64 ± 0.05, respectively; P s < 0.01). The levels of AMY, TNF-α and DAO in serum were also significantly increased(917 ± 62 U/L vs 6870 ± 810 U/L, 59.7 ± 14.3 ng/L vs 180.5 ± 20.1 ng/L, and 10.37 ± 2.44 U/L vs 37.89 ± 5.86 U/L, respectively; P s < 0.01). The apoptosis index of intestinal epithelial cells also differed significantly between the SAP and control rats(0.05 ± 0.02 vs 0.26 ± 0.06; P < 0.01). The serum levels of DAO and TNF-α, and the intestinal apoptosis index significantly correlated with s PLA2 expression in the intestine(r = 0.895, 0.893 and 0.926, respectively; Ps < 0.05). Thelevels of s PLA2, AMY, TNF-α, and DAO in the QYT, VER, and DEX groups were all decreased compared with the SAP group, but not the control group. Qingyi decoction intervention, however, gave the most therapeutic effect against intestinal barrier damage, although the onset of its therapeutic effect was slower. CONCLUSION: Qingyi decoction ameliorates acute pancreatitis-induced intestinal barrier injury by inhibiting the overexpression of intestinal s PLA2. This mechanism may be similar to that of verapamil.

Qingyi decoction protects against myocardial injuries induced by severe acute pancreatitis

BACKGROUND We studied the protective effects of Qingyi decoction(QYD)(a Traditional Chinese Medicine)against severe acute pancreatitis(SAP)-induced myocardial infarction(MI).AIM To study the function and mechanism of QYD in the treatment of myocardial injuries induced by SAP.METHODS Ultrasonic cardiography,hematoxylin and eosin staining,immunohistochemistry,qRT-PCR,western blot,enzyme-linked immunosorbent assays,and apoptosis staining techniques were used to determine the effects of QYD following SAP-induced MI in Sprague-Dawley rats.RESULTS Our SAP model showed severe myocardial histological abnormalities and marked differences in the symptoms,mortality rate,and ultrasonic cardiography outputs among the different groups compared to the control.The expression of serum cytokines[interleukin(IL)-1?,IL-6,IL-8,IL-12,amyloidβ,and tumor necrosis factor-α]were significantly higher in the SAP versus QYD treated group(P<0.05 for all).STIM1 and Orai1 expression in myocardial tissue extracts were significantly decreased post QYD gavage(P<0.001).There was no significant histological difference between the 2-aminoethyl diphenylborinate inhibitor and QYD groups.The SAP group had a significantly higher apoptosis index score compared to the QYD group(P<0.001).CONCLUSION QYD conferred cardio-protection against SAP-induced MI by regulating myocardial-associated protein expression(STIM1 and Orai1).

Qingyi decoction attenuates intestinal epithelial cell injury via the calcineurin/nuclear factor of activated T-cells pathway

BACKGROUND Recent studies have demonstrated that dysfunction of the intestinal barrier is a significant contributing factor to the development of severe acute pancreatitis(SAP).A stable intestinal mucosa barrier functions as a major anatomic and functional barrier,owing to the balance between intestinal epithelial cell(IEC)proliferation and apoptosis.There is some evidence that calcium overload may trigger IEC apoptosis and that calcineurin(CaN)/nuclear factor of activated Tcells(NFAT)signaling might play an important role in calcium-mediated apoptosis.AIM To investigate the potential mechanisms underlying the therapeutic effect of Qingyi decoction(QYD)in SAP.METHODS A rat model of SAP was created via retrograde infusion of sodium deoxycholate.Serum levels of amylase,tumor necrosis factor(TNF-α),interleukin(IL)-6,D-lactic acid,and diamine oxidase(DAO);histological changes;and apoptosis of IECs were examined in rats with or without QYD treatment.The expression of the two subunits of CaN and NFAT in intestinal tissue was measured via quantitative realtime polymerase chain reaction and western blotting.For in vitro studies,Caco-2 cells were treated with lipopolysaccharide(LPS)and QYD serum,and then cell viability and intracellular calcium levels were detected.RESULTS Retrograde infusion of sodium deoxycholate increased the severity of pancreatic and intestinal pathology and the levels of serum amylase,TNF-α,and IL-6.Both the indicators of intestinal mucosa damage(D-lactic acid and DAO)and the levels of IEC apoptosis were elevated in the SAP group.QYD treatment reduced the serum levels of amylase,TNF-α,IL-6,D-lactic acid,and DAO and attenuated the histological findings.IEC apoptosis associated with SAP was ameliorated under QYD treatment.In addition,the protein expression levels of the two subunits of CaN were remarkably elevated in the SAP group,and the NFATc3 gene was significantly upregulated at both the transcript and protein levels in the SAP group compared with the control group.QYD significantly restrained CaN and NFATc3 gene expression in the intestine,which was upregulated in the SAP group.Furthermore,QYD serum significantly decreased the LPS-induced elevation in intracellular free Ca^(2+)levels and inhibited cell death.CONCLUSION QYD can exert protective effects against intestinal mucosa damage caused by SAP and the protective effects are mediated,at least partially,by restraining IEC apoptosis via the CaN/NFATc3 pathway.

Analysis of Clinical Effect of Wumen Qingyi Decoction on Acute Pancreatitis

[Objectives]To examine the effects of Wumen Qingyi Decoction on inflammatory responses in patients with acute pancreatitis(AP).[Methods]Eighty patients with mild or severe AP were randomly allocated to a treatment group(Wumen Qingyi Decoction+baseline treated)or a control group(baseline treated).All patients were managed conservatively.In addition,the Group A received Wumen Qingyi Decoction for 400 mL/d for 7 d.Laboratory parameters,condition of disease and therapeutic effect indexes,and so on,between the two groups were compared.[Results]The recovery of serum levels of amylase(AMS),C reaction protein(CRP),and tumor necrosis factor(TNF-α),interleukin1(IL-1),IL-6,IL-10,as well as the scores of Balthazar and BISAP in Treatment group were quicker than those in Control group(P<0.05).In addition,the improvement of organic dysfunction in Treatment group was better than that in Control group.[Conclusions]The course of combined Wumen Qingyi Decoction and basic treatment of western medicine could effectively adjust the body's inflammatory response to promote the recovery process of acute pancreatitis.

Clinical observation of hysteroscopic surgery combined with ectopic pregnancy ⅱ decoction and methotrexate in the treatment of cesarean scar pregnancy

Objective:To explore the effectiveness and safety about the treatment of Caesarean Scar Pregnancy combined hysteroscopic surgery with extopic pregnancy Ⅱ decoction and methotrexate(MTX).Methods: A total of 80 cases of CSP patients admitted by our hospital from January 2014 to March 2017 were selected as the subjects. According to the treatment way, the patients were divided into experimental group (n=40) and control group (n=40). The control group was given MTX 50 mg/m2, IM once;and the experimental group was given extopic pregnancy Ⅱ decoction on the basis of the treatment given to the control group;the 8th day hysteroscopic surgery. Routine treatment was given after surgery. Experimental group continued to take extopic pregnancy Ⅱ decoction until monitoring the serum beta-hcg level drops below normal. The general information and curative effect, HCG levels before and after 4, 7 and 11d of treatment;mass diameter before and after 11 d of treatment, menstruation recovery time and the incidence of adverse reactions in 2 groups were observed.Results:After hysteroscopic surgery pretreatment with extopic pregnancy Ⅱ decoction and MTX, HCG levels after 4, 7 and 11d were significantly lower than before, it gradually reduced by time prolonged, and research group was lower than control group, the differences were statistically significant. After treatment with different drugs, the size of pregnancy package in the observation group was significantly smaller than that in the control group. Compared with the control group, the he package block size, beta HCG time and vaginal bleeding time were significantly reduced.Conclusion: It has significant clinical effect of hysteroscopic surgery combined with ectopic pregnancy Ⅱ and MTX in the treatment of CSP. It has worthy of clinical promotion to control the amount of blood, avoid intrauterine adhesion caused by uterine artery embolization and infection et al and reduce burden of the physical and economic of patients.

Network Pharmacology Research of Qingyi Decoction(清胰汤)in the Treatment of Acute Pancreatitis

Presently,clinically specific drugs are absent for acute pancreatitis(AP).Numerous clinical investigations have extolled the notable efficacy of Qingyi Decoction(QYD,清胰汤)in the management of AP.However,the molecular mechanisms are lacking.Therefore,we analyzed pharmacological mechanisms of QYD in treating AP through network pharmacology.As for the network pharmacology,173active compounds and 1,073 active target genes for QYD were identified.Of these,884 active target genes correlated with AP among the 11128 AP-associated genes and were linked to the 173 active compounds.In addition,GO functional enrichment and KEGG pathway enrichment revealed that these target genes were mainly enriched in cancer signaling,neuroactive ligand-receptor interactions,lipids and atherosclerosis,cAMP signaling,central carbon metabolism in cancer,and calcium signaling pathways.Finally,molecular docking was employed to assess the binding affinity between target proteins and their associated compounds.This study identified critical compounds and potential target genes.Our study may serve as a foundation for subsequent investigations on the therapeutic potential of QYD in treating AP.

Research Progress of Qingyi Decoction(清胰汤)in Treating Acute Pancreatitis

Acute pancreatitis(AP)is one of the most common digestive system diseases.AP is associated with high rate of hospitalization and death risk,but it lacks specific and effective therapies.Qingyi Decoction(清胰汤)is the basic formula for AP treatment.Qingyi Decoction can improve symptoms,inhibit inflammatory,ameliorate AP-induced organ injury via multiple pathways and targets,as demonstrated in many preclinical and clinical studies.This review summarized the progress of the clinical studies and mechanisms of Qingyi Decoction,aimed to provide valuable research information for the future clinical application and molecular mechanism research of Qingyi decoction.

Intervention effect and mechanism of Jisheng Shenqi Decoction plus Panax notoginseng and Bionjia on CCl4-induced hepatic fibrosis rat model

Objective:To investigate the intervention effect and specific mechanism of Jisheng Shenqi Decoction plus Panax notoginseng and Turmeric on carbon tetrachloride(CCl4)-induced liver fibrosis in rats.Methods:SPF SD rats were randomly divided into control group,model group,and Chinese medicine treatment(low,medium and high dose)groups.The model group and Chinese medicine treatment group were given intraperitoneal injection of 40%CCl4 olive oil solution twice a week.A rat model of liver fibrosis was replicated by the method for 8 weeks.After successful modeling,each drug-administered group was gavaged with corresponding drugs,and the control group and model group were gavaged with equal volume of distilled water,once a day,for 4 weeks.After the last intragastric administration,HE staining and Masson staining were used to observe the pathological morphology of liver tissue,and liver function(ALT,AST)was detected;ELISA method was used to determine transforming growth factorβ(TGF-β),angiotensin II(Ang-Ⅱ),chitinase 3-like protein 1(CHI3L1),interleukin-1(IL-1),interleukin-6(IL-6),tumor necrosis factor-α(TNF-α)content;The expression levels of type I,type III collagen(Col-Ⅰ,Col-Ⅲ)and TGF-βmRNA were determined by RT-PCR.Results:①HE and Masson staining showed that a large number of liver cells in the model group were inflamed and necrotic,the collagen fibers in the liver tissue were extensively proliferated,the fibrous septa were interconnected,and the pseudolobules were formed.Compared with the model group,the levels of ALT,AST,TGF-β,Ang-Ⅱ,CHI3L1,IL-1,IL-6 and TNF-αin the traditional Chinese medicine treatment group were decreased,while the levels of Col-Ⅰ,Col-ⅢThe expressions ofⅢand TGF-βmRNA were decreased,and the effect was most obvious in the middle and high dose groups of traditional Chinese medicine(P<0.01).Conclusion:Jisheng Shenqi Decoction combined with Panax notoginseng and Biejia can significantly improve liver fibrosis induced by CCl4 in rats,and its mechanism may be related to the down-regulation of angiotensin-converting enzyme(ACE)-angiotensin II(Ang-II)-angiotensin II receptor 1(AT1R)signaling pathway related gene expression,reducing the level of related cytokines,promoting the degradation of extracellular matrix and so on.

鳖甲煎丸辅助治疗对慢性乙型肝炎早期肝硬化患者肝功能、基质金属蛋白酶-2及血管紧张素-Ⅱ水平的影响

目的:探讨慢性乙型肝炎早期肝硬化患者应用鳖甲煎丸辅助治疗的效果及对其肝功能、血管紧张素-Ⅱ(AngiotensinⅡ,AngⅡ)、基质金属蛋白酶-2(Matrix metalloprpteinase-2,MMP-2)水平的影响。方法:抽签法将我科2021年7月至2023年7月间124例慢性乙型肝炎早期肝硬化患者分2组,各62例,常规组行恩替卡韦片等常规疗法,研究组加服鳖甲煎丸辅助治疗,4 w作1疗程,共3疗程,治疗3疗程后比较其临床疗效及期间不良反应情况,采用肝功能、炎症因子、血液指标评价其对患者肝功能、AngⅡ、MMP-2等有关指标的影响。结果:与常规组相比,研究组总有效率高,研究组3疗程末凝血酶原活动度及白蛋白水平较高,总胆红素及丙氨酸转移酶水平较低,肿瘤坏死因子-α、白细胞介素-1β较低,血清AngⅡ、MMP-2较低,差异有统计学意义(P<0.05),期间患者均无药物有关不良反应出现。结论:慢性乙型肝炎早期肝硬化患者应用鳖甲煎丸辅助治疗效果显著且安全,能有效降低患者炎症因子及AngⅡ、MMP-2水平,并显著改善其肝功能。

清胰Ⅱ号对香猪重症急性胰腺炎胰肺损害的保护作用

目的 观察重症急性胰腺炎 (severeacutepancreatitis ,SAP)模型血浆淀粉酶、内毒素、IL 1β、IL 6、肺、胰腺的变化及清胰Ⅱ号对其的保护作用。 方法 用 16只贵州香猪 ,雌雄不拘 ,随机分为 2组 ,各组n =8:生理盐水 (NS)组 ;中药清胰Ⅱ号 (ChineseMedicineQingyiⅡ ,CMQ)组。推注 5 %牛磺脱氧胆酸钠 (0 .5ml/kg体重 )复制SAP模型。分别于制模前 ,制模后 1、6、12、2 4、4 8、72、96h采静脉血 ,检测血浆中淀粉酶、内毒素、IL 1β、IL 6浓度。光镜下 ,观察胰、肺组织的病理变化。 结果 CMQ可减轻SAP猪的胰腺及肺的病理性损伤 ,可减轻胰出血、坏死程度和减轻肺间质水肿、肺泡毛细血管壁缺血、缺氧程度 ,显著降低各时间点 (除制模前、制模后 1小时外 )血浆内毒素浓度和血清淀粉酶、IL 1β、IL 6的浓度 (P <0 .0 1)。结论 清胰Ⅱ号可减轻内毒素血症 ,抑制内毒素对全身各器官、组织的损伤 ;减少早期炎症介质IL 1β、IL 6的产生 ,减轻其引发的一系列损伤反应。对胰肺有保护作用。

清胰Ⅱ号方对重症急性胰腺炎大鼠肠黏膜屏障功能的影响

目的探讨清胰Ⅱ号方对重症急性胰腺炎(severe acute pancreatitis,SAP)大鼠肠黏膜屏障功能的影响。方法选取48只SD大鼠制备SAP模型,造模后随机分为模型组及清胰Ⅱ号方治疗组(治疗组),每组24只。另选取8只大鼠作为假手术组。造模后麻醉苏醒即开始干预,治疗组给予清胰Ⅱ号方(1mL/100g)灌胃,假手术组及模型组给予等体积生理盐水灌胃,各组灌胃均6h/次,干预后6、12、24h每组取8只大鼠,开腹后测腹水量,测血清二胺氧化酶(diamine oxidase,DAO)及D-乳酸浓度;取胰腺及回肠做病理检查,并进行胰腺病理评分;取回肠做扫描电镜检查。结果假手术组无腹水,胰腺及回肠病理无明显异常。与假手术组比较,模型组6h时腹水量、DAO、D-乳酸、病理评分均升高,差异均有统计学意义(P<0.05)。模型组6～24h时DAO、D-乳酸、病理评分逐渐升高,差异均有统计学意义(P<0.05),镜下见组织结构紊乱、间质水肿、出血,大量中性粒细胞浸润,局部灶性或片状肠坏死。与本组12h比较,模型组24h腹水量增多,差异有统计学意义(P<0.05)。治疗组6～24h时D-乳酸、病理评分逐渐升高,差异均有统计学意义(P<0.05),与本组12h比较,治疗组24h腹水量增多,DAO升高,差异均有统计学意义(P<0.05)。与模型组同期比较,治疗组6～24h各指标均降低,差异均有统计学意义(P<0.05),镜下见肠黏膜组织水肿、充血,少量中性粒细胞浸润,程度较模型组轻。结论清胰Ⅱ号方对SAP大鼠肠黏膜屏障功能有保护作用。

清胰Ⅱ号颗粒剂对急性坏死性胰腺炎大鼠肠道细菌移位的影响

目的观察清胰Ⅱ号颗粒剂对急性坏死性胰腺炎(acute necrotizing pancreatitis,ANP)大鼠肠道细菌移位的影响并探讨其机理。方法将18只SD大鼠随机等分为假手术组、ANP组及治疗组,每组6只;ANP组及治疗组以30g/L牛磺胆酸钠逆行注入胰胆管制作大鼠ANP模型,造模术后1h,治疗组以250g/L清胰Ⅱ号颗粒剂灌胃给药(10mL/kg),6h1次,共3次,假手术组及ANP组用同等剂量生理盐水以相同方式灌胃。造模后24h,取大鼠肝脏、胰腺、脾脏、肠系膜淋巴结组织及回肠内容物行细菌培养及菌种鉴定,用real-time PCR检测回肠组织中高迁徙率族蛋白-1(high mobility group box1,Hmgb1)mRNA表达,ELISA测定回肠组织中一氧化氮(nitric oxide,NO)、内皮素-1(endothelin-1,ET-1)浓度,同时观察胰腺、回肠组织病理改变,测定回肠组织湿/干重比值。结果ANP组胰腺、回肠组织损伤明显,回肠组织Hmgb1mRNA的表达较假手术组上调(P<0.01),NO、ET-1浓度较假手术组升高(P<0.01),分别为(1.67±0.21)μmol/L、(102.18±9.19)ng/L,细菌移位至肝脏、胰腺、脾脏及肠系膜淋巴结;治疗组回肠组织中Hmgb1 mRNA的表达较ANP组下调(P<0.01),NO、ET-1浓度较ANP组降低(P<0.05),分别为(1.39±0.23)μmol/L、(83.15±5.39)ng/L,回肠病理损害程度减轻,细菌移位减少。结论Hmgb1、NO及ET-1浓度在ANP模型大鼠肠道细菌移位中可能具有重要作用,清胰Ⅱ号颗粒剂可能通过下调回肠组织中Hmgb1 mRNA的表达,降低NO、ET-1浓度,减轻胰腺、回肠组织的病理改变,从而抑制肠道细菌移位。

HPLC-ELSD同时测定当归补血总苷中黄芪甲苷和黄芪皂苷Ⅱ

目的建立HPLC-ELSD测定当归补血总苷(黄芪、当归)中的黄芪甲苷和黄芪皂苷Ⅱ的方法。方法色谱柱Kro-mail C18(4.6 mm×250 mm,5μm);流动相为乙腈-水(37.5∶62.5);体积流量0.8 mL/min;ELSD参数:漂移管温度100℃;N2气流体积流量2.60 L/min。结果黄芪甲苷在0.85～6.76μg之间呈良好的线性关系(r=0.999 2),平均回收率为98.8%,RSD为1.50%。黄芪皂苷Ⅱ在1.05～8.4μg之间呈良好的线性关系(r=0.999 4),平均回收率为95.7%,RSD为2.70%。结论该法精密度、重复性良好,简便、快速、准确,适用于当归补血总苷中黄芪甲苷、黄芪皂苷Ⅱ的测定。

加味桃核承气汤治疗Ⅱ型糖尿病的临床和实验研究

本文报道用加味桃核承气汤治疗Ⅱ型糖尿病106例,总有效率79%,与西药优降糖组疗效相当;但降糖幅度和临床主要症状的改善方面均较优降糖组为优。动物实验表明,加味桃核承气汤能降低糖尿病及正常大鼠的空腹血糖浓度,促进β细胞分泌内源性胰岛素,抑制胰及胰外组织分泌胰高血糖素,对胰岛内分泌细胞有一定的修复功能及增加胰岛β细胞的分泌颗粒,刺激肝糖原的合成,抑制肝糖原的分解。认为加味桃核承气汤的作用机理是"益气养阴、活血化瘀、润肠通下"的协同作用。

肾病Ⅱ号方对单纯血尿型IgA肾病红细胞免疫功能的影响

目的探讨肾病Ⅱ号方治疗单纯血尿型IgA肾病的临床疗效及其对红细胞免疫功能的影响。方法采用随机对照研究的方法,将70例单纯血尿型IgA肾病患者分成两组,治疗组予肾病Ⅱ号方,对照组给予血尿安胶囊,观察临床疗效;治疗8周后观察红细胞免疫指标的变化情况。结果肾病Ⅱ号方与血尿安胶囊均能减轻血尿(P<0.05),两组比较无统计学差异(P>0.05);治疗组红细胞C3b受体活性明显升高,红细胞表面吸附的免疫复合物明显降低。结论肾病Ⅱ号方能通过调节红细胞免疫功能治疗IgA肾病血尿。

桃红四物汤Ⅱ号抗血管生成作用及其对KDR/FLK-1表达的影响

目的探讨桃红四物汤(THSWD)Ⅱ号抗血管生成作用及其机理。方法以鸡胚绒毛尿囊膜(CAM)法检测THSWDⅡ号对新生血管的效应,以MTT法检测其对血管内皮细胞ECV304增殖有无抑制作用,并以免疫组化法观察该方对小鼠B16黑色素瘤血管内皮细胞KDR/FLK-1的表达和微血管密度(MVD)计数的影响。结果THSWDⅡ号1 g/mL、2 g/mL组CAM血管指数降低(P<0.01);THSWDⅡ号1 mg/mL、2 mg/mL组ECV304细胞吸光度值降低(P<0.01);THSWDⅡ号5 g/kg、10 g/kg组及THSWDⅡ号10 g/kg+环磷酰胺25 mg/kg组肿瘤重量、KDR/FLK-1的表达、MVD计数均降低(P<0.01)。结论THSWDⅡ号具有抗CAM血管生成、抑制ECV304细胞增殖、抑制小鼠B16黑色素瘤生长的作用。其抗肿瘤作用机制可能与抑制内皮细胞KDR/FLK-1的表达,继而抗血管生成有关。

高效液相色谱法测定鼠用清胰Ⅱ号颗粒剂后血中大黄素变化

目的研究大鼠灌胃给予清胰Ⅱ号颗粒剂后,其效能成分大黄素在大鼠体内的药代动力学过程。方法大鼠单次灌服不同剂量(2.5g/kg及5.0g/kg)的清胰Ⅱ号颗粒剂后,以高效液相色谱(HPLC)法测定其血浆中不同时间点的大黄素浓度,采用DAS2.0药代动力学软件拟合处理药代动力学参数。结果大鼠血浆中大黄素质量浓度在0.1563～10.0000ng/mL范围与峰面积线性关系良好,平均回收率为99.41%,并计算出了相应的药代动力学参数。结论单次灌服不同剂量的清胰Ⅱ号颗粒剂后,大黄素在大鼠体内的药代动力学过程符合二室模型,吸收慢,消除也慢。

CaM/CaMK Ⅱ在脾气虚证大鼠脑肠微环境中的表达及四君子汤干预效应研究

目的:从Ca M信号通路关键基因揭示脾气虚证发生及益气健脾法干预作用机制。方法:脾气虚证大鼠为研究对象,采用实时荧光定量RT-PCR、Western Blot技术检测不同阶段大鼠脑、肠Ca M信号通路关键基因Ca M/Ca MKⅡmRNA和蛋白的动态表达,并分析四君子汤干预效应机制。结果:从大鼠小肠组织看,脾气虚证大鼠相对于正常大鼠Ca M/Ca MKⅡmRNA和蛋白表达升高,经四君子汤治疗后明显降低;从大鼠脑组织看,脾气虚证大鼠相对于正常大鼠Ca M/Ca MKⅡmRNA和蛋白表达降低,经四君子汤治疗后明显升高。结论:脑肠微环境中Ca M信号传导通路关键基因Ca M/Ca MKⅡ的动态表达与脾气虚证形成有关,四君子汤通过影响其表达对脾气虚证起到时相性动态干预。

ZTC1+1-Ⅱ澄清剂用于中药水提液澄清

目的:考察ZTC1+1-Ⅱ澄清剂用于中药水提液的澄清效果。方法:采用HPLC和分光光度法,以2,3,5,4′-四羟基-二苯乙烯-2-O-β-D-葡萄糖(二苯乙烯苷),总多糖和固形物含量为指标,通过正交试验法,考察澄清剂用量、药液浓度、搅拌速度对澄清工艺的影响。结果:中药水提液的最佳澄清条件为:澄清剂用量5%,药液浓度(1∶10),搅拌速度100 r.m in-1。结论:与传统水提醇沉法比较,ZTC1+1-Ⅱ澄清剂澄清工艺能保留水提液中大部分指标成分,且操作简单、安全。ZTC1+1-Ⅱ澄清剂作为絮凝澄清剂可用于精制中药水提液。

桃红四物汤Ⅱ号抑制小鼠B16黑色素瘤生长及VEGF,KDR/FLK-1表达

目的:观察桃红四物汤Ⅱ号对小鼠B16黑色素瘤生长、血管内皮生长因子(VEGF)和血管内皮生长因子受体-2(KDR/FLK-1)表达及肿瘤微血管密度(MVD)值的影响。方法:采用C57BL/6J小鼠皮下接种B16黑色素瘤细胞建立模型,分别给予2.5,5,10 g.kg-1桃红四物汤Ⅱ号水煎剂、环磷酰胺0.05 g.kg-1及联合用药桃红四物汤Ⅱ号10 g.kg-1+环磷酰胺0.025 mg.kg-1,检测各组肿瘤体积、重量、VEGF和KDR/FLK-1表达及肿瘤MVD值。结果:桃红四物汤Ⅱ号5,10 g.kg-1及联合用药组肿瘤体积、重量、VEGF和KDR/FLK-1表达及肿瘤MVD值均较生理盐水组明显降低(P<0.01)。结论:桃红四物汤Ⅱ号能抑制小鼠B16黑色素瘤的生长,其抗肿瘤机制可能与抗血管生成作用有关。