Fanlian Huazhuo formula:A promising therapeutic approach for metabolic associated steatotic liver disease

This article reviews the study,“Fanlian huazhuo formula alleviates high-fat-dietinduced nonalcoholic fatty liver disease by modulating autophagy and lipid synthesis signaling pathway”published in the World Journal of Gastroenterology.The study explores the therapeutic potential of Fanlian Huazhuo formula(FLHZF)in treating metabolic-associated steatotic liver disease(MASLD),demonstrating that FLHZF reduces lipid accumulation,oxidative stress,and liver injury in MASLD models by modulating key signaling pathways involved in lipid metabolism and autophagy.This editorial emphasizes the potential of FLHZF as a treatment for MASLD and calls for further research to verify its clinical efficacy.

Fanlian Huazhuo Formula alleviates high-fat diet-induced nonalcoholic fatty liver disease by modulating autophagy and lipid synthesis signaling pathway

BACKGROUND Fanlian Huazhuo Formula(FLHZF)has the functions of invigorating spleen and resolving phlegm,clearing heat and purging turbidity.It has been identified to have therapeutic effects on type 2 diabetes mellitus(T2DM)in clinical application.Non-alcoholic fatty liver disease(NAFLD)is frequently diagnosed in patients with T2DM.However,the therapeutic potential of FLHZF on NAFLD and the underlying mechanisms need further investigation.AIM To elucidate the effects of FLHZF on NAFLD and explore the underlying hepatoprotective mechanisms in vivo and in vitro.METHODS HepG2 cells were treated with free fatty acid for 24 hours to induce lipid accumulation cell model.Subsequently,experiments were conducted with the different concentrations of freeze-dried powder of FLHZF for 24 hours.C57BL/6 mice were fed a high-fat diet for 8-week to establish a mouse model of NAFLD,and then treated with the different concentrations of FLHZF for 10 weeks.RESULTS FLHZF had therapeutic potential against lipid accumulation and abnormal changes in biochemical indicators in vivo and in vitro.Further experiments verified that FLHZF alleviated abnormal lipid metabolism might by reducing oxidative stress,regulating the AMPKα/SREBP-1C signaling pathway,activating autophagy,and inhibiting hepatocyte apoptosis.CONCLUSION FLHZF alleviates abnormal lipid metabolism in NAFLD models by regulating reactive oxygen species,autophagy,apoptosis,and lipid synthesis signaling pathways,indicating its potential for clinical application in NAFLD.

Antidepressant effects of Peiyuan Jieyu formula in a mouse model of chronic stress in conjunction with lipopolysaccharide-induced depression

Objective:To explore the mechanism of the Peiyuan Jieyu formula in treating depression by assessing its impact on a lipopolysaccharide-induced(LPS-induced)depression mouse model.Methods:We created a mouse model of depression by exposing mice that had previously received chronic stress to intraperitoneal LPS injections.The mice were divided into the following groups:control,model,fluoxetine,Tiansi Yin,Sini powder,and low-,medium-,and high-dose Peiyuan Jieyu formula groups.Forced swim and tail suspension tests were used to assess the efficacy of the depression(despair)model,and weight gain rates were also measured.Furthermore,serum levels of various depression and inflammation-associated molecules,including tumor necrosis factor-a(TNF-a),interferon-γ(IFN-γ),tryptophan,5-hydroxytryptamine,kynurenine(KYN),and kynurenic acid(KA)were assessed.Furthermore,the expression levels of ionic calcium-binding adaptor molecule-1(IBA-1)and indoleamine 2,3-dioxygenase(IDO)mRNA in hippocampal microglia were measured.Results:The model group displayed greater despair-associated immobility,which was shortened in response to various doses of Peiyuan Jieyu formula.Furthermore,formula administration significantly reduced serum TNF-a levels and hippocampal IDO mRNA expression.The high formula dose also reduced IFN-γand IBA-1 levels,the latter was also decreased in response to the medium formula dose.However,the low formula dose reduced serum KYN level and KYN/tryptophan(TRP)and KYN/KA ratios.Conclusion:The Peiyuan Jieyu formula holds immense potential in treating depression in a mouse model,potentially inhibiting inflammation and improving TRP-KYN metabolic disorders.

Fanlian Huazhuo Formula:A promising herbal preparation for metabolic liver disease

The prevalence of metabolic dysfunction-associated steatotic liver disease(MASLD)has increased significantly in recent decades and is projected to increase further due to the rising obesity rates.MASLD patients are at higher risk of developing advanced liver diseases“cirrhosis and hepatocellular carcinoma”as well as liver-or cardiovascular-related mortality.Existing lipid-lowering therapies failed to reduce the risk of mortality in these patients.Therefore,there is an urgent need for pharmacotherapies that can control and even reverse this disease.Fanlian Huazhuo Formula(FLHZF)is a combination herbal preparation,and its various individual constituents regulate hepatic lipid metabolism,adipose tissue inflammation,and gut microbiota.Despite,these useful effects,limited information is available on its benefits in diet-induced hepatosteatosis.In this article,we discuss the research findings recently published about the therapeutic effects of FLHZF in suppressing MASLD development and underlying mechanisms.Utilizing a series of in vitro and in vivo experiments,the authors demonstrated for the first time that FLHZF suppresses MASLD in male mice possibly by inhibiting hepatic de novo lipogenesis pathways and reducing hepatocyte death.This study paves the way for future investigations aimed at investigating FLHZF’s role in inhibiting lipogenesis particularly using radioactively-labeled glucose and acetate,and governing hepatocyte mitochondrial function,gut microbiome profile,and its effects in other models of MASLD,and female mice.

Mechanism of treating recurrent abortion with “Peiyuan Bushen Antai formula” based on network pharmacology and molecular docking

Objective:To study the effective compound action target signal pathway of Peiyuan bushenan taifang(PYBSATF)has achieved good clinical efficacy in the treatment of recurrent spontaneous abortion(RSA),but its mechanism has not been clarified because of its complex components.In this study,network pharmacology is applied to study the effective compounds,targets and signal pathways of PYBSATF in the treatment of RSA,so as to reveal its pharmacological mechanism of action in the treatment of recurrent spontaneous abortion.Methods:The Traditional Chinese Medicine Systems Pharmacology database(TCMSP)and CNKI are used to obtain the main compounds and drug action targets of PYBSATF.Genecards and the Online Mendelian Inheritance of Man databases(OMIM)are searched to collect the known genes related to RSA,so as to construct compound-target network and screen out the common target proteins and main active compounds.We also use string database to construct a visual protein-protein interaction network(PPI).Cluster Profiler and R software were used to analyze the common targets of drugs and diseases for GO function analysis and KEGG pathway enrichment analysis.Finally,the compound and the protein sequences were conducted according to the node parameters,so that the core protein and core compounds are used to perform molecular docking.Results:186 potential active components and 65 predicted action targets of PYBSATF were screened out.At the same time,1658 genes were also screened out to be closely related to RSA,among which 65genes overlaped with PYBSATF targets and were considered to be related to way of treatment.PPI network showed that VEGFA,IL6,EGFR,MAPK8 and ESR1were the core targets of PYBSATF for the treatment of RSA.GO and KEGG enrichment analysis obtained 93 biological processes of cells(P<0.01)and 87 signaling pathways(P<0.01).PYBSATF played a pharmacological role through a variety of pathways including anti-inflammatory,anti-apoptosis,promoting proliferation and angiogenesis.Molecular docking showed that most active components and key targets of PYBSATF had strong efficiency.Conclusion:Through the study of network pharmacology,it predicted that PYBSATF might treat RSA through multiple targets and multiple signal pathways.Significantly,the predictive targets may be potential targets for treatment of RSA.

化浊解毒生肌方对胃内镜黏膜下剥离术后患者的疗效观察

目的 观察化浊解毒生肌方治疗胃内镜黏膜下剥离术(ESD)后患者的临床疗效。方法 选取2020年10月~2022年10月河北省中医院脾胃病科胃ESD术后的住院患者60例,采用随机数字表法分为治疗组和对照组各30例,治疗组予雷贝拉唑肠溶胶囊加化浊解毒生肌方口服;对照组予雷贝拉唑肠溶胶囊口服。比较两组术后临床症状,出血发生率,内镜下再生黏膜成熟度,血管内皮生长因子(VEGF)、表皮生长因子(EGF)水平等。结果 术后7 d治疗组在改善腹痛、嗳气、烧心反酸及纳呆方面效果优于对照组(P <0.05),术后14 d治疗组在改善腹痛、腹胀、嗳气、纳呆方面优于对照组(P <0.05)。术后72 h后两组出血发生率比较,差异有统计学意义(P <0.05)。术后8周两组溃疡面积比较,差异无统计学意义(P> 0.05);术后8周两组胃小凹形态(A+B型)及规则微血管网所占比例比较,差异有统计学意义(P <0.05)。术后8周治疗组血清VEGF、EGF水平高于对照组,差异有统计学意义(P <0.05)。结论 化浊解毒生肌方能更好改善患者临床症状,减少术后迟发性出血,改善黏膜愈合质量。

化浊解毒活血通络方联合通督调神针刺法治疗急性脑梗死疗效及NLRP3信号通路研究

目的观察化浊解毒活血通络方联合通督调神针刺法治疗急性脑梗死(ACI)的疗效,以及对患者神经功能和NOD样受体热蛋白结构域相关蛋白3(NLRP3)炎性小体信号通路的影响。方法80例ACI患者采用随机数字表法分为两组,对照组采用化浊解毒活血通络方治疗,观察组采用化浊解毒活血通络方联合通督调神针刺治疗。观察两组疗效、神经功能、残疾程度、NLRP3炎性小体信号通路相关分子mRNA表达、炎症因子和氧化应激的差异。结果观察组治疗总有效率高于对照组(P<0.05)。两组治疗后中医证候积分、美国国立卫生院脑卒中量表(NIHSS)、改良RANKIN量表(mRS)评分,外周血单核细胞NLRP3 mRNA、凋亡相关点样蛋白(ASC)mRNA、半胱氨酸蛋白酶-1(Caspase-1)mRNA表达,血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、丙二醛(MDA)水平较治疗前降低(P<0.05),超氧化物歧化酶(SOD)水平较治疗前增高(P<0.05)。观察组治疗后中医证候积分、NIHSS、mRS评分,外周血单核细胞NLRP3 m RNA、ASC mRNA、Caspase-1 mRNA表达,血清TNF-α、IL-6、MDA水平低于对照组(P<0.05),SOD水平高于对照组(P<0.05)。结论化浊解毒活血通络方联合通督调神针刺法可更有效抑制NLRP3炎性小体信号通路,缓解炎症反应和氧化应激,改善神经功能,减轻残疾程度,提高临床疗效。

基于网络药理学研究培元化瘀解毒方治疗胃癌的作用机制

目的探讨培元化瘀解毒方治疗胃癌的网络药理学作用机制。方法利用中医药数据库和文献检索筛选培元化瘀解毒方的生物活性成分,预测其作用靶点,从疾病数据库检索胃癌相关靶点,构建药效分子-靶点网络及蛋白质-蛋白质相互作用(PPI)网络,然后进行KEGG分析、GO富集分析。结果检索获得培元化瘀解毒方中药的有效活性成分206种,药效分子靶点基因211个,有对应靶点信息的有效成分132个,对应关系1131个;检索得到胃癌靶点184个;通过PPI对药物靶点进行扩增得到3592个直接或间接靶点,与疾病靶点取交集得到144个靶点。PPI分析表明,排名靠前的靶点与胃癌密切相关,富集分析也显示这些靶点在癌症通路中被富集。结论本研究初步揭示了培元化瘀解毒方在胃癌治疗中的有效成分、潜在靶点及可能的作用机制,为中西医结合治疗胃癌提供参考。

调平归源法论治慢性萎缩性胃炎近远期临床疗效观察

目的观察以“调平归源”为论治思想的脾胃培源方治疗慢性萎缩性胃炎的近远期疗效观察。方法收集从2018年1月至2022年1月在安徽中医药大学第二附属医院就诊治疗的CAG患者,其中100例通过脾胃培源方治疗,另外100例使用常规西药治疗。观察两组患者治疗前及12周后中医症候积分,24周后中医症候积分、胃镜病理积分、病理疗效等指标情况。结果中医症状积分:12周及24周治疗后两组中医症状积分均降低,差异有统计学意义,且治疗组均优于对照组(P<0.05);胃镜病理:24周治疗后两组各项评分均较前改善,差异有统计学意义,且治疗组效果更好(P<0.05);临床疗效:治疗组总有效率高于对照组(P<0.05)。两组均未有明显不良反应。结论基于“调平归源”法则的脾胃培源方能够改善CAG患者中医症状,缓解萎缩、肠化等病理表现,值得临床推广应用。

慈苓化浊方对痛风大鼠滑膜组织环氧化酶-2、热休克蛋白70表达的影响

目的:分析慈苓化浊方对痛风大鼠滑膜组织中环氧化酶-2(COX-2)、热休克蛋白70(HSP70)表达的影响。方法:选取50只SPF级SD大鼠,10只大鼠作为对照组,另外40只建立痛风模型,将30只建模成功的大鼠分为模型组、药物对照组、慈苓化浊方组,每组10只。观察各组大鼠组织病理学、关节肿胀度、COX-2、HSP70表达、炎症因子、磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(AKT)/叉头框转录因子O亚族1(FoxO1)通路相关因子及其mRNA表达量。结果:与对照组相比,模型组、药物对照组、慈苓化浊方组关节肿胀度、COX-2、肿瘤坏死因子-α(TNF-α)、白介素-1β(IL-1β)、白介素-6(IL-6)、PI3K mRNA、AKT mRNA、FoxO1 mRNA表达量升高,HSP70 mRNA、Caspase-3 mRNA表达量降低(均P<0.05)。与模型组相比,药物对照组、慈苓化浊方组关节肿胀度、COX-2、TNF-α、IL-1β、IL-6、PI3K mRNA、AKT mRNA、FoxO1 mRNA表达量降低,HSP70 mRNA、Caspase-3 mRNA表达量升高(均P<0.05)。与药物对照组相比,慈苓化浊方组关节肿胀度、COX-2、TNF-α、IL-1β、IL-6、PI3K mRNA、AKT mRNA、FoxO1 mRNA表达量降低,HSP70 mRNA、Caspase-3 mRNA表达量升高(均P<0.05)。结论:采用慈苓化浊方干预痛风大鼠,可降低大鼠关节肿胀程度,降低滑膜组织COX-2、HSP70表达,抑制炎症反应,其作用机制可能与抑制PI3K/AKT/FoxO1通路有关。

基于肝脏能量代谢途径变化探讨健脾化浊消脂方对代谢相关脂肪性肝病大鼠的干预机制

目的通过肝脏能量代谢途径研究健脾化浊消脂方(JPHZXZF)防治代谢相关脂肪性肝病大鼠的作用机制。方法将36只雄性SD大鼠随机分为空白组,模型组,阳性药物组,健脾化浊消脂方高、中、低剂量组。空白组饲喂维持饲料,其余五组饲喂高脂饲料同时饮用10%果葡糖浆溶液,连续喂养12周后,各给药组小鼠给予相应药物连续干预4周。末次给药后,采用生化分析仪测定大鼠血清中三酰甘油(TG)、总胆固醇(T-CHO)、低密度脂蛋白胆固醇(LDL-C)、空腹葡萄糖(FBG)含量;试剂盒法检测大鼠肝脏中TG、T-CHO、游离脂肪酸(NEFA)、柠檬酸合成酶(CS)、肉毒碱棕榈酸转移酶-1(CPT-1)、低氧诱导因子-1α(HIF-1α)、乳酸脱氢酶(LDH)含量或活性;用油红O、HE染色观察大鼠肝脏病理变化;采用蛋白免疫印迹法检测大鼠肝脏组织中p-AMPKα、HIF-1α蛋白表达水平。结果JPHZXZF可以显著降低TG、T-CHO、LDL-C、FBG、NEFA、CS、CPT-1、HIF-1α、LDH含量或活性(P<0.05),缓解肝细胞脂质沉积,升高p-AMPKα的蛋白表达水平(P<0.05),降低HIF-1α的蛋白表达水平(P<0.05)。结论JPHZXZF可以有效改善代谢相关脂肪性肝病糖脂代谢紊乱,其作用可能与改变能量代谢途径有关。

温阳化浊通络方体外抑制HIF-1a/Foxm1/smad3信号通路改善系统性硬化病肺微血管损伤

目的利用系统性硬化病(systemic sclerosis,SSc)肺微血管内皮细胞缺氧模型,研究温阳化浊通络方抑制内皮细胞的内皮-间充质转化(EndoMT)改善肺微血管损伤的分子机制。方法利用SSc患者血清培养正常人肺微血管内皮细胞构建SSc肺微血管内皮细胞,液体石蜡封闭法建立SSc肺微血管内皮细胞缺氧模型,并分别用温阳化浊通络方含药血清或HIF-1a抑制剂KC7F2处理,Western blot检测VE-cadherin、CD31、vimentin、HIF-1α、Foxm1、smad3、Tie-1以及vWF的蛋白表达水平,ELISA检测细胞培养液中的E-selectin和ICAM-1的浓度,双荧光素酶报告基因系统检测Foxm1基因启动子活性。结果与对照组相比较,模型组细胞中的VE-cadherin、CD31、HIF-1a、Foxm1、smad3、Tie-1和vWF蛋白表达水平显著降低,vimentin蛋白表达水平以及细胞培养液中E-selectin和ICAM-1的浓度显著增高,同时细胞形态呈现出明显的“纺锤体样”成肌纤维细胞形态,而温阳化浊通络方和KC7F2能够逆转这些缺氧诱导的蛋白表达水平,以及细胞形态的改变。结论温阳化浊通络方能够改善SSc肺微血管损伤,其作用机制可能是抑制HIF-1a/Foxm1/smad3通路介导的肺微血管内皮细胞EndoMT。

High-throughput sequencing analysis of differential microRNA expression in the process of blocking the progression of chronic atrophic gastritis to gastric cancer by Xianglian Huazhuo formula(香连化浊方)

OBJECTIVE:To explore the mechanism of Xianglian Huazhuo formula(香连化浊方,XLHZ)blocking the development of chronic atrophic gastritis(CAG)to gastric cancer(GC)through bioinformatics analysis and in vitro.METHODS:Pathological morphology of gastric mucosa of rats were observed.High-throughput sequencing was used to analyze the miRNA expression profile of gastric mucosa.The miRanda,miRDB and miRWalk databases were used to predict the differential target genes.Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)enrichment analysis were performed for differential target genes.Real-time quantitative reverse transcription polymerase chain reaction(qRTPCR)was used to verify the differentially expressed miRNAs and target genes.Western blot,EdU,wound healing and flow cytometry were used to observe the effect of XLHZ on epithelial-mesenchymal transition(EMT)markers,proliferation,migration,apoptosis and cell cycle of CAG cells in vitro.RESULTS:A total of five differentially expressed miRNAs and four differential target genes were screened in this study.GO analysis showed that the target genes were enriched in regulation of neuron development,regulation of transcription factor activity and regulation of RNA polymerase.KEGG pathways database differences in gene enrichment of target genes in the Wnt signaling pathway,Phospholipase D signaling pathway and mitogen-activated protein kinase signaling pathway.qRTPCR confirmed that miRNAs and its target genes were consistent with the screening results.In vitro,our study revealed that XLHZ could increase the expression of Ecadherin,decrease the expression of transforming growth factorβ1,vimentin andβ-catenin,inhibite the proliferation and migration of CAG cells,cause cell cycle arrest at G0/G1 and G2/M phase,induce the apoptosis of CAG cells,and prevent the progression of CAG to GC.CONCLUSION:This study provided a new idea for the mechanism of blocking the progression of CAG to GC by XLHZ,which may be related to the expression of miR-20a-3p,miR-320-3p,miR-34b-5p,miR-483-3p and miR-883-3p and their target genes transferrin receptor,nuclear receptor subfamily 4 member 2,delta like canonical Notch ligand 1 and a kinase anchor protein 12 in CAG.In the future,we will continue to investigate the linkage between the active ingredients of XLHZ and the relevant miRNAs and their target genes,so as to provide more sufficient experimental basis for clinically effective prevention of CAG to GC.

益气化浊利水方联合针刺对气虚血瘀证2型糖尿病周围神经病变的疗效观察

目的探讨益气化浊利水方联合针刺治疗气虚血瘀证2型糖尿病周围神经病变(Type 2 diabetic peripheral neu-ropathy,T2DPN)的效果。方法选取2021年9月—2022年9月医院收治的96例T2DPN患者为研究对象,以随机数字表法分研究组(48例)、对照组(48例)。对照组给予针刺治疗,研究组在对照组基础上给予益气化浊利水方治疗,两组均持续治疗2周后评价效果。比较两组中医症状评分、周围神经传导速度及临床疗效,对比两组外周血炎症因子、氧化应激因子变化情况,记录两组治疗期间不良事件发生情况。结果两组治疗后的主症、次症中医证候评分均低于治疗前(P<0.05),研究组治疗后中医证候评分均低于对照组(P<0.05)。两组治疗后正中神经、胫后神经、腓总神经的运动神经传导速度(Motor nerve conduction velocity,MNCV)、感觉神经传导速度(Sensory nerve conduction velocity,SNCV)均高于治疗前(P<0.05),研究组治疗后上述指标均高于对照组(P<0.05)。研究组总有效率(91.67%,44/48)高于对照组(77.08%,37/48)(P<0.05)。两组治疗后肿瘤坏死因子-α(Tumor necrosis factor-α,TNF-α)、白细胞介素-6(Inter-leukin-6,IL-6)、C反应蛋白(C-reactive protein,CRP)均低于治疗前(P<0.05),研究组治疗后的TNF-α、IL-6、CRP均低于对照组(P<0.05)。两组治疗后丙二醛(Malondialdehyde,MDA)均低于治疗前,超氧化物歧化酶(Superoxide dis-mutase,SOD)、总抗氧化能力(Total antioxidant capacity,TAOC)均高于治疗前(P<0.05),研究组治疗后的MDA均低于对照组,SOD、TAOC均高于对照组(P<0.05)。两组总不良事件发生率比较,差异无统计学意义(P>0.05)。结论益气化浊利水方联合针刺治疗气虚血瘀证T2DPN可改善患者症状、周围神经传导速度,增强治疗效果,抑制外周血炎症因子分泌、减轻氧化应激损伤,安全性良好。

番连化浊方对急性高脂血症小鼠胆固醇代谢紊乱的调节作用

目的:探讨番连化浊方对急性高脂血症小鼠胆固醇代谢紊乱的调节作用。方法:采用Triton-WR1339构建C57BL/6小鼠急性高脂血症模型,给药5 d后,测定血清中总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、谷草转氨酶(GOT)、谷丙转氨酶(GPT)含量;苏木精-伊红(HE)染色观察肝脏病理变化;油红O染色检测肝脏内脂质累积情况;蛋白质印迹法检测肝脏去唾液酸糖蛋白受体1(ASGR1)、肝X受体α(LXRα)、三磷酸腺苷结合盒转运蛋白A1(ABCA1)、ABCA5、细胞色素P4507A1(CYP7A1)蛋白表达变化。结果:与模型组比较,番连化浊方能显著降低血清中TC、TG、LDL-C、GOT、GPT含量,同时升高HDL-C含量(均P<0.05);显著上调ABCA1、ABCG5、LXRα、CYP7A1蛋白表达水平,显著下调ASGR1蛋白表达水平(均P<0.05);显著减少肝细胞内脂质累积,改善肝脏病理形态。结论:番连化浊方可能通过调控ASGR1/LXRα/CYP7A1信号通路促进急性高脂血症小鼠的胆固醇外排,降低血脂。

基于多指标综合评分法优化升阳化浊降糖方的提取工艺

目的 优选升阳化浊降糖方的最佳提取工艺。方法 采用正交试验设计,以莫诺苷、马钱苷、芍药苷、甘草苷、甘草酸、毛蕊异黄酮葡萄糖苷、淫羊藿苷、吴茱萸碱、吴茱萸次碱9种成分质量浓度及固形物质量的综合评分为评价指标,对提取次数、提取时间、加水量进行考察,确定最佳的提取工艺。结果 确定的提取工艺为:提取3次,每次1 h,第1次加入10倍量水,第2、3次加入8倍量水;3批验证试验平均综合评分为90.11。结论 优选的工艺稳定可行,为升阳化浊降糖方的后续研发工作奠定了基础。

益气行瘀补肾化浊方对糖尿病肾病患者的临床疗效及肾功能指标的影响

目的探究益气行瘀补肾化浊方对糖尿病肾病(diabetic kidney disease,DKD)患者的临床疗效及肾功能相关指标的影响。方法选取2022年6月—2024年1月武威市中医医院收治的200例DKD患者(肾虚络瘀证)为研究对象,根据不同的治疗方法分成对照组、研究组,每组100例。对照组给予常规西医治疗,研究组在对照组基础上给予益气行瘀补肾化浊方治疗。比较两组治疗前后肾功能指标、临床疗效。结果治疗后,与对照组相比,研究组肾小球滤过率水平更高,血肌酐、24 h尿蛋白定量、尿微量白蛋白/尿肌酐比值水平更低,差异有统计学意义(P均<0.05)。研究组治疗总有效率高于对照组,差异有统计学意义(P<0.05)。结论益气行瘀补肾化浊方联合常规西医治疗在改善DKD患者的肾功能及提升临床疗效等方面具有较为明显的优势。

益气化浊利水方联合别嘌醇治疗慢性心力衰竭合并高尿酸血症的临床效果研究

目的探讨益气化浊利水方联合别嘌醇治疗慢性心力衰竭(CHF)合并高尿酸血症的效果。方法以随机数字表法将2021年8月—2023年8月就诊的105例CHF合并高尿酸血症分为3组,每组35例。3组均给予常规治疗,在此基础上,中药组给予益气化浊利水方治疗,别嘌醇组给予别嘌醇治疗,联合组给予益气化浊利水方联合别嘌醇治疗,均治疗3个月。比较3组临床疗效、血清尿酸、左心室射血分数(LVEF)、左心室舒张末期内径(LVEDD)、左心室收缩末期内径(LVESD)、血栓素B_(2)(TXB_(2))、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)、超敏C反应蛋白(hs-CRP)、N末端脑钠肽前体(NT-proBNP)、6 min步行距离、一氧化氮(NO)、内皮素(ET)、降钙素基因相关肽(CGRP)及不良反应。结果联合组总有效率94.29%(33/35)高于中药组74.29%(26/35)、别嘌醇组71.43%(25/35)(P<0.05),但中药组与别嘌醇组比较,无显著差异(P>0.05)。治疗后联合组LVESD、LVEDD、NT-proBNP、hs-CRP、TXB_(2)、TNF-α、ET、IL-6低于中药组、别嘌醇组,6 min步行距离大于中药组、别嘌醇组,LVEF、NO、CGRP高于中药组、别嘌醇组(P<0.05),但中药组与别嘌醇组比较,无显著差异(P>0.05);治疗后血清尿酸联合组低于别嘌醇组低于中药组(P<0.05);3组不良反应总发生率比较,无显著差异(P>0.05)。结论益气化浊利水方联合别嘌醇对CHF合并高尿酸血症患者疗效可靠,可调节血清尿酸、炎性因子及NT-proBNP水平,改善血管内皮功能,促进心功能恢复,增强运动能力,且安全性高。

固本培元方治疗脾肾阳虚型癌因性疲乏临床观察

目的探讨固本培元方治疗脾肾阳虚型癌因性疲乏的临床效果。方法选择脾肾阳虚型癌因性疲乏患者120例,按随机数字表法分为对照组和观察组,各60例。对照组采用西医治疗,观察组在对照组基础上加用固本培元方,观察周期为4周。比较两组患者治疗后Piper疲乏量表(PFS)评分、中医证候评分、生命质量评分、机体功能状态评分,以及治疗期间不良反应情况。结果治疗后,观察组PFS评分和中医证候评分均低于对照组,卡氏(KPS)评分和生命质量评分均高于对照组(P<0.05);且观察组血常规、肝功能、肾功能、尿常规、粪便常规相关指标恢复正常比例均明显高于对照组(P<0.05)。结论固本培元方能够显著改善脾肾阳虚型癌因性疲乏患者的疲乏状态,提升其生命质量和机体功能状态,改善中医证候,安全性更高。

化浊解毒方治疗慢性萎缩性胃炎癌前病变的临床研究

目的观察化浊解毒方对慢性萎缩性胃炎(CAG)伴胃黏膜上皮中、重度不典型增生(ATP)及不完全肠上皮化生(IM)癌前病变临床症状、胃镜病理学及幽门螺旋杆菌(Hp)的影响。方法将确诊为慢性萎缩性胃炎癌前病变的120例患者随机分为治疗组和对照组两组,分别给予化浊解毒方汤剂和胃复春片治疗。治疗结束后比较两组患者的临床症状、胃镜病理学及Hp转阴率的改变情况。结果临床症状总有效率比较,化浊解毒方组为86.67%,胃复春组为71.67%,差异有统计学意义(P<0.05);胃镜病理学检查总有效率比较,化浊解毒方组为78.33%,胃复春组为60.00%,差异有统计学意义(P<0.05);Hp的转阴率比较,化浊解毒方组为73.17%,胃复春组为35.89%,差异有统计学意义(P<0.01)。结论在浊毒理论指导下运用化浊解毒方治疗慢性萎缩性胃炎癌前病变具有良好疗效。其作用机制除与对抗幽门螺旋杆菌有着密切关系外,还可能与增强胃肠动力、调节免疫功能、保护胃黏膜等存在相关性。