Objective To explore the pharmacological mechanism of the traditional Chinese medicine（TCM） herbal pair of Rhizomacoptidis and Artemisia capillaris in the treatment of chronic atrophic gastritis（CAG） based on the network pharmacology and molecular docking.Methods The active ingredients, targets and molecular structures of the TCM herbal pair of Rhizomacoptidis and Artemisia capillaris searched in the traditional Chinese medicine systems pharmacology database and analysis platform（TCMSP）. The targets of CAG were searched in the GeneCards, the Comparative Toxicogenomics Database（CTD） and the Therapeutic Target Database（TTD）. Using the Cytoscape, a protein-protein interaction（PPI） network and a drug-ingredient-target-disease network diagram were established by introducing the intersections of the targets of both the TCM herbal pair of Rhizomacoptidis and Artemisia capillaris, and CAG. The common active ingredients and targets were obtained by a cluster analysis on the two networks, which were further subjected to GO and KEGG enrichment analyses using the Database for Annotation, Visualization and Integrated Discovery（DAVID）. Finally, molecular docking of the common active ingredients and targets was performed using the AutoDock and PyMOL. Results A total of 26 active ingredients were screened from the TCM herbal pair of Rhizomacoptidis and Artemisia capillaris, with 86 corresponding targets. A total of 639 targets of CAG were identified. Taking the intersection, a total of 38 targets were finally obtained. The core components are quercetin, isorhamnetin, β-sitosterol, etc Among them, interleukin 6（IL-6）, tumor necrosis factor（TNF）, Jun（Jun proto-oncogene） and others were above the average degree. GO enrichment analysis yielded 98 biological processes（BP）, including the positive regulations of the transcription of RNA polymerase II promoter, nitric oxide biosynthesis and gene expressions; 21 cell components（CC）, including extracellular space, extracellular region and cell surface; and 18 molecular functions（MF）, including enzyme binding, transcription factor binding and cytokine activity. KEGG pathway enrichment analysis obtained 54 pathways that were significantly enriched in the intersected targets, including cancer signaling pathways, TNF signaling pathway, and mitogen-activated protein kinase（MAPK） signaling pathway. Molecular docking data revealed an acceptable binding between the compounds and targets, that was favorable to form a stable structure. Conclusion Multiple active ingredients of the TCM herbal pair of Rhizomacoptidis and Artemisia capillaris are able to inhibit the aggravation of CAG to gastric cancer via multiple targets and signaling pathways, which may even reverse the atrophy.

目的 观察葛根芩连汤对幽门螺杆菌(Hp)感染人正常胃黏膜上皮(GES-1)细胞增殖与凋亡的影响及相关机制.方法 按照葛根芩连汤干预剂量的不同、是否有Hp感染将人GES-1 细胞分为空白对照组、模型组、葛根芩连汤低剂量组(10 μmol/L)、葛根芩连汤中剂量组(20 μmol/L)、葛根芩连汤高剂量组(40 μmol/L)及阳性药对照组(阿莫西林5 μmol/L).培养结束后,采用细胞增值检测分析法(CCK-8 法)检测细胞存活率,酶联免疫吸附法(ELISA)检测上清液肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)和IL-6 水平,流式细胞术检测细胞凋亡率,实时荧光定量聚合酶链式反应(RT-qPCR)检测细胞p38、丝裂原活化蛋白激酶2(MK2)mRNA表达,蛋白免疫印迹(Western bloting)法检测细胞p38、MK2 蛋白表达.结果 与空白对照组比较,模型组人GES-1 细胞存活率降低(P<0.05);与模型组比较,葛根芩连汤各剂量组与阳性药对照组人GES-1 细胞存活率均升高(P<0.05),且葛根芩连汤各剂量组效应呈剂量依赖性(P<0.05);阳性药对照组与葛根芩连汤高剂量组人GES-1 细胞存活率比较差异无统计学意义(P>0.05).与空白对照组比较,模型组TNF-α、IL-1β和IL-6 均升高(P<0.05);与模型组比较,葛根芩连汤各剂量组与阳性药对照组TNF-α、IL-1β和IL-6 均降低(P<0.05),且葛根芩连汤各剂量组效应呈剂量依赖性(P<0.05);阳性药对照组与葛根芩连汤高剂量组TNF-α、IL-1β和IL-6 比较差异均无统计学意义(P>0.05).与空白对照组比较,模型组人GES-1细胞凋亡率升高(P<0.05);与模型组比较,葛根芩连汤各剂量组和阳性药对照组人GES-1 细胞凋亡率降低(P<0.05),且葛根芩连汤各剂量组效应呈剂量依赖性(P<0.05);阳性药对照组和葛根芩连汤高剂量组人GES-1 细胞凋亡率比较差异无统计学意义(P>0.05).与空白对照组比较,模型组人GES-1 细胞p38、MK2 mRNA和蛋白表达水平均升高(P<0.05);与模型组比较,葛根芩连汤各剂量组和阳性药对照组人GES-1 细胞p38、MK2 mRNA和蛋白表达水平均降低(P<0.05),且葛根芩连汤各剂量组效应呈剂量依赖性(P<0.05);阳性药对照组和葛根芩连汤高剂量组人GES-1 细胞p38、MK2 mRNA和蛋白表达比较差异均无统计学意义(P>0.05).结论 葛根芩连汤可有效提高Hp感染后人GES-1 细胞增殖率,同时降低细胞凋亡水平,其机制可能与抑制p38/MK2 信号通路、降低细胞炎性反应有关.

Background: Infection with Helicobacter pylori (H. pylori) can cause chronic gastritis and other digestive tract diseases, and represents a public health concern. Current anti-H. pylori treatment can result in antibiotic resistance and other adverse reactions. Huangqi Jianzhong decoction (HQJZD) is a prescription form of traditional Chinese medicine for chronic gastritis that increases probiotics and inhibits H. pylori. In this study, its anti-bacterial activity against H. pylori receives a preliminary evaluation, and a pharmacology analysis is performed to predict its underlying mechanisms. Methods: Human GES-1 cells are divided into a blank control group, a model group, a HQJZD low-dose (2.08 mg·mL−1), a high-dose group (4.16 mg·mL−1), and a positive control group (amoxicillin, 5 μg·mL−1). After culture, the CCK-8 method is used to detect cell viability; flow cytometry is used to detect cell apoptosis rate; and RT-qPCR is used to detect the expression of mRNA virulence factors, including HpPrtC, OPiA, IceA1, and BabA2. Network pharmacology analysis and molecular docking were performed to explore the mechanisms of HQJZD in treating H. pylori gastritis, based on its anti-H. pylori infection effect. Results: We noted lower cell survival rates in the model group, but higher apoptosis rates and mRNA expressions of HpPrtC, OPiA, IceA1, and BabA2 than in the control group (p < 0.05). Compared to the model group, the cell survival rate of each dosage group of Huangqi Jianzhong decoction and the positive control group increased significantly, while the apoptosis rate and the mRNA expressions of HpPrtC, OPiA, IceA1, and BabA2 were decreased significantly. The effect in each HQJZD group was dose-dependent (p < 0.05). Network pharmacological analysis involving 159 signaling pathways was used to screen 6 key active components of HQJZD and 102 potential target proteins for the treatment of H. pylori-related gastritis. The molecular docking results revealed that the 6 active compounds had a strong binding ability with the target proteins of ALB, IL-6, AKT1, IL-1B, and JUN. Conclusion: HQJZD effectively increases the proliferation rate of human GES-1 cells after infection, while reducing the level of apoptosis. The mechanism may be related to multiple components, multiple targets and pathways, which provides a scientific basis for further elucidating the mechanism of action, the pharmacodynamic material basis, and the clinical application of HQJZD against H. pylori infection.

目的 研究急性胰腺炎患者辅助性T细胞17(Th17)/调节性T细胞(Treg)细胞平衡与白细胞介素23(IL-23)/白细胞介素17(IL-17)炎症轴的关系.方法 选择2018年6月—2021年6月河北省中医院收治的63例急性胰腺炎患者为观察组,另于同期选择63名健康成年人作为对照组,其中观察组依据急性胰腺炎严重程度分为轻度急性胰腺炎(MAP)19例、中度急性胰腺炎(MSAP)23例、重度急性胰腺炎(SAP)11例.检测两组外周血Th17、Treg细胞比例和血清IL-23、IL-17水平,比较观察组和对照组、不同严重程度急性胰腺炎患者的Th17、Treg、IL-23、IL-17水平,以Person系数检验急性胰腺炎患者Th17/Treg细胞平衡与IL-23/IL-17炎症轴的相关性.结果 与对照组相比,观察组Th17水平、Th17/Treg值较低,Treg、IL-23、IL-17水平较高(P<0.05);Th17、IL-23、IL-17水平及Th17/Treg值比较,MAPMSAP>SAP(P<0.05);经相关性分析,Th17、Th17/Treg值与IL-23、IL-17呈正相关,Treg与IL-23、IL-17呈负相关,差异有统计学意义(P<0.05).结论 IL-23、IL-17、Th17、Treg水平均与急性胰腺炎患者的严重程度相关,并且随着炎症反应的加重,Th17/Treg比值增加,Th17/Treg细胞失衡越来越严重,这对临床治疗急性胰腺炎有一定指导意义.

目的 解析真实世界京津冀地区溃疡性结肠炎患者的中医证候分布规律,为该病临床治疗提供借鉴.方法 基于国家中医临床研究基地(河北省中医院)建立的医院信息系统数据库,对京津冀地区5家三甲医院第一诊断为溃疡性结肠炎的住院患者之入院科室、中医证候分布、性别与年龄分层的中医证候分布等真实世界数据进行描述性分析.结果 共有286例患者纳入分析,京津冀地区溃疡性结肠炎的中医分布依次为浊毒内蕴证、脾虚湿阻证、肝郁脾虚证、瘀阻肠络证、脾肾阳虚证、寒热错杂证、热毒炽盛证.性别分层结果显示,男性以浊毒内蕴证最常见,女性以肝郁脾虚证最为常见.年龄分层分析结果显示,18岁以下患者以肝郁脾虚证多见,18～45岁患者以浊毒内蕴证多见,46～65岁患者以浊毒内蕴证多见,65岁以上患者以脾肾阳虚证多见.结论 京津冀地区溃疡性结肠炎患者总体以浊毒内蕴证最为常见,而不同性别、年龄分层证候分布特点各有不同.

目的 观察化浊解毒方对溃疡性结肠炎(UC)模型大鼠结肠黏膜病理形态及血清肿瘤坏死因子α(TNF-α)、γ干扰素(IFN-γ)含量的影响,探讨其作用机制.方法 将60只雄性Wistar大鼠按照随机数字表法分为正常组15只及造模组45只,造模组采用2,4,6-三硝基苯磺酸(TNBS)/乙醇法诱导UC大鼠模型,并将造模成功的大鼠(42只)按照随机数字表法分为模型组、美沙拉嗪组及化浊解毒方组,每组14只.造模后,模型组予蒸馏水4 mL/(kg·d)灌胃;美沙拉嗪组予美沙拉嗪混悬液0.3 g/(kg·d)灌胃;化浊解毒方组予化浊解毒方混悬液20 g/(kg·d)灌胃.灌胃14 d后,比较各组大鼠疾病活动指数(DAI)评分、结肠黏膜损伤指数(CMDI)评分及血清TNF-α、IFN-γ含量.结果 与正常组比较,模型组、美沙拉嗪组、化浊解毒方组DAI评分均升高(P＜0.05);与模型组比较,美沙拉嗪组、化浊解毒方组DAI评分均降低(P＜0.05);与美沙拉嗪组比较,化浊解毒方组DAI评分降低(P＜0.05).与正常组比较,模型组、美沙拉嗪组、化浊解毒方组溃疡、炎症及病变深度评分均升高(P＜0.05);与模型组比较,化浊解毒方组溃疡、炎症及病变深度评分均降低(P＜0.05),美沙拉嗪组溃疡、炎症评分均下降(P＜0.05),病变深度评分无明显变化(P＞0.05);与美沙拉嗪组比较,化浊解毒方组溃疡、炎症及病变深度评分均降低(P＜0.05).与正常组比较,模型组血清TNF-α、IFN-γ均升高(P＜0.05),美沙拉嗪组、化浊解毒方组血清TNF-α均升高(P＜0.05);与模型组比较,美沙拉嗪组、化浊解毒方组血清TNF-α、IFN-γ均降低(P＜0.05);与美沙拉嗪组比较,化浊解毒方组血清TNF-α、IFN-γ均降低(P＜0.05).结论 化浊解毒方能够调整血清细胞因子,进而调控免疫机制,降低DAI,改善UC模型大鼠结肠黏膜的病理损伤.

目的 观察化浊解毒方对溃疡性结肠炎(UC)模型大鼠血清白细胞介素(IL)-6、IL-10含量及结肠黏膜中CD4+、CD8+T淋巴细胞表达的影响.方法 将60只健康Wistar大鼠随机分为4组,即空白组、模型组、美沙拉嗪组、化浊解毒方组.采用2,4,6-三硝基苯磺酸(TNBS)/乙醇复合法建立UC大鼠模型,各组分别灌胃生理盐水及相应药物.计算各组大鼠的疾病活动指数(DAI)评分,采用酶联免疫吸附法检测大鼠血清IL-6、IL-10的含量,采用免疫组化法检测大鼠结肠黏膜中CD4+、CD8+T淋巴细胞的表达.结果 与空白组比较,模型组大鼠DAI评分、血清IL-6含量、结肠黏膜中CD8+T淋巴细胞表达水平明显升高,血清IL-10含量及结肠黏膜中CD4+T淋巴细胞表达水平明显降低,差异均有统计学意义(P＜0.05);与模型组比较,美沙拉嗪组与化浊解毒方组大鼠DAI评分、血清IL-6含量、结肠黏膜中CD8+T淋巴细胞表达水平明显降低,血清IL-10含量及结肠黏膜中CD4+T淋巴细胞表达水平明显升高,差异均有统计学意义(P＜0.05);美沙拉嗪组与化浊解毒方组大鼠结肠黏膜中CD4+T淋巴细胞表达水平比较差异有统计学意义(P＜0.05).结论 化浊解毒方能明显降低血清促炎因子IL-6含量,升高血清抑炎因子IL-10含量,调节结肠黏膜T淋巴细胞的表达,从而减轻、抑制炎症反应.

随着人民群众对中医药服务需求的不断增长,近年来,中医药事业取得了快速发展,中医医院职业化管理受到越来越多的关注和重视.中医医院职业化管理方法在职业化管理诸因素中居于关键地位.文章从战略管理、文化管理、流程管理、现场管理四个方面阐述了河北省中医院职业化管理方法的探索实践,论证引入职业化管理方法对于快速提升中医医院管理水平、提高医院综合服务能力发挥着关键作用.