Study on the mechanism of Renshen Gansong herb in the treatment of paroxysmal atrial fibrillation based on network pharmacology

Objective:To explore the target gene and mechanism of effective components of Renshen-Gansong in the treatment of paroxysmal atrial fibrillation based on network pharmacology.Methods:The chemical constituents of Renshen-Gansong drug pairs were searched by TCMSP traditional Chinese medicine database.The potentially effective components were screened under the conditions of bioavailability(OB)≥30%and drug-like(DL)≥0.18,and the potential targets were predicted by TCMSP database.The human gene name corresponding to the potential target was found by Uniprot database,and the disease target of paroxysmal atrial fibrillation was searched by Genecards database,the intersection target was mapped with the potential target of drug pair,the Wayne diagram was drawn,and the disease-drug-component-target network map was constructed by Cytoscape3.7.2.The PPI protein interaction network map was constructed by STRING database to select the core targets,and finally GO analysis and KEGG analysis were carried out.Results:A total of 28 active components and 45 effective targets were obtained.GO enrichment analysis showed that the main pathways were neurotransmitter receptor activity,ion gated channel activity,passive transmembrane transporter activity,G protein coupled neurotransmitter receptor activity and so on.KEGG pathway enrichment analysis showed that the main pathways were IL-17 signal pathway,calcium signal pathway,TNF signal pathway and so on.Conclusion:Renshen-Gansong has a synergistic effect on the treatment of paroxysmal atrial fibrillation through multi-targets,multi-pathways and multiple signal pathways,which provides a basis for further study of drug mechanism and clinical guidance.

Mechanism of Baihu Renshen decoction on T2DM rats based on mitochondrial autophagy mediated by PINK1/Parkin

Background:This study will be aimed at investigating the effects of Baihu Renshen decoction(BHRS)on type 2 diabetes rats and on macromolecular enzyme 1(PINK1)/E3 ubiquitin protein ligase(Parkin)pathway.Methods:The experiment was divided into four groups:control group,model group,metformin group and BHRS low-dose group and high-dose group.Forty male rats were selected as samples and randomly assigned to at least one test group.Finally,there are 18 rats in each group.Except for the control group,the rats within the different teams got a high-fat diet associate in nursing an intraperitoneal injection of streptozotocin to make a type 2 diabetes mellitus(T2DM)rat model.The organic chemistry and inflammatory indexes of rats in every cluster were analyzed and compared once four weeks of intragastric administration of comparable reagents to review the therapeutic impact of BHRS on T2DM.In addition,we determined the pathological changes of ductal gland tissue of T2DM rats after treatment,and compared the expression of mitochondrial phagocytosis related proteins in ductal gland tissue of rats in each group.Results:FBG,LDL-C,TC,TG,MDA,IL-1,IL-6,TNF-,and mitophagy-related proteins COXIV,P62,VDAC1,and TOM20 were elevated in the model group compared to the control group,while HDL-C,SOD,GSH-Px,and mitophagy-related proteins PINK1,Parkin,and LC3II/I were decreased(P<0.05 or P<0.01).The expressions of FBG,TC,TG,LDL-C,MDA,IL-1,IL-6,TNF-,and mitophagy-related proteins COXIV,P62,VDAC1,and TOM20 were lowered in the BHRS group,while the expressions of HOMA-,HDL-C,SOD,GSH-Px,and mitophagy-related proteins PINK1,Parkin,and LC3II/I were(P<0.05 or P<0.01).After therapy with BHRS,hematoxylin-eosin staining showed that the intensity of pancreatic acinar staining increased,and islet cells became clear boundaries that were,regularly arranged,and with reduced vacuoles reduced.Conclusion:BHRS has a clear therapeutic effect on T2DM,which may be achieved by regulating mitochondrial autophagy through the PINK1/Parkin pathway.

Protective Effect of Renshen Yangrong Decoction(人参养荣汤) on Bone Marrow against Radiation Injury in Mouse

Objective：To explore the effect of Renshen Yangrong Decoction（人参养荣汤,RYD） in protecting bone marrow from radiation injury.Methods：One hundred and eighty Kuming mice were subjected to the three tests for anti-radiation injury effect evaluation,i.e.the test of peripheral white blood cell（WBC） count, the test of bone marrow nucleated cell count,and the bone marrow micronucleus test,using 60 mice for each test.The mice in each test were divided into 6 groups：the blank control group,the model control group,the positive control group treated by Shiyiwei Shenqi Tablet（十一味参芪片,1.0 g/kg）,and three RYD groups treated with high（42.0 g/kg）,moderate（21.0 g/kg）,and low（10.5 g/kg） doses of crude drugs of RYD,with 10 mice in each group.The treatment was given by gastrogavage perfusion continuously for 7-14 days before mice received ^（60）Co-γray radiation and continued until the end of the experiment.The body weights of the mice were monitored,the changes in peripheral WBC and bone marrow nucleated cells were counted,and the variation in bone marrow micronucleated cells was observed on the respective appointed days.Results：A significant decrease in body weight,peripheral WBC count,and bone marrow nucleated cell count,as well as marked changes in bone marrow micronucleated cells were observed in the mice after radiation,indicating that the radiation injury model was successfully established.As compared with the model control group,the decrease in body weight,peripheral WBC count,and bone marrow nucleated cell count,as well as the increase in bone marrow micronucleus cell count in the high dosage RYD treated group were obviously inhibited or lessened （P0.05 or P0.01）.Conclusion：RYD showed obvious protective effect in mice with bone marrow injury induced by radiation.

Anti-fatigue Effect of Renshen Yangrong Decoction(人参养荣汤) in Mice

Objective： To explore the anti-fatigue effect of Renshen Yangrong Decoction （人参养荣汤 RYD） in mice. Methods： One hundred Kunming mice were randomly divided into 5 groups with 20 mice in each group. The negative control group was treated with distilled water, the positive control group was treated with Shiyiwei Shenqi Tablet （十一味参芪片 1.0 g/kg）, the high-, medium- and low-dose RYD groups were treated with 42.0, 21.0 and 10.5 g/kg of RYD daily, respectively, by gastric infusion. At the end of the 7-day treatment, loaded swimming time, organ wet weight and coefficient, serum glucose, urea nitrogen, and hepatic glycogen levels were determined. The outcomes were compared among groups. Results： As compared with the negative control group, the loaded swimming time was significantly increased in the positive control group, specifically the medium- and high-dose RYD groups （P〈0.01）. In addition, the wet weights and coefficients of the spleen and thymus, and the serum glucose and hepatic glycogen contents were increased, whereas serum urea nitrogen level was significantly decreased in the positive control group and the high dose RYD group （P〈0.05 or P=〈0.01）. Conclusion： RYD showed an anti-fatigue effect in mice.

Efficacy of Renshen(Radix Ginseng) plus Fuzi(Radix Aconiti Lateralis Preparata) on myocardial infarction by enhancing autophagy in rats

OBJECTIVE:To elucidate the protective effects of Renshen(Radix Ginseng)and Fuzi(Radix Aconiti Lateralis Preparata)on myocardial infarction(MI)through regulating myocardial autophagy.METHODS:Thirty-one male Sprague-Dawley rats were randomized into five groups(n=6 or 7 for each).After treatment for 3 weeks,electrocardiogram(ECG)and cardiac function were recorded.Hematoxylin and eosin(HE)staining was used to detect pathological changes in the heart.Enzyme-linked immunosorbent assay(ELISA)was used to detect serum B-type brain natriuretic peptide(BNP),cardiac troponin T(c Tn T),tumor necrosis factor-α(TNF-α),and serum inflammatory cytokines.Metabolomic analysis was used to identify differential biomarkers of MI in rats.Immunohistochemistry and western blotting were used to detect BNP,cTnT,TNF-α,LC3B,Beclin-1,p62,and adenosine monophosphate activated protein kinase(AMPK)expression in cardiac tissue.RESULTS:Fuzi(Radix Aconiti Lateralis Preparata)alone or Renshen(Radix Ginseng)plus Fuzi(Radix Aconiti Lateralis Preparata)markedly ameliorated cardiac dysfunction and abnormal ECGs,demonstrated by decreases in the heart weight/body weight ratio,BNP,and c Tn T.Pro-inflammation cytokine interleukin(IL)-1αsignificantly decreased and anti-inflammatory cytokine IL-10 significantly increased in Renshen(Radix Ginseng)single or Renshen(Radix Ginseng)plus Fuzi(Radix Aconiti Lateralis Preparata)groups compared with the control group.HE results suggested that co-treatment produced a greater reduction in cardiomyocyte cross-sectional area than Renshen(Radix Ginseng)or Fuzi(Radix Aconiti Lateralis Preparata)alone.Renshen(Radix Ginseng)plus Fuzi(Radix Aconiti Lateralis Preparata)reversed these changes to different degrees in MI rats.Furthermore,Renshen(Radix Ginseng)plus Fuzi(Radix Aconiti Lateralis Preparata)down-regulated LC3 B,Beclin-1,and AMPK expression in cardiac tissue and upregulated p62 expression.CONCLUSIONS:Renshen(Radix Ginseng)plus Fuzi(Radix Aconiti Lateralis Preparata)may have a greater effect on heart injury induced by MI in rats than Fuzi(Radix Aconiti Lateralis Preparata)treatment alone,and the underlying mechanism may be associated with the regulation of myocardial autophagy and anti-inflammation effects.These results provide fresh insight into the mechanism of co-treatment with Renshen(Radix Ginseng)and Fuzi(Radix Aconiti Lateralis Preparata)for MI.

Efficacy of Renshen Sanqi Chuanxiong formula for preventing vascular aging

OBJECTIVE:To evaluate the efficacy of Renshen Sanqi Chuanxiong formula(RSCF)for preventing vascular aging,and to investigate the possible molecular mechanism underlying the actions of RSCF.METHODS:Potentially active components and their relatively direct targets were identified by combining drug-likeness(DL)screening using a target identification process.Vascular aging-associated targets for RSCF were obtained by selecting common genes not only from potential targets but also from human vascular aging-associated genes.Cytoscape 3.2.1 software was employed to visualize the complex compound-target and target-function networks.Biological process and molecular function were assessed,and the Kyoto Encyclopedia of Genes and Genomes and pathway enrichment analyses were performed using Clue GO.Pathways directly associated with vascular aging were integrated into a"vascular aging-related"pathway.RESULTS:Altogether,122 potentially active components of RSCF were identified through DL screening,and their corresponding 692 direct targets were retrieved via target prediction and identification.We identified 49 vascular aging-associated targets for RSCF by overlapping the 692 potential targets with 146 human vascular aging-associated genes.The results from the compound-target network indicated that most components acted on common targets and displayed synergistic action,which showed that the magnifying effects of RSCF were based on these common targets.The target-function network revealed that each target was involved in multiple function modules,suggesting that RSCF was multi-functional during treatment of vascular aging.The results of the Clue GO analysis indicated that most of the targets were associated with the hypoxia-inducible factor 1(HIF-1)signaling pathway.The results from the pathway analysis also indicated that an integrative vascular aging-related pathway mainly included an angiogenesis regulation module,cell-survival module,and oxidative stress-resistance module.CONCLUSION:Our results suggested that many components act synergistically on common targets to delay vascular aging,and each target is involved in multiple functional modules.The Clue GO analysis indicated that most of the targets were connected to the HIF-1 signaling pathway,FOXO signaling pathway,and thyroid hormone signaling pathway.

Elucidation of Immune Regulation Mechanism of Renshen Guben Oral Liquid by Network Pharmacology and Molecular Docking

Objective:To investigate the mechanism of Renshen Guben oral liquid(RSGB)enhancing immune function.Materials and Methods:Network pharmacology and molecular docking were used to intuitively demonstrate the mechanism of immune regulation of RSGB.Results:A total of 112 active compounds of RSGB were found,and 501 targets were predicted.Furthermore,2974 immune targets were obtained from UniProt and NCBI Gene databases,and 111 common targets of RSGB and immunity were obtained.Among them,interleukin(IL)6,tumor necrosis factor,AKT1,VEGFA,STAT3,MAPK1,SRC,EGFR,IL1B,and PTGS2 might be the key targets for RSGB to improve immunity.ClueGO and Kyoto Encyclopedia of Genes and Genomes analysis showed that the immunoregulatory mechanism of RSGB may find a relation with the B cell receptor signaling pathway and T cell receptor signaling pathway.Furthermore,this study preliminarily explored the mechanism of RSGB improving menopausal syndrome,polycystic ovary syndrome,and cancer-related fatigue by enhancing immunity.Conclusions:RSGB can improve the body's immunity through multicomponent,multitarget,and multipathway.In addition,RSGB can also improve the immune capacity of the body to assist in the treatment of diseases,which has great potential as an immunomodulator.

Effects of extracts from Renshen(Radix Ginseng), Sanqi(Radix Notoginseng), and Chuanxiong(Rhizoma Chuanxiong) on F-actin in senescent microvascular endothelial cells

OBJECTIVE: To investigate the effects of extracts from Renshen(Radix Ginseng), Sanqi(Radix Notoginseng), and Chuanxiong(Rhizoma Chuanxiong) on the endothelial actin cytoskeleton in senescent human cardiac microvascular endothelial cells(HCMECs), and to propose the possible mechanism underlying the actions.METHODS: Lentiviral mediated RNA interference was applied to a replicative senescent HCMEC model by knocking down heat shock protein 27(HSP27)gene. Cells were treated with extracts from Renshen(Radix Ginseng), Sanqi(Radix Notoginseng), and Chuanxiong(Rhizoma Chuanxiong) at final concentrations of 50, 100, and 200 mg/L, respectively and with 10 μM resveratrol for 48 h. Untreated cells were used as controls. Senescence was detected by senescence β-galactosidase staining and cell proliferation was analyzed by cell counting kit-8 assays.Secreted nitric oxide levels were detected by nitrate reductase. Morphological changes of F-actin and G-actin were observed by laser scanning confocal microscopy. Protein and gene expression of Factin and HSP27 was detected by western blotting.RESULTS: Compared with the control group, the proportion of senescent HSP27 shRNA cells treated with the extracts was decreased and their proliferation was increased. In the extract intervention group, F-actin around the cell periphery became irregular and jagged fractures formed gradually and then dissipated. Moreover, some dynamic actin stress fiber filaments appeared. The G-actin stretched to the cell periphery and punctate staining was scattered in the cytoplasm. In addition, the mean optical density value of F/G-actin was decreased significantly and the protein expression of F-actin was downregulated.CONCLUSION: The extracts delayed microvascular endothelial cell senescence by downregulating the expression of F-actin through HSP27.

白虎加人参汤对2型糖尿病大鼠抗氧化应激作用及机制研究

目的:研究白虎加人参汤(BHJRS)对2型糖尿病(T2DM)模型大鼠抗氧化应激的作用,并初步探讨其作用机制。方法:随机取8只SD大鼠作为对照组(NC组),其余SD大鼠采用高脂高糖联合低剂量腹腔注射STZ(45 mg/kg)制备T2DM大鼠模型。将成模大鼠随机分为模型(DM)组、阳性药[盐酸二甲双胍(Met),200 mg/kg]组、BHJRS高剂量组(BHJRS-H,BHJRS溶液37.8 g/kg)、BHJRS低剂量组(BHJRS-L,BHJRS溶液18.9 g/kg),连续给药8周。测定各组大鼠第0、2、4、6、8周空腹血糖(FBG),检测糖化血红蛋白(HbAlc)、胰岛素(INS)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)水平并计算ISI值,观察胰腺组织病理学形态变化;检测胰腺组织中B淋巴细胞瘤-2基因(Bcl-2)、胱天蛋白酶3(Caspase-3)、Bcl-2相关X蛋白(Bax)的mRNA和蛋白水平;检测胰腺组织中蛋白激酶B(AKT)/糖原合成激酶-3β(GSK-3β)/核因子NF-E2相关因子(Nrf2)信号通路关键蛋白的表达。结果:与DM组比较,Met组、BHJRS-H组和BHJRS-L组显著降低T2DM大鼠FBG、血清中HbAlc、MDA水平(P<0.05),显著升高血清中INS、CAT、SOD、GSH-Px水平和ISI值(P<0.05);显著上调胰腺组织中p-AKT/AKT、p-GSK-3β/GSK-3β、n-Nrf2、血红素加氧酶-1(HO-1)水平(P<0.05),显著下调Bax/Bcl-2、Caspase-3、n-Fyn水平(P<0.05),胰腺组织病理变化均不同程度改善。结论:BHJRS对胰腺组织有一定的抗氧化应激作用,其原因可能在于调节AKT/GSK-3β/Nrf2信号通路中相关蛋白的表达有关。

人参、知母调控NR2B-CaMKⅡ-AMPAR1通路防治糖尿病认知功能障碍作用研究

目的 观察人参、知母防治糖尿病认知功能障碍(diabetic cognitive impairment,DCI)的作用,并探讨其机制。方法 采用高脂高糖饲料联合腹腔注射链脲佐菌素(STZ)(70 mg/kg)建立DCI小鼠模型,除空白组,造模成功后随机分为模型组、二甲双胍组(30 mg/kg)、多奈哌齐组(30 mg/kg)、人参组(3.6 g/kg)、知母组(10.8 g/kg)、人参知母组(3.6、7.2 g/kg),每组8只。连续灌胃给药30 d,记录各组小鼠体质量和血糖。给药结束用Moriss水迷宫法进行行为学测试,酶联免疫吸附测定(ELISA)法检测小鼠血清中糖化血红蛋白(GHbA1c);苏木素-伊红(HE)染色法观察海马组织病理变化,Western blot法检测NR2B、钙调蛋白激酶Ⅱ(CaMKⅡ)、α-氨基-3-羟基-5-甲基-4-异唑-丙酸谷氨酸受体1(AMPAR1)蛋白的表达。结果 与模型组相比,人参组(3.6 g/kg)、知母组(10.8 g/kg)、人参知母组(3.6、7.2 g/kg)小鼠体质量增长,血糖下降(P<0.05,P<0.01),逃避潜伏期、探索距离显著缩短(P<0.05,P<0.01),站台穿越次数、目标象限游泳时间显著增加(P<0.05,P<0.01),GHbA1c降低(P<0.05,P<0.01),小鼠海马CA1区神经细胞更加整齐紧密,脑组织中NR2B、AMPAR1蛋白表达显著下调(P<0.01),CaMKⅡ蛋白表达显著上调(P<0.01)。结论 人参知母可改善DCI,其机制可能与调控NR2B-CaMKⅡ-AMPAR1通路有关。

基于氧化应激途径探讨人参益脉方干预血管老化作用机制

目的观察人参益脉方对ApoE^(-/-)小鼠氧化应激及血管老化的影响,探讨其干预血管老化的作用机制。方法将40只ApoE^(-/-)小鼠随机分为模型组、西药组(瑞舒伐他汀,2.6 mg/kg)及中药低、高剂量组(人参益脉方,4.29、8.58 g/kg),每组10只,另取10只C57BL/6J小鼠作为正常组。采用西式饮食饲料喂养ApoE^(-/-)小鼠建立血管老化模型,同时各给药组分别予相应药物灌胃,正常组和模型组灌胃等体积纯净水,连续12周。HE染色及Masson染色观察小鼠主动脉组织形态变化,ELISA检测血清氧化型低密度脂蛋白(ox-LDL)含量,比色法测定血清活性氧(ROS)、谷胱甘肽(GSH)、谷胱甘肽还原酶(GPX)、烟酰胺腺嘌呤二核苷酸(NAD^(+))含量,Western blot检测主动脉组织沉默信息调节因子1(SIRT1)、p21、p53、NADPH氧化酶4(NOX4)蛋白表达。结果与正常组比较,模型组小鼠主动脉可见脂质沉积,内膜及中膜明显增厚,弹性纤维减少,胶原纤维增多;血清ox-LDL、ROS含量显著升高(P<0.01),GSH、GPX、NAD^(+)含量显著降低(P<0.01);主动脉组织SIRT1蛋白表达显著降低(P<0.05),p21、p53蛋白表达显著升高(P<0.01,P<0.05)。与模型组比较,各给药组主动脉内膜可见少量脂质沉积,各层膜结构较清晰,胶原纤维减少;各给药组血清ox-LDL、ROS含量显著降低(P<0.01),GSH含量显著升高(P<0.05,P<0.01),中药低剂量组NAD^(+)含量显著升高(P<0.05);中药高剂量组主动脉组织p21、NOX4蛋白表达显著升高(P<0.05,P<0.01)。与西药组比较,中药高剂量组ROS含量显著降低(P<0.01),p53蛋白表达显著降低(P<0.05)。与中药低剂量组比较,中药高剂量组p21蛋白表达显著降低(P<0.01),NOX4蛋白表达显著升高(P<0.01)。结论人参益脉方可能通过调节氧化应激水平和相关蛋白表达减轻血管内皮损伤,从而发挥改善血管老化作用。

中西医结合治疗重症黏液型铜绿假单胞菌性肺炎1例并文献回顾

总结1例重症黏液型铜绿假单胞菌性肺炎患者的中西医诊疗过程,分析探讨铜绿假单胞菌性肺炎的中医诊疗思路。患者因“反复咳嗽、咳痰、气促10余年,再发加重10 d”来诊,诊断为慢性阻塞性肺疾病急性加重期(AECOPD)Ⅱ型呼吸衰竭、支气管哮喘、支气管扩张、2型糖尿病,遂入院治疗。入院后因病情危重,予气管插管接呼吸机辅助通气,又因肺泡灌洗液高通量基因测序示铜绿假单胞菌序列数73659,加用抗感染治疗。以气管插管接呼吸机辅助通气联合抗感染治疗至氧合指数正常后,拔除气管插管,予高流量湿化氧疗续贯。之后患者再发呼吸急促、高热、烦躁,伴口干、汗少,考虑抗感染治疗已持续近2周,可能出现抗生素诱导的发热等不良反应,遂暂停使用抗生素,先后应用大青龙汤、大承气汤(灌肠)、白虎加人参汤进行中医治疗。经中医治疗后,患者发热症状逐渐消退,痰培养提示黏液型铜绿假单胞菌(全敏),最终病情平稳出院。以往中医药治疗铜绿假单胞菌感染多采用清肺化痰、泻热通腑法,对扶正关注较少。根据上述病例治疗情况,笔者认为在以中药治疗铜绿假单胞菌性肺炎过程中,应加强对正气的关注,根据正气强弱及时调整治疗方案。

人参归脾丸防治环磷酰胺化疗胃肠道反应的实验研究

目的探究人参归脾丸对环磷酰胺致胃肠道反应小鼠的干预作用。方法选取60只SPF级BALB/c小鼠随机分为阴性对照组,模型组,盐酸昂丹司琼片组[2.4 mg/(kg·d)]及人参归脾丸高剂量组[5.4 g/(kg·d)]、中剂量组[2.7 g/(kg·d)]、低剂量组[1.35 g/(kg·d)],每组10只。除阴性对照组外其余5组动物分别以80 mg·kg^(-1)剂量的环磷酰胺进行隔日腹腔注射,共注射3次,造模同时连续灌胃给予相应药物6 d,每日观察动物状态。隔日称量各组小鼠造模后的体重,给药结束检测胃液pH值,计数小鼠肠道派氏结(PP结),免疫组化法检测小鼠胃肠道组织中TLR4蛋白的表达。结果人参归脾丸能够改善环磷酰胺造模小鼠精神状态,促进模型小鼠体重增长,增加PP结数量,提高胃液pH值,下调胃、十二指肠、空肠及回肠组织TLR4蛋白的相对表达量。结论人参归脾丸对环磷酰胺化疗所致胃肠道反应有一定的预防治疗作用,其机制可能与调节胃肠道TLR4蛋白表达有关。

人参-五味子药对对PCPA失眠大鼠神经递质及cAMP/Epac/Raf1信号通路的作用机制研究

目的通过观察人参-五味子药对对失眠大鼠下丘脑中神经递质及其cAMP/Epac/Raf1信号通路水平的影响,探讨人参-五味子药对对PCPA失眠大鼠的作用机制。方法将60只SD大鼠随机分为空白组、模型组、地西泮组、人参-五味子低剂量组、中剂量组和高剂量组,每组10只。除空白组外,其余5组连续3 d对大鼠进行腹腔注射对氯苯丙氨酸(PCPA)复制失眠模型。模型复制成功后,人参-五味子药对低、中、高剂量组给药浓度分别为0.3、0.9、2.7 g/mL,地西泮组给药浓度为0.002 g/mL,模型组、空白组每天生理盐水灌胃,各组每日灌胃2 mL,连续给药14 d。观察记录各组大鼠的行为学变化;采用HE(苏木素-伊红)染色法检测大鼠下丘脑组织病理形态的改变;ELISA(酶联免疫吸附法)测定大鼠下丘脑中甘丙肽(GAL)、去甲肾上腺素(NE)、5-羟色胺(5-HT)、腺苷(Ado)水平;RT-PCR(实时荧光定量聚合酶链式反应)检测大鼠下丘脑中Eapc、Raf1mRNA的表达;IHC(免疫组织化学染色法)检测大鼠下丘脑中cAMP蛋白的含量。结果和空白组相比:模型组大鼠下丘脑病理切片损伤明显;GAL、5-HT、Ado含量显著下降(P<0.05),NE含量显著上升(P<0.05),下丘脑Eapc、Raf1 mRNA表达显著下降(P<0.05),下丘脑cAMP蛋白表达显著下降(P<0.05),差异有统计学意义。与模型组相比:地西泮组、人参-五味子低、中、高剂量组下丘脑病理切片损伤明显改善;地西泮组、人参-五味子中、高剂量组GAL、5-HT、Ado含量显著上升(P<0.05),NE含量显著下降(P<0.05),下丘脑Eapc、Raf1 mRNA表达显著上升(P<0.05),下丘脑cAMP蛋白表达显著上升(P<0.05),差异有统计学意义。结论人参-五味子药对可能通过上调cAMP/Epac/Raf1信号通路,缓解PCPA大鼠失眠症状。

许德公人参黄精杏麦饮对小鼠免疫增强活性研究

目的探究许德公人参黄精杏麦饮对小鼠免疫功能的作用,阐明其免疫增强的作用机制。检测各浓度许德公人参黄精杏麦饮对脾脏淋巴细胞的安全浓度、脾淋巴细胞因子分泌水平变化、淋巴细胞亚群的变化。方法将40只BALB/c小鼠随机分为4组(n=10),包括空白对照组,许德公人参黄精杏麦饮高、中、低剂量(1.2、0.6、0.3 mg/g)组,给药28 d后检测小鼠胸腺及脾脏指数,然后通过脾淋巴细胞转化实验、免疫器官组织学观察、小鼠血清免疫细胞因子水平变化、淋巴细胞亚群分布变化,评价许德公人参黄精杏麦饮的免疫调节作用。结果干预后的脾脏淋巴细胞的安全浓度最优为500μg/mL;淋巴细胞CD_(4)^(+)/CD_(8)^(+)的比例显著升高。此外,脾脏淋巴细胞分泌白细胞介素2(interleukin-2,IL-2)、白细胞介素6(interleukin-6,IL-6)、γ干扰素(interferon-γ,IFN-γ)及肿瘤坏死因子α(tumor necrosis factor-α,TNF-α)水平均得到不同程度的上调。与空白对照组比较,高剂量许德公人参黄精杏麦饮能明显增加小鼠免疫器官脾脏指数(P<0.05);低、中、高剂量许德公人参黄精杏麦饮均能促进淋巴细胞增殖反应(P<0.05);小鼠脾脏白髓生发中心和边缘区淋巴细胞增生明显;能持续诱导脾脏淋巴细胞中CD_(4)^(+)和CD_(8)^(+)高表达。结论许德公人参黄精杏麦饮可以显著增强机体免疫力,其预防和治疗免疫功能失调相关疾病有较好的应用前景。

人参枳椇子口服液的解酒保肝作用研究

目的:研究人参枳椇子口服液(GROL)的解酒保肝作用。方法:将50只小鼠随机分空白组、模型组、GROL高剂量组、GROL低剂量组和阳性药联苯双酯对照组,每组10只。灌胃给药4周后用50%乙醇一次灌胃建立小鼠急性醉酒模型,考察GROL对小鼠基本生理活动、小鼠血清及肝组织中相关指标,观察肝组织病理切片,评价其解酒保肝作用。采用乙醇诱导AML12肝细胞损伤模型,检测GROL干预后对乙醇刺激的AML12细胞上清液中谷丙转氨酶(GPT)、谷草转氨酶(GOT)、活性氧(ROS)水平的影响。结果:GROL组小鼠醉酒时间显著延长,睡眠、醒酒时间显著缩短;血清中乙醇浓度、GPT、GOT水平显著降低;肝细胞损伤情况有所改善;GROL组肝组织中超氧化物歧化酶(SOD)活性和谷胱甘肽过氧化物酶(GSH)水平明显提高,丙二醛(MDA)含量明显降低。对体外培养的AML12肝细胞,GROL可以逆转乙醇引起的肝细胞ALT和AST活性的升高以及过度生成的ROS量。结论:GROL具有良好的防醉、解酒和保肝作用,其发挥作用的途径可能与促进体内乙醇代谢、增强内源性抗氧化酶的活性有关。

四逆加人参汤联合美托洛尔、胺碘酮治疗冠心病合并室性心律失常的临床研究

目的:探究四逆加人参汤联合美托洛尔、胺碘酮治疗冠心病合并室性心律失常的效果。方法:选择2022年4月—2024年4月在湖南中医药大学第一附属医院治疗的冠心病合并室性心律失常患者94例,随机分为两组。对照组(n=47)予以美托洛尔、胺碘酮治疗,观察组(n=47)在对照组基础上加四逆加人参汤治疗。对比两组临床疗效、左心室重构情况、细胞因子、心率变异性(HRV)、QT间期离散度(QTd)、炎症因子。结果:观察组总有效率高于对照组,差异有统计学意义(P<0.05)。治疗后,观察组左室舒张末期容积(LVEDV)、左室收缩末期容积(LVESV)均小于对照组,血管性血友病因子(vWF)、纤溶酶原激活物抑制剂-1(PAI-1)、内皮素-1(ET-1)、C反应蛋白(CRP)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)均低于对照组,QTd短于对照组,左室射血分数(LVEF)高于对照组,窦性心搏R-R间期标准差(SDNN)、每5分钟窦性心搏R-R间期平均值标准差(SDANN)、相邻窦性心搏R-R间期差值均方根(RMSSD)均长于对照组,差异均有统计学意义(P<0.05)。结论:四逆加人参汤联合美托洛尔、胺碘酮可改善冠心病合并室性心律失常患者左心室重构、HRV、QTd,作用机制可能与降低CRP、TNF-α、IL-6、vWF、PAI-1、ET-1有关。

人参五味子汤治疗肺脾气虚证支气管哮喘患儿的疗效及对其气道炎症、免疫功能的影响

目的 探讨人参五味子汤加减治疗肺脾气虚证支气管哮喘患儿的疗效及对其气道炎症、免疫功能的影响。方法 选取2020年1月—2021年3月期间安徽省六安市中医院收治的肺脾气虚证哮证的患儿108例,按随机数字表法分为对照组和观察组,每组各54例。对照组患儿给予布地奈德混悬液雾化治疗,观察组在对照组基础上给予人参五味子汤加减,两组患儿均治疗1周。观察比较两组患儿临床疗效,治疗前后血气状态[血氧分压(Partial Pressure of Oxygen in Arterial Blood,PaO_(2))、二氧化碳分压(Partial Pressure of Carbon Dioxide in Arterial Blood,PaCO_(2))、血氧饱和度(Oxygen Saturation of Arterial Blood,SaO_(2))]、气道炎症因子[血清中转化生长因子β1(Transforming Growth Factor-β1,TGF-β1)、单核细胞趋化蛋白-1(Monocyte Chemoattractant Protein-1,MCP-1)、嗜酸细胞阳离子蛋白(Eosinophil Cationic Protein,ECP)]、免疫功能[IgA、IgG、IgM]、中医证候、肺功能[肺功能第一秒用力呼气量(Forced Expiratory Volume in 1 second,FEV1)、用力肺活量(Forced Vital Capacity,FVC)及第一秒用力呼气量与用力肺活量比率(Forced Expiratory Volume in 1 second/Forced Vital Capacity,FEVl/FVC)]。结果 治疗后观察组总有效率94.44%(51/54)明显高于对照组81.48%(44/54),差异有统计学意义(P<0.05)。治疗后两组患儿气道炎症因子TGF-β1、MCP-1、ECP水平均明显低于治疗前,差异有统计学意义(P<0.05);且观察组气道炎症因子TGF-β1、MCP-1、ECP水平均明显低于对照组,差异有统计学意义(P<0.05)。治疗后两组患儿免疫功能IgG、IgA、IgM水平均较治疗前升高,差异有统计学意义(P<0.05);且观察组免疫功能IgG、IgA、IgM水平均明显高于对照组,差异有统计学意义(P<0.05)。治疗后两组患儿主症、次症、体征及总积分均较治疗前明显降低,差异有统计学意义(P<0.05);且观察组主症、次症、体征及总积分均明显低于对照组,差异有统计学意义(P<0.05)。治疗后两组患儿肺功能FEV1、FVC及FEV1/FVC水平均较治疗前升高,差异有统计学意义(P<0.05);且观察组肺功能FEV1、FVC及FEV1/FVC水平均明显高于对照组,差异有统计学意义(P<0.05)。治疗后两组患儿血气指标PaO_(2)、SaO_(2)水平均较治疗前升高,PaCO_(2)水平均较治疗前降低,差异有统计学意义(P<0.05);且观察组血气指标PaO_(2)、SaO_(2)水平均明显高于对照组,PaCO_(2)水平明显低于对照组,差异有统计学意义(P<0.05)。结论 人参五味子汤加减能显著提高肺脾气虚证支气管哮喘患儿的临床治疗效果,改善临床证候,减轻炎性反应,提升其免疫功能并改善患儿肺功能。

白虎加人参汤对高尿酸血症肾病小鼠保护作用及机制研究

目的白虎加人参汤对高尿酸血症肾病(HN)小鼠的保护作用及机制研究。方法将C57BL/6小鼠48只随机分为正常组、模型组、阳性药物组和白虎加人参汤组。正常组小鼠灌胃0.5%羧甲基纤维素钠(CMC-Na),其余各组小鼠灌胃次黄嘌呤500 mg/kg和腹腔注射氧嗪酸钾200 mg/kg诱导高尿酸血症肾病小鼠模型,阳性药物组每日灌胃非布司他5 mg/kg,白虎加人参汤组小鼠每日灌胃白虎加人参汤54 g/kg,连续给药21d。采集小鼠血清及肾脏组织,测定小鼠血清中SUA、Scr和BUN含量;HE染色,镜下观察小鼠肾脏的病理变化;测定小鼠肾脏组织中GSH-Px、SOD、CAT及MDA水平;ELISA法测定小鼠血清中TNF-α、IL-6和IL-1β表达;Western blot法测定小鼠肾脏组织中AKT/GSK-3β/Nrf2信号通路和NLRP3炎性小体相关蛋白表达。结果生化结果显示,白虎加人参汤能够降低高尿酸血症肾病小鼠血清中SUA、Scr和BUN水平。HE染色结果显示,白虎加人参汤可以减轻高尿酸血症肾病小鼠肾脏损伤。白虎加人参汤能够抑制高尿酸血症肾病小鼠肾脏组织中MDA表达,促进GSHPx、SOD和CAT的表达,抑制TNF-α、IL-6和IL-1β表达;Western blot结果显示,白虎加人参汤能够促进高尿酸血症肾病小鼠肾脏组织中p-AKT、p-GSK-3β、Nrf2和HO-1蛋白表达,抑制NLRP3、Caspase1、IL-1β蛋白表达。结论白虎加人参汤通过激活AKT/GSK-3β/Nrf2信号通路,抑制NLRP3炎性小体,改善高尿酸血症肾病小鼠氧化应激和炎症,减轻高尿酸血症肾病。

自拟参芪补味汤治疗慢性阻塞性肺疾病稳定期肺脾气虚证的临床观察

【目的】观察自拟参芪补味汤(由黄芪人参汤化裁而来)治疗慢性阻塞性肺疾病(简称慢阻肺)稳定期肺脾气虚证患者的临床疗效。【方法】将110例慢阻肺稳定期肺脾气虚证患者随机分为对照组和观察组,每组各55例。对照组给予噻托溴铵吸入粉雾剂吸入治疗,观察组在对照组的基础上给予参芪补味汤治疗,疗程为3个月。观察2组患者治疗前后肺功能指标[第1秒用力呼气容积(FEV1)、用力肺活量(FVC)、一秒率(FEV1/FVC)]、改良英国医学研究学会呼吸困难指数(mMRC)评分、6 min步行试验(6MWT)、慢阻肺患者自我评估测试(CAT)评分和中医证候积分的变化情况,并评价2组患者的临床疗效和用药安全性。【结果】(1)脱落情况方面,研究过程中,观察组有1例患者剔除,2例患者脱落,对照组有3例患者脱落,最终对照组和观察组各有52例患者纳入疗效统计。(2)疗效方面,治疗3个月后,观察组的总有效率为80.77%(42/52),对照组为67.31%(35/52),组间比较(χ^(2)检验),观察组的疗效略优于对照组,但差异无统计学意义(P>0.05)。(3)肺功能指标方面,治疗后,对照组的FEV1、FEV1/FVC和观察组的FEV1、FVC、FEV1/FVC均较治疗前明显改善(P<0.05),且观察组对各项肺功能指标的改善幅度均明显优于对照组(P<0.05)。(4)6MWT及mMRC、CAT评分方面,治疗后,2组患者的6MWT及mMRC、CAT评分均较治疗前明显改善(P<0.05),且观察组的改善幅度均明显优于对照组(P<0.05)。(5)中医证候积分方面,治疗后,2组患者的中医证候积分均较治疗前明显降低(P<0.05),且观察组的降低幅度明显优于对照组(P<0.05)。(6)安全性方面,治疗过程中,2组患者均未发生明显不良反应,且患者的各项安全性指标均无异常变化。【结论】在常规西药治疗基础上联合参芪补味汤治疗慢阻肺稳定期肺脾气虚证患者疗效确切,可有效改善患者通气功能,缓解患者临床症状,提高患者生活质量,延缓患者肺功能减退。