OBJECTIVES:To explore the mechanism of Xiezhuo Jiedu Recipe (XZJD) for improving ulcerative colitis (UC). METHODS:SD rat models of UC were randomized into 5 groups (n=10) for daily gavage with saline, mesalamine, or low-, medium- or high-dose XZJD for 14 days, with 10 normal rats with saline gavage as the control group. Pathological changes in the colon of the rats were observed using HE staining, and serum IL-6, IL-10 and IL-17 levels and their expressions in the colon tissues were determined with ELISA and immunohistochemistry. The expressions of occludin and ZO-1 and percentages of Th17 and Treg cells in the colon tissues were detected using immunofluorescence staining and flow cytometry; the mRNA and protein expressions of ROR-γt and Foxp3 were detected with RT-PCR and Western blotting. RESULTS:The rat models of UC showed obvious colonic mucosal damage with massive inflammatory cell infiltration, increased IL-6 and IL-17 levels and lowered IL-10 level in both the serum and colonic tissues, reduced expression levels of occludin and ZO-1, increased Th17 and lowered Treg cell percentages, increased RORγt mRNA and protein expressions, and reduced Foxp3 mRNA and protein expressions in the colonic tissue. Treatment with XZJD significantly alleviated inflammatory response in the colonic mucosa and effectively reversed the changes in IL-6, IL-17 and IL-10 levels, expressions of occludin and ZO-1, percentages of Th17 and Treg cells, and the expressions of RORγt and Foxp3 in the colonic tissues of UC rats. CONCLUSIONS:XZJD can alleviate pathologies in the colonic mucosa in UC rats possibly by regulating Th17/Treg immune balance.

The genetic architecture underlying traits associated with Type 1 Gaucher disease (GD1) remains insufficiently explored. We integrated genomic structural equation modeling and multiple post-genome-wide association study (GWAS) methodologies to prioritize candidate SNPs associated with GD1-related variation, identifying 15 loci with strong statistical support. Subsequently, diverse transcriptome-wide association approaches were employed to pinpoint susceptibility gene signals strongly correlated with GD1. For selected candidate genes, we explored the potential structural consequences of missense variants using integrated structure prediction, molecular dynamics simulations, and AI-based thermodynamic stability analyses. These analyses suggested that the mutations may alter protein structure and dynamics, with possible consequences for protein stability and biological function. Next, we screened a large set of publicly available traits to identify GD1-related factors and biomarkers with potential relevance. Finally, a summary data-based polygenic risk score (PRS) was utilized to examine risk associations between 22 autosomes and GD1. Collectively, by modeling a GD1-related phenotype without direct prior measurement, this study provides an initial overview of the shared genetic architecture associated with GD1.

Background:ATG16L1 (Autophagy Related 16 Like 1) is a key regulatory protein in the autophagy pathway. Although previous studies have established a significant association between the ATG16L1 genotype and Crohn's disease (CD) susceptibility, the specific molecular mechanism of its high-frequency missense variant rs2241880 has yet to be systematically elucidated. Methods:In this study, we first confirmed the important role of ATG16L1 in CD pathogenesis through genome-wide association study analysis and Western blot, as well as qRT-PCR. Subsequently, high-precision structural prediction, protein model-based dynamic simulation, and AI model thermodynamic stability analysis were innovatively integrated. The thermal shift assay (TSA) was employed to validate the structural stability of the mutant, while the pull-down assay was used to examine its binding capacity with WIPI2b. Results:The results show that ATG16L1 plays a significant role in the pathogenesis of CD. The mutation causes the protein's overall conformation to become more compact, significantly increasing the rigidity of key functional regions, and enhancing the structural and thermodynamic stability, which in turn affects the cleavage efficiency of caspase-3 and the function of the WD40 domain. The results of the TSA experiment provided evidence for the computational findings. The pull-down assay confirmed that the binding capacity of the mutant to WIPI2b was significantly impaired. Conclusion:This finding not only provides the first molecular mechanism of the ATG16L1 T300A mutation, offering an important theoretical basis for understanding CD susceptibility differences, but also provides insights for precision medicine interventions and gene editing strategies.

The pathogenesis and treatment of colorectal cancer (CRC) continue to be areas of ongoing research, especially the benefits of traditional Chinese medicine (TCM) in slowing the progression of CRC. This study was conducted to investigate the effectiveness and mechanism of action of modified Lichong decoction (MLCD) in inhibiting CRC progression. We established CRC animal models using azoxymethane/dextran sodium sulfate (AOM/DSS) and administered high, medium, or low doses of MLCD or mesalazine (MS) for 9 weeks to observe MLCD alleviation of CRC. The optimal MLCD dose group was then subjected to metagenomic and RNA sequencing (RNA-seq) to explore the differentially abundant flora and genes in the control, model and MLCD groups. Finally, the mechanism of action was verified using WB, qRT‒PCR, immunohistochemistry and TUNEL staining. MLCD inhibited the progression of CRC, and the optimal effect was observed at high doses. MLCD regulated the structure and function of the intestinal flora by decreasing the abundance of harmful bacteria and increasing that of beneficial bacteria. The differentially expressed genes were mainly associated with the Wnt/β-catenin pathway and the cell cycle. Molecular biology analysis indicated that MLCD suppressed the Wnt/β-catenin pathway and the epithelial–mesenchymal transition (EMT), inhibited abnormal cell proliferation and promoted intestinal epithelial cell apoptosis. MLCD mitigated the abnormal growth of intestinal epithelial cells and promoted apoptosis, thereby inhibiting the progression of CRC. This inhibition was accomplished by modifying the intestinal microbiota and disrupting the Wnt/β-catenin pathway and the EMT. Therefore, MLCD could serve as a potential component of TCM prescriptions for CRC treatment.

Objective: To explore the mechanism of Shugan Jianpi Qingre Fang in the treatment of functional dyspepsia (FD) by using ultrahigh-performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UHPLC-QTOFMS). Methods: 30 clean healthy Wistar rats were randomly divided into 3 groups, of 10 rats: Normal Group, Model Group and Shugan Jianpi Qingre Group. The functional dyspepsia model was made by "Guo's clamping tail method" and "irregular feeding method". The model time was 7 days. The rats in the traditional Chinese Medicine Group were given 13.98 G/kg/D of Shugan Jianpi Qingre Fang, and the rats in the normal group and the model group were given the same volume of distilled water once daily for 14 days. On the 22nd day of the experiment, the rats in each group were euthanized, blood was collected, plasma samples were prepared and metabonomics analysis was performed, to estimate the differential metabolites (15 potential biomarkers, such as Choline, proline, Taurine, glutamic acid, Glutathione, l-citrulline, Tryptophan, and eicosapentaenoic acid (EPA)) and find the main differential metabolic pathways. Results: In the model group, the level of estrone significantly increased whereas the level of the other metabolites significantly decreased. After the intervention of "Shugan Jianpi Qingre Fang", the level of Choline, proline, Taurine, glutamic acid and mannose in the plasma of the model group significantly regressed. It is better to include figures and p values. Conclusions: Shugan Jianpi Qingre Fang may play an important role in the treatment of Functional Dyspepsia, by regulating glucose metabolism, energy metabolism, affecting nerve signal transduction and enhancing antioxidant capacity. Compound Chinese medicine has the characteristics of multi-angle and multi-target.

Ulcerative colitis (UC) is a chronic and immune-mediated inflammatory disorder characterized by abdominal pain, diarrhoea, and haematochezia. The goal of clinical therapy for UC is mucosal healing, accomplished by regenerating and repairing the intestinal epithelium. Paeoniflorin (PF) is a natural ingredient extracted from Paeonia lactiflora that has significant anti-inflammatory and immunoregulatory efficacy. In this study, we investigated how PF could regulate the renewal and differentiation of intestinal stem cells (ISCs) to improve the regeneration and repair of the intestinal epithelium in UC. Our experimental results showed that PF significantly alleviated colitis induced by dextran sulfate sodium (DSS) and ameliorated intestinal mucosal injury by regulating the renewal and differentiation of ISCs. The mechanism by which PF regulates ISCs was confirmed to be through PI3K-AKT-mTOR signalling. In vitro, we found that PF not only improved the growth of TNF-α-induced colon organoids but also increased the expression of genes and proteins related to the differentiation and regeneration of ISCs. Furthermore, PF promoted the repair ability of lipopolysaccharide (LPS)-induced IEC-6 cells. The mechanism by which PF regulates ISCs was further confirmed and was consistent with the in vivo results. Overall, these findings demonstrate that PF accelerates epithelial regeneration and repair by promoting the renewal and differentiation of ISCs, suggesting that PF treatment may be beneficial to mucosal healing in UC patients.

目的:探讨泄浊解毒方对溃疡性结肠炎(UC)大鼠肠道菌群、白细胞介素-10(IL-10)的影响.方法:50只雄性Wistar大鼠中随机抽取8只大鼠设为对照组,其余42只大鼠采用2,4,6-三硝基苯磺酸(TNBS)诱导UC模型,3 d后处死两只大鼠,确定是否造模成功.将剩余40只大鼠随机分成模型组、柳氮磺吡啶组及泄浊解毒方低、中、高剂量组,每组8只,分别给予相应药物.连续给药14 d后,观察大鼠症状和体征、结肠黏膜损伤指数、结肠组织形态、血清中白细胞介素-10(IL-10)含量,以及粪便中乳酸杆菌、双歧杆菌、肠杆菌、肠球菌含量.结果:造模后成功复制UC模型,粪便中乳酸杆菌、双歧杆菌含量减少,肠杆菌、肠球菌含量增多,IL-10含量减少.治疗后,泄浊解毒方各组大鼠症状及体征明显改善,粪便中乳酸杆菌、双歧杆菌含量升高,肠杆菌、肠球菌含量降低,IL-10含量升高,且泄浊解毒方高剂量组效果优于其他组.结论:泄浊解毒方对UC大鼠结肠黏膜损伤具有显著保护作用,以高剂量组为佳,其机制可能与调节肠道菌群平衡、增强血清中抗炎因子IL-10的释放有关.

Aim To predict the targets of Modified Danggui Shaoyao San（MDSS） in the treatment of chronic atrophic gastritis（CAG） based on network pharmacology and vertify the results based on experimention. Methods TCMSP,SWISS TARGETS,GENE CARDS and OMIM databases were used to screen the therapeutic targets of MDSS for CAG. STRING database and Cytoscape software were used to construct the protein interaction network and screen the core targets. Metascape database was used for GO analysis and KEGG enrichment pathways. And molecular docking was used for target validation. CAG rat model was prepared by N-methyl-N′-nitroso-N-nitroguanidine free drink combined with sodium salicylate gastric lavage. The pathology of rat gastric mucosa was observed by hematoxylin-eosin staining, and the ultrastructure of epithelial cells was observed by transmission electron microscopy. The serum IL-6 and IL-10 content was detected by enzyme-linked immunosorbent assay, and the expression of JAK2,STAT3,p-STAT3,c-MYC mRNA and protein in rats was detected by qPCR and Western blot. Results MDSS acted on 189 targets, mainly involved in response to oxidative stress and apoptotic signaling pathway. KEGG analysis related to pathways in cancer and JAK-STAT signaling pathway. The experimental results showed that the MDSS could improve the degree of atrophy of gastric mucosa in CAG rats and improve the status of epithelial cells, down-regulate the serum IL-6 content of CAG rats, up-regulate the IL-10 content, and reduce the expression of JAK2,STAT3,p-STAT3,c-MYC mRNA and protein in gastric mucosa with statistical significance. Conclusions MDSS treats CAG through multiple active ingredients, targets, and pathways, the mechanism of which may be related to the inhibition of the JAK2/STAT3 signaling pathway.

溃疡性结肠炎(ulcerative colitis, UC)是一种慢性非特异性肠道炎性疾病,病因未明,反复发作,目前尚无彻底治愈的方法. 有研究显示,近 30 年来中国UC发病率快速上升,目前仍未达到最高峰,预计在接下来的25 年里将持续增加[1] . 中国中西医结合学会消化系统疾病专业委员会在 2010 年、2017 年分别制(修)订了《溃疡性结肠炎中西医结合诊疗共识》(以下分别简称2010 年《共识》 、2017 年《共识》),为该病的诊断与治疗提供了有效的指导.

Objective:To explore the potential mechanism of Tianshui Dichang Decoction in the treatment of ulcerative colitis through network pharmacology and experimental verification.Methods:The active components and targets of Tianshui Dichang Decoction were screened by TCMSP. The related targets of ulcerative colitis were screened by OMIM, GeneCard and TTD databases, and the effective component targets of Tianshui Dichang Decoction were intersected with the potential targets of ulcerative colitis. The PPI network was constructed by STRING database to screen the core targets, and the "Chinese materia medica-disease-active components-target" network was constructed by Cytoscape 3.8.0 software. GO function and KEGG pathway enrichment analysis were carried out using Metascape database. 48 mice were divided into control group, model group, mesalazine group (0.3 g/kg) and Tianshui Dichang Decoction low-, medium-, and high-dosage groups (7.5,15 and 30 g/kg) according to random number table method, with 8 mice in each group. Except the control group, the ulcerative colitis model was established in other groups. After 7 days of intervention with corresponding drugs, the disease activity index (DAI) was scored, the pathological changes of colon were observed by HE staining, and the expressions of IL-6, STAT3mRNA and protein in colon tissue were detected by PCR and Western blot methods.Results:Totally 127 active components in Tianshui Dichang Decoction and 560 targets of ulcerative colitis were obtained. 89 intersecting targets of Tianshui Dichang Decoction and ulcerative colitis were obtained, and the core targets included IL6, TNF, IL1B, AKT1, TP53, VEGFA, JUN, PTGS2, CXCL8, CCL2, STAT3, MMP9 and so on. Oxidative stress response, lipopolysaccharide metabolism, bacterial response, signal transduction and other biological processes were mainly involved, mainly through the cancer pathway, IL17, TNF, MAPK and other signal pathways to play a role in the treatment of ulcerative colitis. The results of experimental verification showed that the DAI score, the expressions of IL-6 and STAT3 protein in colon tissue of Tianshui Dichang Decoction medium- and high-dosage groups.decreased ( P<0.05). The levels of IL-6 and STAT3 mRNA in colon tissue decreased in the Tianshui Dichang Decoction low-, medium- and high-dosage groups.groups ( P<0.05). Conclusion:Tianshui Dichang Decoction has a certain therapeutic effect on UC through component-multitarget-signal pathway, and its mechanism is related to regulating IL-6/STAT3 signal pathway and inhibiting intestinal mucosal inflammation.

目的:采用网状Meta分析的方法评价不同中成药联合西药治疗慢性萎缩性胃炎(CAG)的疗效及安全性.方法:计算机检索相关数据库,筛选各数据库建库至2021年1月1日所发表的不同中成药治疗CAG的随机对照试验(RCT),按照"Cochrane风险偏倚评估工具"进行质量评价,应用Stata 14.0进行数据分析.结果:最终纳入32个RCTs,涉及6种口服中成药,3 962例患者.网状Meta分析结果显示:在提高临床疗效方面排序为:摩罗丹＞气滞胃痛颗粒＞胃苏颗粒＞枳术宽中胶囊＞香砂养胃丸＞胃复春片分别联用常规西药;在提高胃镜疗效方面排序为:摩罗丹＞香砂养胃丸＞胃复春片＞枳术宽中胶囊＞气滞胃痛颗粒分别联用常规西药;在Hp根除率方面排序为:枳术宽中胶囊＞气滞胃痛颗粒＞摩罗丹颗粒分别联用常规西药;用药安全性方面:总体上治疗组相较于对照组不良反应发生的频次、类型明显下降,所有研究均未因不良反应事件而停药.结论:本研究初步评价了六种中成药在改善CAG结局指标方面的疗效及排序情况,但由于纳入研究的局限性,方法学质量普遍不高,应谨慎选择用药,未来仍需开展多中心、大样本、高质量的RCT予以验证.

目的 通过隐结构模型方法 诠释名老中医"调肝守恒"治疗慢性胃炎经验,运用网络药理学探讨"调肝守恒"核心组方治疗慢性胃炎的潜在靶标及作用机制.方法 利用TCMSP数据库筛选组方具有成药可能性较大以及口服吸收较佳的候选活性成分;通过GeneCards数据库筛选获得慢性胃炎相关预测靶点,并与潜在活性成分的作用靶点进行交集分析,获得组方治疗慢性胃炎的靶点;采用Cytoscape软件,构建"药物-活性成分-作用靶点"网络图;借助String数据库平台构建蛋白质相互作用网络,筛选核心靶点;利用Cytoscape软件中的ClueGO插件对共同作用靶蛋白进行GO生物功能注释与KEGG富集分析.结果 发现组方中包含的59个候选成分可能作用于疾病的101个靶点,候选成分中槲皮素、木犀草素、山柰酚可能是组方发挥作用的关键成分,生物学功能涉及凋亡、增殖、炎症反应等多方面,交集基因富集于MAPK信号通路、PI3K/AKT信号通路等经典炎症-肿瘤信号通路.结论 隐结构模型方法 诠释名老中医遣方用药以"调肝守恒"为路法,提供临床实践用药范式与借鉴.组方治疗慢性胃炎是多靶点、多成分、多通路的复杂过程,其可能是通过调节以上关键蛋白表达及信号通路,来发挥改善慢性胃炎相关症状,延缓、阻断炎-癌转化的作用.

目的:基于网络药理学和实验验证,探讨香连化浊方治疗慢性萎缩性胃炎(CAG)的作用机制.方法:利用中药系统药理学技术平台(TCMSP)、SWISS TARGETS数据库、基因组注释数据库平台(GENE CARDS)、在线人类孟德尔遗传数据库(OMIM)筛选香连化浊方和疾病的作用靶点,利用STRING数据库、Cytoscape软件构建蛋白互作网络,筛选核心靶点,利用Metascape数据库进行基因本体论(GO)分析与京都基因与基因组百科全书(KEGG)通路富集分析.制备CAG大鼠模型后予香连化浊方干预治疗,观察大鼠胃黏膜组织病理学改变,采用免疫组化、实时荧光定量聚合酶链式反应(qPCR)对核心靶点进行验证.结果:网络药理学结果显示香连化浊方中口服利用度较高的成分有珊瑚甙、过氧化苯甲酰内酯、芍药花酮等;主要活性成分槲皮素、木犀草素、山柰酚等作用于192个靶点,生物学途径主要为参与蛋白磷酸化正调控、氧化应激反应、损伤应答、凋亡信号通路等;细胞组分主要包括膜侧、膜筏、细胞外基质、细胞质的核周围区域等;分子功能包括激酶结合、转录因子结合、蛋白域特异性结合、蛋白激酶活性等.KEGG富集通路与磷脂酰肌醇-3-激酶-丝氨酸苏氨酸蛋白激酶(PI3K-AKT)信号通路、肿瘤坏死因子信号通路、细胞凋亡通路.实验验证研究发现香连化浊方治疗后大鼠胃黏膜萎缩病理程度减轻,胃组织核心靶点AKT1、C-MYC的蛋白表达明显下调(P＜0.05),胃组织Cmyc mRNA表达明显下调(P＜0.05).结论:香连化浊方中有效成分槲皮素、木犀草素、山柰酚等可能通过下调Cmyc mRNA、AKT1、C-MYC蛋白表达抑制胃黏膜细胞过度增殖实现对CAG的治疗作用.

目的 探讨疏肝化浊中药对幽门螺杆菌相关性慢性萎缩性胃炎患者生活质量的影响.方法 选取2018年1月～2019年1月共收治90例罹患慢性萎缩性胃炎患者作为研究对象,根据给药方案不同将患者分为中药组(n=30)、西药组(n=30)和中西药组(n=30),中药组患者给予疏肝化浊中药治疗,西药组患者给予雷贝拉唑肠溶胶囊+阿莫西林+左氧氟沙星胶囊+胶体果胶铋治疗,中西药组患者用药方法同中药组和西药组,比较三组临床疗效、胃镜病理评分、中医证候评分以及生活质量评分.结果 治疗后,中西药组胃镜病理评分和中医证候评分均低于中药组和西药组,且中西药组总有效率明显高于中药组和西药组,差异均有统计学意义(P<0.05);治疗后,中西药组生活质量评分明显高于中药组和西药组(P<0.05).结论 中西药合用对改善患者症状,治疗幽门螺杆菌相关性萎缩性胃炎方面的优势明确,能够改善胃内环境,减轻杀菌药物的不良反应.

慢性萎缩性胃炎是以胃黏膜上皮和腺体萎缩、数目减少甚至消失,或伴有肠上皮化生、异型增生等为特征的慢性消化系统疾病."心之浊毒"是国医大师李佃贵教授"浊毒理论"的重要组成部分,其创新性提出从"心之浊毒"论治慢性萎缩性胃炎,以化浊解毒、宁心健脾为治则,创立化浊解毒养心方,并辨证辅以芳香化浊开心窍、温燥祛浊健心阳、清热泄浊除心火、养血祛浊安心神、重镇降浊定心志、活血排浊通心脉法,取效颇佳.

张锡纯认为胃气以降为顺,胃气不降导致胃痞发生,而胃气不降之关键在于五脏功能失常,即心肺阳虚、肝脾失调、肾虚冲逆皆可引起胃气不降而致胃痞.据此,张锡纯认为应从五脏论治胃痞,提出通降胃气、宣通心肺、行气利湿、升肝扶脾、纳肾降冲等治法,并自拟理饮汤、升降汤、理痰汤等方,灵活运用生赭石、厚朴、清半夏、桂枝、茵陈、生麦芽、白术等药物,值得学习借鉴.

目的 基于肠道菌群变化探讨健脾泄浊解毒方对缓解期溃疡性结肠炎(UC)模型大鼠复发的干预效果.方法 在85只大鼠中随机取10只作为空白组,剩余75只大鼠通过结肠灌注2,4,6-三硝基苯磺酸(TNBS)与50％乙醇的混合液进行第1次造模(期间死亡3只),再将剩余72只大鼠随机分为模型组、柳氮磺胺吡啶组、健脾泄浊解毒方低剂量组及健脾泄浊解毒方高剂量组,每组18只,各组再随机处死2只大鼠观察以确定造模成功.除空白组正常喂养外,模型组予0.9％氯化钠注射液10 mL/kg灌胃,柳氮磺胺吡啶组予柳氮磺胺吡啶混悬液0.3 g/kg灌胃,健脾泄浊解毒方低、高剂量组分别予健脾泄浊解毒方药液8.0、16.0 g/kg灌胃.灌胃14 d后空白组随机取5只大鼠,其余各组随机取8只大鼠,处死后留取粪便标本,并将模型组、柳氮磺胺吡啶组、健脾泄浊解毒方低剂量组及健脾泄浊解毒方高剂量组剩余大鼠再次予TNBS与50％乙醇的混合液进行第2次灌注造模,继续正常喂养2 d后,各组大鼠全部处死,留取粪便标本.比较各组大鼠第1次造模治疗后及第2次造模后粪便标本中乳酸杆菌、双歧杆菌、肠杆菌及肠球菌DNA相对表达情况.结果 与第1次造模治疗后比较,柳氮磺胺吡啶组及健脾泄浊解毒方低剂量组第2次造模后乳酸杆菌及双歧杆菌相对表达量均降低(P<0.05),肠杆菌及肠球菌相对表达量均升高(P<0.05),空白组、模型组及健脾泄浊解毒方高剂量组第2次造模后乳酸杆菌、双歧杆菌、肠杆菌及肠球菌相对表达量比较差异无统计学意义(P>0.05).第2次造模后组间比较,模型组乳酸杆菌及双歧杆菌相对表达量均低于空白组(P<0.05),肠杆菌及肠球菌相对表达量均高于空白组(P<0.05);健脾泄浊解毒方高剂量组乳酸杆菌及双歧杆菌相对表达量均高于模型组(P<0.05),肠杆菌及肠球菌相对表达量均低于模型组(P<0.05),而柳氮磺胺吡啶组及健脾泄浊解毒方低剂量组乳酸杆菌、双歧杆菌、肠杆菌及肠球菌相对表达量与模型组比较差异均无统计学意义(P>0.05).结论 高剂量健脾泄浊解毒方能以肠道菌群为作用靶点,通过提高乳酸杆菌、双歧杆菌相对含量,降低肠杆菌、肠球菌相对含量,使有益菌较有害菌数量占据主导,调节肠道菌群紊乱状态,进而维持肠道微环境的长久稳态,保持机体健康,有效预防UC复发.

目的:系统评价青黛制剂治疗溃疡性结肠炎的疗效与安全性.方法:采用系统评价方法,检索中国知网、万方数据知识服务平台、中国生物医学文献数据库(CBM)、维普中文期刊服务平台、PubMed数据库、Cochrane Library数据库、Embase数据库、Cochrane临床对照试验中心注册数据库(CENTRAL),检索时间为各数据库建库至2021年6月1日,收集青黛制剂治疗溃疡性结肠炎的随机对照试验(RCT),根据纳入排除标准对相关文献资料进行筛选、提取,应用Cochrane风险偏倚评估工具对纳入文献进行质量评价,采用Revman 5.3软件进行Meta分析.结果:共纳入文献34篇,涉及溃疡性结肠炎患者2596例.Meta分析结果显示,青黛制剂治疗溃疡性结肠炎的临床疗效优于对照组,差异有统计学意义[RR=1.17,95％CI(1.12,1.23),P<0.00001],且单用青黛制剂治疗[RR=1.17,95％CI(1.08,1.27),P=0.0002]与青黛联合对照组药物治疗[RR=1.16,95％CI(1.11,1.23),P<0.00001]的临床疗效比较,差异无统计学意义(P>0.05);观察组在改善患者肠镜疗效[RR=1.18,95％CI(1.06,1.31),P=0.003]及中医证候积分[SMD=-0.41,95％CI(-0.64,-0.19),P=0.004]方面均优于对照组,差异均有统计学意义(P<0.05),安全性指标结果较好.结论:青黛制剂治疗溃疡性结肠炎疗效确切,在临床疗效、肠镜疗效、中医证候积分方面具有优势,且安全性较好,但受纳入文献数量及质量影响,上述结论尚需更多高质量文献进行验证.

肝脾同调为治疗消化系统疾病常见的治法,又是张仲景治未病思想的体现,肝脾在五行中相互克制,功能上相互依存.仲景善从脾论治六经病变,调和肝脾亦为仲景组方之一大原则,掌握肝脾同调的理论精髓,对于消化系统诸多疾病的治疗、转归及预后意义重大.

慢性萎缩性胃炎( chronic atrophic gastritis, CAG)又称为胃癌前期病变,主要是由于胃黏膜上皮反复遭受损害而出现的一种慢性难治性消化系统疾病.内镜下可见黏膜红白相间,以白为主,皱襞变平,甚则消失;病理可见固有腺体萎缩、肠化[1].临床表现为上腹部胀满、疼痛,嗳气,食欲不振,消瘦等.近年来,由于人们的生活习惯与饮食结构的改变,CAG的发病率正在逐年递增.