Background: Postmenopausal Osteoporosis (PMOP) is characterized by decreased bone mass and deterioration of bone microarchitecture, leading to increased fracture risk. Current treatments often have adverse effects, necessitating safer alternatives. Kaempferol, a flavonoid identified as a key active component of the traditional Chinese medicine Yishen Gushu formula, has shown promise in improving bone health, but its mechanisms in PMOP treatment remain unclear. Objective: The aim of this study was to investigate the therapeutic effects and underlying mechanisms of kaempferol in the treatment of PMOP. Methods: A bilateral ovariectomized (OVX) rat model was established to simulate PMOP. Sixty female Sprague-Dawley rats were divided into six groups: Sham operation, OVX control, OVX with alendronate (ALN), and OVX with kaempferol at doses of 10, 20, and 40 mg/kg. Treatments were administered orally once daily for 12 weeks. Assessments included Bone Mineral Density (BMD), trabecular microarchitecture via histopathology, organ morphology, organ indices, and serum levels of bone metabolism markers (TRACP-5b, BALP, ALP, Ca, P, and Fe) as well as liver and kidney function indicators (ALT, AST, CREA, and urea). Tandem Mass Tag (TMT) quantitative proteomics and bioinformatics analyses were conducted on femur samples to identify differentially expressed proteins (DEPs). Key DEPs were validated using parallel reaction monitoring (PRM), immunohistochemistry, and molecular docking. Results: Kaempferol significantly improved BMD and enhanced trabecular microarchitecture in OVX rats in a dose-dependent manner, comparable to ALN, without causing hepatic, renal, or estrogen- like side effects. Serum bone metabolism markers were normalized with kaempferol treatment. Proteomic analysis identified 902 DEPs associated with kaempferol treatment, involved in processes such as bone remodeling, skeletal system development, and osteoclast function. Key signaling pathways affected included NF-κB, PI3K-AKT, and HIF-1. Notably, kaempferol downregulated five key DEPs—Rac2, Ddb1, Cdc42, Rpl19, and Hist2h4-in the femur, which are crucial for osteoclast resorptive activity, migration, adhesion, and cell cycle progression. Conclusion: Kaempferol exerts therapeutic effects on PMOP by inhibiting key proteins involved in osteoclast function, thereby reducing bone resorption and promoting bone health. These findings suggested that kaempferol is a potential safer alternative for PMOP treatment. Further research is recommended to explore its clinical applications and elucidate detailed mechanisms. conclusion: Kaempferol may reduce osteoclast resorptive activity, migration, adhesion ability, and polarization level, increase apoptosis, and slow the cell cycle of osteoclasts by inhibiting Hist2h4, Cdc42, and Rac2 protein expression, thus exerting an anti-PMOP effect. other: None.

BACKGROUND:Safer and more effective drugs are needed for the treatment of acute pancreatitis (AP). Qingjie Huagong decoction (QJHGD) has been applied to treat AP for many years and has shown good clinical effects. However, the potential mechanism has not yet been determined.PURPOSE:To investigate the role and underlying mechanism of the effects of QJHGD on AP both in vitro and in vivo.METHODS:QJHGD was characterized by UHPLC-Q-Orbitrap-MS. The protective effect of QJHDG and the underlying mechanism were investigated in MPC-83 cells in vitro. A caerulein-induced AP model was established to evaluate the protective effect of QJHGD in mice. CCK-8 assays were used to detect cell viability. The contents of inflammatory mediators were determined by ELISA. Expression levels of circRNA, miRNA and mRNA were determined by qRT-PCR. Protein expression was determined using Western blot. Pancreatic tissues were assessed by hematoxylin and eosin staining as well as immunohistochemical and immunofluorescence analyses. Pull-down and luciferase activity assays were performed to determine the regulatory relationships of circHipk3, miR-193a-5p and NLRP3.RESULTS:Our results confirmed that mmu-miR-193a-5p was sponged by mmu-circHipk3, and NLRP3 was a target of miR-193a-5p. In vitro experiments showed that QJHGD enhanced MPC-83 cell viability by regulating circHipk3 sponging mir-193a-5 targeting NLRP3 and inhibiting pyroptosis-related factors. Finally, we showed that QJHGD ameliorated pancreatic tissue injury in AP mice via this pathway.CONCLUSION:This study demonstrate that QJHDG exerted its anti-AP effects via the circHipk3/miR-193a-5p/NLRP3 pathway, revealing a novel mechanism for the therapeutic effect of QJHDG on AP.

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OBJECTIVE:To identify the core targets of Rheum palmatum L. and Salvia miltiorrhiza Bge., (Dahuang-Danshen, DH-DS) and the mechanism underlying its therapeutic efficacy in acute pancreatitis (AP) using a network pharmacology approach and validate the findings in animal experiments.METHODS:Network pharmacology analysis was used to elucidate the mechanisms underlying the therapeutic effects of DH-DS in AP. The reliability of the results was verified by molecular docking simulation and molecular dynamics simulation. Finally, the results of network pharmacology enrichment analysis were verified by immunohistochemistry, Western blot analysis and real-time quantitative PCR, respectively.RESULTS:Sixty-seven common targets of DH-DS in AP were identified and mitogen-activated protein kinase 3 (MAPK3), Janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3), protein c-Fos (FOS) were identified as core targets in the protein interaction (PPI) network analysis. Gene ontology analysis showed that cellular response to organic substance was the main functions of DH-DS in AP, and Kyoto Encyclopedia of Genes and Genomes analysis showed that the main pathway included Th17 cell differentiation. Molecular docking simulation confirmed that DH-DS binds with strong affinity to MAPK3, STAT3 and FOS. Molecular dynamics simulation revealed that FOS-isotanshinone II and STAT3-dan-shexinkum d had good binding capacity. Animal experiments indicated that compared with the AP model group, DH-DS treatment effectively alleviated AP by inhibiting the expression of interleukin-1β, interleukin-6 and tumor necrosis factor-α, and blocking the activation of Th17 cell differentiation (P<0.01).CONCLUSION:DH-DS could inhibit the expression of inflammatory factors and protect pancreatic tissues, which would be functioned by regulating Th17 cell differentiation-related mRNA and protein expressions.

目的 探讨清解化攻汤对急性胰腺炎(AP)大鼠肠黏膜屏障的保护作用及机制.方法 采用雨蛙素联合脂多糖腹腔注射建立AP大鼠模型,造模完成后立即按分组予相应药物干预,观察胰腺和回肠组织HE染色后的病理变化及回肠组织病理评分;检测血清淀粉酶、内毒素、血清炎性因子肿瘤坏死因子α(TNF-α)及白介素6(IL-6)水平;免疫组化法检测回肠组织Toll样受体4(TLR4)、磷酸化核因子κB(p-NF-κB)及紧密连接蛋白Occludin的表达.结果 与假造模组比较,模型组大鼠胰腺和回肠组织损伤明显,回肠组织病理评分明显升高(P＜0.01),血清淀粉酶、TNF-α、IL-6、内毒素显著升高(均P＜0.01),回肠黏膜TLR4和p-NF-κB表达明显升高,而Occludin明显下降(均P＜0.01);与模型组比较,中药组和西药组大鼠胰腺和回肠组织损伤有所改善,中药组回肠组织病理评分明显下降(P＜0.05),血清淀粉酶、TNF-α、IL-6、内毒素明显下降(均P＜0.01),回肠黏膜TLR4和p-NF-κB蛋白表达明显下降,而Occludin明显升高(均P＜0.01);与西药组比较,中药组大鼠胰腺和回肠组织损伤略有改善,回肠组织病理评分无统计学差异(P＞0.05),血清淀粉酶、TNF-α、IL-6、内毒素均有所下降(内毒素P＜0.01,其余均P＜0.05),回肠黏膜TLR4表达有所下降(P＜0.05),而p-NF-κB及Occludin差异无统计学意义(均P＞0.05).结论 清解化攻汤对急性胰腺炎大鼠肠黏膜屏障有保护作用,其机制可能与抑制TLR4/NF-κB信号通路活化及降低血清炎性细胞因子表达水平有关.

Background: The Qingjiehuagong decoction (QJHGD), which has been used in clinical trials to treat acute pancreatitis (AP), has demonstrated encouraging results. Methods: In this particular investigation, we used both metabolomics and network pharmacology to investigate the fundamental processes and targets that QJHGFD employs to cure AP. Results: Using a cerulein-induced rat model of AP, we showed that QJHGD effectively improved pancreatic tissue damage and reduced serum levels of AMY, LPS, IL-1β, IL-6, IL-8 and TNF-α. In total, 28 blood entry compounds derived from QJHGD were identified by ultra-performance liquid chromatography-high resolution mass spectrometry technology. The intersecting target genes of 108 genes associated with identified compounds in QJHGD and AP disease genes were identified using a network pharmacology approach. The protein interaction network revealed AKT1, TNF-α, IL-6, VEGFA, and TP53 as important targets. Gene ontology analysis showed that response to stimulus, molecular function regulator and organelle part were the main functions, and Kyoto Encyclopedia of Genes and Genomes analysis showed that 20 pathways such as AGE-RAGE signaling pathway in diabetic complications and the IL-17 signaling pathway were the main pathways involved in the anti-AP effects of QJHGD. Thirty-two potential metabolic markers and 13 possible metabolic pathways were identified by metabolomics analysis. Combined network pharmacological analysis revealed that QJHGD affects four metabolic pathways (tryptophan metabolism; glycolysis and gluconeogenesis metabolism; valine, leucine and isoleucine degradation metabolism; the urea cycle and metabolism of arginine, proline, glutamate, aspartate and asparagine), five metabolites (indole-3-acetate, pyruvate, methylmalonate, L-citrulline, N-acetyl-l-glutamate) and four related targets (AKT1, ALDH2, NOS2, NOS3) to combat inflammation. The strong affinity of QJHGD’s interactions with its primary targets was established by molecular docking and molecular dynamics simulations. Conclusion: This research investigate the critical targets and mechanisms of QJHGFD for treating AP. The results of this investigation provide novel tactics and complementary techniques for the clinical treatment of AP.

目的 运用网络药理学的研究方法,初步分析独活寄生汤治疗退行性腰椎管狭窄症(DLSS)的作用机制.方法 通过中药系统药理学数据库与分析平台(TCMSP)检索和筛选独活寄生汤方药物的活性成分,同时在GeneCards、OMIM数据库中检索DLSS的靶点.利用Venny平台得到独活寄生汤治疗DLSS的潜在作用靶点.利用STRING数据库和Cy-toscape软件构建独活寄生汤治疗DLSS的"单味药—活性成分—作用靶点"网络和蛋白质相互作用网络(PPI),并通过David数据库对独活寄生汤治疗DLSS的作用靶点进行基因本体(GO)和京都基因与基因组百科全书(KEGG)通路富集分析,研究独活寄生汤治疗DLSS的作用机制,并通过分子对接来模拟活性成分作用于靶蛋白的结合情况.结果 共探索出独活寄生汤主要涉及1939个有效活性成分及对应292个潜在靶点,DLSS靶点1258个,筛选出共同靶点122个.经PPI互作图显示蛋白ALB、AKT1、IL-6、IL-1B、CASP3等存在较多连线.药物-活性成分-靶点网络图显示,度值较高的活性成分主要涉及柚皮素、芒柄花黄素、甘草查尔酮A、黄芩素等,被影响较多的靶点为PTGS2、ESR1、HSP90AA1等.GO功能分析提示,关键靶点基因在生物过程(BP)主要参与了对氧化应激的反应、对脂多糖的反应、细胞对化学应激的反应等,在分子功能(MF)主要参与了脱氧核糖核酸-结合转录因子结合、信号受体激活剂活性、肽结合等,在细胞成分(CC)主要参与了膜筏、膜微区、囊腔等细胞结构,由此推测,治疗作用机制可能与信号转导蛋白、活性酶调节、炎症反应等有关.KEGG通路富集分析提示,关键通路主要涉及AGE-RAGE、IL-17、TNF等信号通路.结论 借助网络药理学的研究方法,发现独活寄生汤治疗DLSS具有多靶点、多通路的特点,从抗炎、抗氧化、抗纤维化、抑制破骨细胞活性、促进成骨细胞活性等多个机制发挥治疗作用.

目的:探讨清解化攻汤对急性胰腺炎(AP)大鼠肠黏膜屏障及血清炎症因子的干预作用.方法:24只SD大鼠随机分成假造模组、模型组、西药组及中药组,每组各6只,运用雨蛙素联合脂多糖腹腔注射建立大鼠AP模型,成模后按分组给予相应药物干预,观察回肠组织的病理改变情况;检测血清淀粉酶、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、白细胞介素-10(IL-10)、D-乳酸及内毒素水平;Western blot检测回肠组织紧密连接蛋白Occludin的表达情况.结果:与假造模组比较,模型组回肠组织病理损伤明显,回肠黏膜绒毛略不规整或破损,肠上皮下间隙稍见增宽,与固有层分离增大,局部炎性细胞浸润增多,内皮下及固有层充血及出血明显增多,模型组血清淀粉酶、TNF-α、IL-1β、IL-10、D-乳酸及内毒素水平明显升高(P＜0.01),回肠组织Occludin蛋白相对表达量明显下降;与模型组比较,西药组和中药组病理改变明显减轻,血清淀粉酶、TNF-α、IL-1β、D-乳酸及内毒素水平均明显下降(P＜0.01),血清IL-10及回肠Occludin蛋白相对表达量均明显增高(P＜0.01);与西药组比较,中药组血清淀粉酶、D-乳酸及内毒素水平降幅更明显(P＜0.05).结论:清解化攻汤对AP大鼠的肠黏膜屏障有一定的保护作用,而且该方可降低血清促炎细胞因子水平,提高抑炎细胞因子水平,对AP大鼠血清炎症因子有明显的调控作用.

The mortality of gastric cancer ranks fourth in the world. Therefore, the research on the pathogenesis, development, metastasis and treatment of gastric cancer is particularly important. Based on the clinical characteristics of gastric cancer in traditional Chinese and Western medicine, this study summarized and analyzed the currently applied animal models, and analyzed the clinical goodness of fit in terms of animal models according to the clinical diagnostic characteristics of traditional Chinese and Western medicine. For the evaluation of the model, western medicine pays attention to pathology and cytology, whereas pays less attention to other aspects. In traditional Chinese medicine, there are few studies on animal disease-syndrome models combined with gastric cancer. The main method is using ‘medicine verification syndrome type’ to study the pathogenesis and drugs. While analyzing the clinical goodness of fit in terms of animal models of gastric cancer, this study analyzed the advantages and disadvantages of various models and summarized the scope of their applications, and puts forward the existing problems, so as to further improve the animal model of gastric cancer and make it more in line with the requirements of clinical disease-syndrome, provide referential animal models for the basic research of integrated traditional Chinese and Western medicine, and better serve the basic research of traditional Chinese and Western medicine.

胃癌是一种发生在消化系统高死亡率、临床治疗效果不佳的恶性肿瘤.目前临床上治疗胃癌的效果不佳且预后较差,发病机制尚未清晰,常涉及多条信号通道.Wnt/β-catenin通路作为消化系统肿瘤信号经典传导通路之一,其异样激活会启动靶基因及相关因子转录、翻译、表达进程,与胃黏膜病变甚至胃癌的发生进展息息相关.中医药作为我国几千年一直延续下来的医学,在防治疾病过程中重视整体观念辨证论治.鉴于中医宏观调控与西医微观调控互补关系,协同中医药靶向治疗胃癌已经成为新的医学热点.因此,立足于近年研究者关于中医药干预Wnt/β-catenin信号通路影响胃癌细胞增殖、凋亡、侵袭转移、自我更新等方面的研究,科学总结阐述中医药能够干预靶向Wnt/β-catenin信号通路上的靶点、效应点防治胃癌的机理,这有利于为中医药临床靶向治疗胃癌提供系统的科学依据.

目的 采用网络药理学与分子对接技术探讨脊髓伤方治疗脊髓损伤(SCI)的作用机制.方法 通过中药系统药理学数据库与分析平台(TCMSP)与中国知网(CNKI)数据库筛选脊髓伤方的活性成分及其作用靶点,运用人类基因数据库(GeneCards)、在线人类孟德尔遗传数据库(OMIM)和治疗靶标数据库(TTD)等数据库挖掘SCI的疾病相关靶点;最终获取中药复方活性成分作用靶点与疾病相关靶点的交集靶点.运用Cytoscape 3.7.2 软件与STRING数据库分别构建"活性成分-潜在作用靶点"和蛋白互作网络(PPI),筛选出潜在核心靶点;运用R软件和Metascape平台分别用于分析基因本体(GO)功能和京都基因与基因组百科全书(KEGG)途径的富集;对潜在靶点进行GO和KEGG富集分析.利用AutoDock Tools 1.5.6软件对关键化合物与核心靶点进行分子对接验证.结果 共筛选获取138个活性成分及111个潜在作用靶点;获取到槲皮素、木犀草素、山柰酚、汉黄芩素、β-胡萝卜素等核心活性成分,白蛋白(ALB)、白介素6(IL-6)、丝氨酸/苏氨酸激酶1(AKT1)、管内皮生长因子A(VEGFA)、半胱氨酸天冬氨酸蛋白酶3(CASP3)、表皮生长因子受体(EGFR)、表皮生长因子(EGF)、转录因子AP-1(JUN)、白介素1B(IL1B)、转录3的信号换能器和激活子(STAT3)等核心靶点;共筛选获取179条信号通路,关键通路包括糖尿病并发症中晚期糖基化终产物及其受体(AGE-RAGE)信号通路、磷脂酰肌醇3-激酶-蛋白激酶B(PI3K-AKT)信号通路、缺氧诱导因子-1(HIF-1)信号通路、松弛素(RLX)信号通路、甲状腺激素(TH)信号通路、叉头盒O(FoxO)信号通路、阿佩林(AP)信号通路等.分子对接结果的最小结合能均

目的 系统评价中药多途径治疗急性胰腺炎并发腹间隔室综合征疗效。方法 检索中国知网、万方、维普、Sinomed、PubMed、Embase、Cochrane Library自建库至2020年12月1日收录的中医药治疗急性胰腺炎并发腹间隔室综合征的临床试验，RevMan5.3软件进行荟萃分析。结果 共纳入17项研究，共1 033例病人；荟萃分析显示，与西药基础治疗比较，中西药联用可显著降低腹内压[标准化均数差（SMD）95%CI：-0.63（-0.83,0.43）]；与西药基础治疗比较，联用中药组可显著降低急性生理学和慢性健康状况评价Ⅱ（APACHE Ⅱ）评分[SMD 95%CI：-0.65（-0.87,0.43）]；与西药基础治疗比较，联用中药组可有效缩短排便恢复时间[SMD 95%CI：-0.68（-1.14,0.22）]；此外，小样本的研究表明中西医结合相较于单纯西药治疗可降低病人死亡情况[比值比（OR）95%CI:1.04（-1.91，-0.16）]。结论 中药治疗急性胰腺炎并发腹间隔室综合征可降低腹内压、减少临床APACHE Ⅱ评分、缩短病人排便恢复时间。

目的 基于数据整合研究(处方挖掘、网络药理学、分子对接及动力学模拟)探讨陈国忠治疗慢性萎缩性胃炎(chronic atrophic gastritis,CAG)组方规律、作用靶点和潜在机制.方法 基于门诊电子病历系统建立"慢性萎缩性胃炎处方用药"数据库,以频数统计、关联分析、系统聚类探讨处方核心药团和聚类新方;网络药理学分析构建药物-成分-靶点网络图,对核心基因富集分析;分子对接及动力学模拟验证核心药靶结合的稳定性.结果 纳入129张处方,162味中药,用药寒温并用、辛开苦降,多入肺脾胃经;核心药团为黄芩、半夏、甘草,聚类为类小柴胡汤等5种新方.核心药团共98个活性成分,作用的54个主要靶点富集到脂多糖反应、PI3K-Akt等1904个生物过程与319条信号通路.核心药团主要成分槲皮素、黄芩素、豆甾醇与关键靶点PTGS2经分子对接及动力学分析显示均稳定结合.结论 陈国忠治疗慢性萎缩性胃炎用药辛苦、寒温并举,善用黄芩、半夏、甘草与柴胡等组成类小柴胡汤,治疗少阳阳明不利证;并拟三白汤诸方健脾温阳降逆、行气利湿除痞.核心药团主要成分与PTGS2等关键靶点稳定结合,多途径协同调控胃黏膜增殖、凋亡等相关通路发挥治疗作用.

Objective:To evaluate the clinical efficacy of TCM Qingjie Huagong Decoction combined with routine internal medicine in the treatment of severe acute pancreatitis with cholelithiasis (bile duct stones) in the early stage.Methods:Thirty-two patients with severe acute pancreatitis combined with cholelithiasis in the first affiliated Hospital of GuangXi University of Traditional Chinese Medicine were selected and randomly divided into two groups with 16 in each, both groups were treated for 14 days. Serum amylase (AMS) was detected by iodine-starch colorimetry, GOT and GPT were detected by continuous monitoring method, and CRP, IL-6 and procalcitonin (PCT) were detected by immune transmission turbidimetry. Acute Physiological and Chronic Health Score Ⅱ (APACHE Ⅱ), CT Severity Index Score (CTSI) and Modified Marshall Score were used to evaluate the severity of SAP. The recovery time of body temperature, the relief time of abdominal distension pain, the recovery time of bowel sounds and the total hospital stay were observed and recorded to evaluate the clinical effect.Results:The total effective rate was 93.8% (15/16) in the treatment group and 75.0% (12/16) in the control group. There was significant difference between the two groups ( χ2=8.19, P=0.042). After treatment, the level of AMS, WBC, CRP, PCT, AST, ALT and IL-6 in the treatment group were lower than those in the control group ( t values were 14.3, 7.24, 9.63, 5.48, 7.05, 7.33, 28.34, respectively, all Ps<0.05); After treatment, the time for body temperature to return to normal [(2.91±0.12)d vs. (3.78±0.38)d, t=8.76], the time for relief of abdominal distension pain [(4.77±0.68)d vs. (7.13±1.55)d, t=9.52], the time for recovery of bowel sounds [(3.90±1.80)d vs. (4.89±1.38)d, t=2.98] and the total hospital stay [(22.60±2.80)d vs. (30.37±3.89)d, t=7.88] in the treatment group were all significantly shorter than those in the control group ( P<0.01); APACHE Ⅱ, CTSI and the Modified Marshall Score in the treatment group were lower than those in the control group ( t values were 11.82, 12.72, 7.71, respectively, all Ps<0.01). Conclusion:Qingjie Huagong Decoction combined with ERCP and conventional western medicine therapy can reduce the level of inflammation in patients with cholelithiasis in the early stage of SAP, relieve clinical symptoms and improve clinical efficacy.

目的 运用网络药理学和分子对接分析大黄治疗急性胰腺炎(acute pancreatitis,AP)的分子作用机制.方法 运用TCMSP、TCMID、Swiss Target Prediction数据库筛选大黄的活性成分及靶点,GeneCards、OMIM数据库筛选AP的靶点.然后利用Cytoscape软件构建大黄"活性成分-药物靶点"网络、大黄治疗AP的"活性成分-疾病靶点"网络,在STRING数据库构建PPI网络,Metascape数据库和R语言进行GO和KE GG富集分析.最后通过分子对接验证前期所得的核心活性成分与核心靶点结合的可能性.结果 查询得到大黄活性成分192个,AP靶点1882个.大黄治疗AP主要且核心的前3个活性成分为beta-sitosterol、aloe-emodin、EUPA-TIN,大黄治疗AP核心靶点为HSP90AA1.GO富集分析集中于对有毒物质反应等,KE GG富集分析则显著富集在与AP密切相关的p53信号通路.分子对接显示结合性好、构象稳定.结论 大黄可通过p53信号通路影响与AP相关的基因、蛋白表达,从而抑制细胞凋亡,缓解AP的炎症损伤.

目的 系统评价不同黏度骨水泥经皮椎体后凸成形术(PKP)治疗骨质疏松性椎体压缩骨折(OVCF)的有效性与安全性.方法 计算机检索自建库至2021年4月18日收录在中国知网(CNKI)、万方(Wanfang)、维普(VIP)、PubMed、中国生物医学文献数据库(CBM)、The Cochrane library等数据库的文献,搜索有关PKP中采用高低黏度骨水泥治疗OVCF的随机对照试验(RCT)文献,并以手工检索相关论文.由2位评价员独立筛选文献、提取资料及评价纳入研究的方法学质量后,采用Review 5.3软件进行Meta分析.结果 共纳入12篇RCT文献,共1089例患者,其中高黏度组544例,低黏度组545例.Meta分析结果表明:与对照组相比,研究组在降低术后视觉模拟量表(VAS)评分(MD=-0.43,95％CI:-0.67～-0.19,P<0.01)、Oswestry功能障碍指数(ODI)(MD=-3.89,95％CI:-6.32～-1.47,P<0.01)、Cobb角(MD=-1.78,95％CI:-2.08～-1.48,P<0.00001)、减少骨水泥注入量(MD=-0.18,95％CI:-0.34～-0.02,P<0.05)、缩短手术时间(MD=-6.91,95％CI:-12.84～-0.99,P<0.05)和恢复伤椎高度(MD=3.01,95％CI:1.15～4.86,P<0.01)方面均明显优于对照组;与对照组相比,研究组在降低术后骨水泥渗漏率(RR=0.40,95％CI:0.32～0.51,P<0.01)和其他并发症发生率(RR=0.55,95％CI:0.39～0.78,P<0.01)方面均明显低于对照组.结论 与低黏度骨水泥相比,PKP中选用高黏度骨水泥具备更好的临床疗效及安全性.然而,上述结论仍需更多高质量、多中心的RCT进一步证实.

目的 系统评价超声骨刀(UBC)与高速磨钻(HSD)经颈椎后路减压术治疗颈椎退行性疾病(CDD)的有效性及安全性.方法 检索在2021年5月之前公开发表在中国知网(CNKI)、万方数据库、维普中文科技期刊数据库(VIP)、中国生物医学文献数据库(CBM)、PubMed和EMbase等数据库的文献,搜索有关UBC与H SD经颈椎后路减压术治疗CDD的临床文献,由两位评价者独立筛选文献、提取资料并评价纳入研究的偏倚风险后,运用Stata/SE 12.0软件进行meta分析.结果 共纳入14项研究,UBC、HSD组患者分别为379、427例.Meta分析结果显示,与HSD组比较,UBC组患者的手术总时间(MD=-20.78,95％CI:-31.68～-9.88)、术中总出血量(MD=-57.97,95％CI:-110.14～-5.81)、术后引流量(MD=-53.69,95％CI:-89.80～-17.59)、并发症发生率(MD=0.52,95％CI:0.32～0.85)、术后视觉模拟评分(VAS,MD=-0.80,95％CI:-1.23～-0.37)均低于HSD组,差异均有统计学意义(P<0.05).两组在日本骨科协会评分(JOA)比较,差异无统计学意义(MD=0.01,95％CI:-0.15～0.17,P>0.05).结论 与HSD相比,在颈椎后路减压术治疗CDD中UBC具有提高减压速度,失血量小、并发症少的优势.

目的:采用转录组高通量测序探讨清解化攻方抑制重症急性胰腺炎(SAP)炎症反应的可能机制.方法:雨蛙素联合脂多糖腹腔注射法复制SAP大鼠模型,观察空白组、模型组、中药组大鼠胰腺组织湿/干比重、血清淀粉酶、内毒素、IL-6、IL-8表达水平及病理组织改变情况;RNA-seq测序检测大鼠胰腺组织基因表达差异,筛选清解化攻方抑制炎症反应的核心基因、生物学功能及信号通路;Real-time PCR验证测序结果.结果:与模型组比较,中药组大鼠胰腺湿/干比重显著下降(P＜0.01);ELISA及胰腺病理结果表明中药组大鼠胰腺水肿、炎性因子释放以及胰腺炎症反应显著改善.测序表明中药组上调1 701个、下调1 602个胰腺差异基因,从而调节免疫炎症反应、趋化因子介导通路等生物过程,并下调TNF-α/NF-κB、MAPK、趋化因子等信号通路.中药组TNF-α、NF-κB p65、IKK β、p38MAPK、ERK1、IL-1 β较模型组表达显著下降,IκBα表达显著增加,与测序结果一致.结论:清解化攻方能有效抑制重症急性胰腺炎大鼠炎症反应,可能机制与调节TNF-α/NF-κB、MAPK等信号通路相关.

目的 探讨尿液羧肽酶B激活肽(carboxypeptidase B activating peptide,CAPAP)作为急性重症胰腺炎(severe acute pancrea-titis,SAP)早期标志物的诊断价值.方法 检索PubMed、Embase、Web of Science、中国知网、万方以及维普数据库,时间为1995年1月至2021年3月.RevMan5.3制作QUADAS-2量表评估文献质量,Stata 16.0软件荟萃分析及绘制综合受试者工作特征(summary receiver operating characteristic,SROC)曲线,TSA 0.9.5.10 Beta软件试验序贯分析.结果 纳入9项研究,研究无阈值效应,CAPAP诊断SAP的灵敏度、特异度、阳性似然比(postive likelihood ratio,PLR)、阴性似然比(negative likelihood ratio,NLR)、诊断比值比(diagnostic oddsratio,DOR)分别为0.84、0.92、10、0.17、59;SROC曲线下面积为0.94;亚组分析提示,发表年份、研究区域和检测方法不是异质性来源;发表偏倚及敏感性分析提示文献存在发表偏倚;试验序贯分析提示需纳入更大的样本量验证CAPAP对SAP的诊断效能.结论 尿液CAPAP可以作为SAP诊断困难时的辅助指标,仍需多中心、大样本、前瞻性的研究予以验证.

目的 研究清解化攻方调节重症急性胰腺炎(SAP)模型大鼠肠道菌群及对肠黏膜屏障的影响.方法 采用雨蛙素联合脂多糖腹腔注射法复制SAP大鼠模型,观察各组大鼠生存状态,检测大鼠血清中血清淀粉酶、白细胞介素10(IL-10)、IL-18、IL-1β水平,观察大鼠胰腺及小肠组织的病理变化,检测大鼠小肠组织中闭合蛋白(Occludin)、闭锁连接蛋白1(ZO-1)、高迁移率族蛋白B1(HMGB1)的表达水平;利用16SrRNA高通量测序检测大鼠肠道菌群结构和相对丰度.结果 经清解化攻方干预后,SAP模型大鼠腹部膨胀症状明显减轻,精神状态恢复较好;血清中血清淀粉酶、IL-18水平显著降低(P＜0.05),IL-10水平显著升高(P＜0.05);胰腺组织坏死区域、炎症细胞浸润减少,肠上皮细胞结构紊乱程度有所缓解,肠黏膜上皮脱落减少;小肠组织中HMGB1蛋白表达水平显著降低(P＜0.05),Occludin、ZO-1蛋白表达水平均显著升高(P＜0.05).16S rRNA高通量测序结果显示,清解化攻方可升高大鼠肠道拟杆菌门、乳酸杆菌属等益生菌群的相对丰度,减少厚壁菌门等有害菌群的定植.结论 清解化攻方可通过上调小肠组织Occludin、ZO-1蛋白表达,下调HMGB1蛋白表达,改善肠黏膜屏障损伤,并可调节不同菌群的相对丰度从而达到保护肠道的作用.