The etiology of gastric cancer (GC) is increasingly defined by the complex interplay within the oral-gastric microbial axis. This conceptual shift extends beyond the classical Helicobacter pylori (H. pylori) model. Instead, it encompasses a broader polymicrobial network. Mechanisms underlying ectopic colonization of oral pathobionts are examined alongside their synergistic contributions to mucosal dysbiosis. Remodeling of the tumor microenvironment is discussed through the analysis of critical functional modules, including biofilm formation, metabolic reprogramming, and immune dysregulation. Carcinogenesis is reportedly promoted by specific genotoxic metabolites and perpetuation of chronic inflammation. Diagnostic capabilities are evaluated with a focus on noninvasive biomarkers, where integration of artificial intelligence for risk stratification is identified as a transformative tool for early detection. Furthermore, therapeutic perspectives are expanded by evidence linking microbial composition to the efficacy of immune checkpoint inhibitors and chemotherapy. Strategies for prevention and treatment are proposed based on restoration of microbial homeostasis. Collectively, a roadmap for translating microbiome research into personalized clinical practice for gastrointestinal malignancies is provided by this review.

Introduction: Liver inflammation in Non-Alcoholic Fatty Liver Disease (NAFLD) is shaped by immune regulation. This study examines the contribution of immune-related genes to NAFLD pathogenesis. Methods: Single-cell analysis identified key immune cell clusters and subtypes. Differential expression, machine learning, and expression profiling were used to screen key genes, which were then used to construct a nomogram predicting NAFLD risk. Immune infiltration analysis characterized immune states, and pseudotime analysis tracked key gene expression along T-cell differentiation. Reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blotting were used to validate gene expression. Results: T cells were identified as the key immune cells, with regulatory T cells (Tregs) as the critical subtype. CXCR4, DUSP1, and ID2 were downregulated in NAFLD and supported a nomogram with good predictive performance. Immune infiltration analysis showed differences in six immune cell types, including Tregs, between NAFLD and controls. Pseudotime analysis showed increased CXCR4, DUSP1, and ID2 expression in Tregs and cytotoxic T lymphocytes (CTLs) at late differentiation, while NAFLD samples showed reduced DUSP1 and ID2 expression in RT-qPCR and Western blot assays. Discussion: Treg-centered immune dysregulation and the downregulation of CXCR4, DUSP1, and ID2 are closely linked to NAFLD pathology. The context-dependent nature of these genes precludes simple protective or pathogenic labels. The nomogram capturing single-cell-derived immune signatures outperforms conventional clinical predictors and offers mechanistic insight. Pseudotime analysis provides the first continuous view of T-cell activation trajectories in NAFLD. A ceRNA network involving NEAT1/XIST and miR-15b-5p may explain DUSP1 suppression. However, small validation cohorts (n = 3/group), the absence of functional experiments, and PBMC-based profiling limit causal inference; replication in larger intrahepatic cohorts is necessary before clinical translation. Conclusion: T cells, especially Tregs, and CXCR4, DUSP1, and ID2 are central to Non-Alcoholic Fatty Liver Disease and may serve as diagnostic and therapeutic targets.

INTRODUCTION:Salvianolic acid B (SAB), as one of the major water-soluble compounds of Salvia miltiorrhiza, has proved to effectively reduce elevated portal pressure in cirrhotic rats. However, the short halflife and in vivo retention time of SAB affect its pharmacodynamics. Therefore, in this study, we prepared albumin nanoparticles loaded with SAB (SAB-ALB-NPs) to improve the in vivo retention time of the drug and enhance bioavailability. METHODS:We prepared and characterized SAB-ALB-NPs, including particle size, polydispersity index (PDI), zeta potential, stability, EE, in vitro release, and pharmacokinetics. Subsequently, we investigated the effects and potential mechanisms of SAB-ALB-NPs in CCl4-induced portal hypertension (PHT) mice models, and it was found that angiotensin-II (Ang-II) induced proliferation and contraction in hepatic stellate cells (HSCs). The CCl4 (0.3:1 in corn oil, 1mL/kg) was injected repeatedly, leading to the PHT mice model. The effect of SAB-ALB-NPs on PHT mice was evaluated by hematoxylin-eosin, Sirius red staining, immunohistochemistry, and Western blot. RESULTS:We successfully prepared SAB-loaded albumin nanoparticles with smaller-sized particles, lower PDI and zeta potential with stable properties, and higher EE. Importantly, the SAB-ALB-NPs notably prolonged the in vitro release of SAB. SAB-ALB-NPs significantly reduced portal pressure, inhibited inflammation (decrease the concentration of TNF-α and IL-6) and hepatotoxicity of the liver (down-regulated the level of ALT and AST) against fibrous tissue hyperplasia, and reduced collagen deposition in the liver. Afterward, we used Ang-II to facilitate the proliferation of HSCs and induce HSC cell contraction. Cotreatment of SAB-ALB-NPs markedly inhibited Ang II-induced effects on cell proliferation and contraction and improved apoptosis. Importantly, SAB-ALB-NPs were preliminarily found to inhibit the expression of RhoA and ROCK II in Ang-II- treated HSC and CCl4-induced PHT mice, suggesting that SAB-ALB-NPs may participate in the regulation of RhoA/ROCK II pathway. CONCLUSION:SAB-ALB-NPs improved portal hypertension by suppressing inflammation and inhibiting HSCs activation and proliferation to attenuate liver fibrosis. This therapeutic function of SAB-ALB-NPs may be owing to SAB-ALB-NPs regulating the RhoA/ROCK2 pathway, which may be one of its molecular mechanisms for reducing portal hypertension.

BACKGROUND:Hepatocellular carcinoma accounts for 90% of primary liver malignancies and ranks as the fourth leading cause of global cancer mortality. DNA methylation drives HCC pathogenesis by orchestrating tumor suppressor silencing and oncogenic pathway activation, fundamentally governing tumor heterogeneity and therapeutic resistance. While alterations in white blood cell counts have emerged as independent prognostic indicators in HCC progression, their causal relationship with tumor epigenetics remains unclear. Given that HCC tumors actively secrete cytokines and remodel systemic immunity through epigenetic mechanisms, peripheral white blood cell dynamics serve as a compelling surrogate for studying tumor-driven immune dysregulation and identifying methylation-based therapeutic targets. METHODS:We integrated DNA methylation profiles from The Cancer Genome Atlas-Liver Hepatocellular Carcinoma (TCGA-LIHC) with summary statistics from six genome-wide association studies of white blood cell counts. Using these data, we applied a two-sample Mendelian Randomization (MR) framework to systematically investigate the causal effects of HCC-related CpG sites on white blood cell counts. The robustness of our findings was established through stringent criteria, comprehensive sensitivity analyses, and Bayesian colocalization, followed by functional validation with TCGA data and a transcriptome-wide association study (TWAS). RESULTS:Our analysis identified 26 HCC-specific CpG sites with causal effects on white blood cell counts. A multi-step validation pipeline integrating Bayesian colocalization and tumor-specific expression analysis robustly confirmed three core mediator genes: BTN3A2, TRIM27, and S100A12. TWAS provided independent, gene-level validation, revealing BTN3A2 as a powerful regulator of lymphocyte and neutrophil counts, TRIM27 as a key immunometabolic checkpoint, and S100A12 as a modulator of innate immunity. CONCLUSION:This study establishes epigenome-immune crosstalk in HCC by identifying BTN3A2, S100A12 and TRIM27 as central methylation-immunoregulatory hubs. The discovered methylation-immune axes provide mechanistic insights for developing combination therapies targeting epigenetic checkpoints to reverse immunosuppressive microenvironments in advanced HCC.

Background:Peptic ulcer (PU) and cardiovascular disease (CVD) are significant chronic illnesses, particularly in the elderly. This study investigates the relationship between PU and CVD in older adults and the impact on mortality risk. Methods:This study was conducted utilizing data from a nationwide health survey of the elderly in China. Kaplan-Meier curves and log-rank tests were applied in survival analysis to evaluate mortality differences between the groups. Stratified models were applied to evaluate the effects of factors. Results:This study included 3,636 participants. CVD was significantly associated with an increased PU risk (OR = 1.31, 95%CI 1.03-1.66, p = 0.04), while PU had no significant effect on CVD incidence (OR = 1.08, 95%CI 0.77-1.51, p = 0.64). Mortality risk was significantly higher in the CVD group (HR = 1.22, 95%CI 1.03-1.45, p = 0.02) compared to the non-comorbid group. No significant difference in mortality was observed between the PU-only and combined PU-CVD groups. Stratified analysis identified advanced age (≥75 years) (HR = 1.45, 95%CI 1.06-1.87, p < 0.01) and male gender (HR = 1.29, 95%CI 1.05-1.62, p < 0.01) as significant mortality risk factors among PU patients. Conclusion:PU does not have a significant impact on overall mortality or the prognosis of CVD patients. CVD was a risk factor for PU, but PU did not significantly increase CVD risk. A higher mortality risk was observed in older and male PU patients. These findings suggest the need for gender-sensitive and age-stratified management strategies for PU in high-risk groups.

Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as the most prevalent chronic liver disease worldwide, but there has long been a lack of effective therapeutic drugs. Thyroid hormone (TH) and its receptor THR-β play pivotal roles in hepatic metabolism, positioning THR-β as a promising therapeutic target for MASLD. Notably, Resmetirom, a selective THR-β agonist, gained FDA approval in 2024 for MASLD treatment, and several other THR-β agonists are currently undergoing preclinical or clinical studies. While these agents demonstrate effective in alleviating hepatic steatosis, inflammation, and fibrosis in MASLD, the disease heterogeneity and drugs' adverse reactions remain key challenges. Therefore, further research is necessary to comprehensively assess their clinical efficacy and safety. This review summarizes the mechanisms by which TH/THR-β influences MASLD and recent advances in THR-β-targeted pharmacotherapy, aiming to enhance understanding of its therapeutic potential and promote drug development and clinical applications.

Liver cirrhosis is the terminal stage of various acute and chronic liver diseases and ranks 11th among the most common causes of death worldwide. In recent years, with the progress of clinical research, there has been increasing support from evidence-based medicine for the treatment of liver cirrhosis with integrated traditional Chinese and Western medicine. In 2023, the Chinese Association of Integrative Medicine, the China Association of Chinese Medicine, and the Chinese Medical Association jointly released the first evidence-based guideline in this field, the Guidelines for Integrated Traditional Chinese and Western Medicine Diagnosis and Treatment of Liver Cirrhosis. By combining the latest research at home and abroad, this article provides a detailed interpretation of the highlights in the guideline, including traditional Chinese medicine etiology and pathogenesis, diagnostic progress, disease and syndrome combination, stage-based diagnostic mode, and treatment strategies of integrated traditional Chinese and Western medicine. The aim is to enhance understanding of this guideline among health workers and promote the improvement of the diagnosis and treatment of liver cirrhosis with integrated traditional Chinese and Western medicine.

Abstract Background Previous literature has explored the relationship between chronic atrophic gastritis (CAG) and isolated cancers within the upper gastrointestinal cancers; However, an integrative synthesis across the totality of upper gastrointestinal cancers was conspicuously absent. The research objective was to assess the relationship between CAG and the risk of incident upper gastrointestinal cancers, specifically including gastric cancer, oesophageal cancer, and oesophagogastric junction cancer. Methods Rigorous systematic searches were conducted across three major databases, namely PubMed, Embase and Web of Science, encompassing the timeline from database inception until August 10, 2023. We extracted the necessary odds ratio (OR) and their corresponding 95% confidence interval (CI) for subsequent meta-analysis. Statistical analyses were conducted using Stata 17.0 software. Results This meta-analysis included a total of 23 articles encompassing 5858 patients diagnosed with upper gastrointestinal cancers. CAG resulted in a statistically significant 4.12-fold elevated risk of incident gastric cancer (OR = 4.12, 95% CI 3.20–5.30). Likewise, CAG was linked to a 2.08-fold increased risk of incident oesophageal cancer (OR = 2.08, 95%CI 1.60–2.72). Intriguingly, a specific correlation was found between CAG and the risk of incident oesophageal squamous cell carcinoma (OR = 2.29, 95%CI 1.77–2.95), while no significant association was detected for oesophageal adenocarcinoma (OR = 0.62, 95%CI 0.17–2.26). Moreover, CAG was correlated with a 2.77-fold heightened risk of oesophagogastric junction cancer (OR = 2.77, 95%CI 2.21–3.46). Notably, for the same type of upper gastrointestinal cancer, it was observed that diagnosing CAG through histological methods was linked to a 33–77% higher risk of developing cancer compared to diagnosing CAG through serological methods. Conclusion This meta-analysis indicated a two- to fourfold increased risk of gastric cancer, oesophageal cancer, and oesophagogastric junction cancer in patients with CAG. Importantly, for the same upper gastrointestinal cancer, the risk of incident cancer was higher when CAG was diagnosed histologically compared to serological diagnosis. Further rigorous study designs are required to explore the impact of CAG diagnosed through both diagnostic methods on the risk of upper gastrointestinal cancers.

原发性胆汁性胆管炎(PBC)是一种病因与发病机制尚未明确的疾病.近几年,通过研究PBC患者代谢物质的改变来寻找其潜在的发病机制和治疗靶点已成为热门.代谢组学通过质谱分析和核磁共振技术对PBC患者的代谢谱进行全面的分析,可以为PBC的诊断和治疗提供帮助.该文综述了近年来代谢组学在PBC中的研究进展,以期为PBC的临床诊断和治疗提供新的思路.

Background: Circular RNA (circRNA) can regulate the progression of hepatocellular carcinoma (HCC). However, the role and potential mechanism of circ_0004913 in HCC are not explored. Methods: Circ_0004913 was identified from two GSE datasets (GSE94508 and GSE97322) as a differentially expressed circRNA between HCC and normal tissues. Levels of circ_0004913, microRNA-184 (miR-184), and hepcidin (HAMP) were determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell proliferation, migration, and invasion were estimated by methyl thiazolyl tetrazolium, colony formation, and Transwell assays, respectively. Levels of all proteins were examined by Western blot. Glucose consumption and lactate and ATP production were analyzed by the glucose, lactate, and ATP assay kits. Dual-luciferase reporter, RNA immunoprecipitation (RIP), and RNA pull-down assays were performed to verify the interactions among miR-184 and circ_0004913 or HAMP. The mice xenograft models were established to assess the effect of circ_0004913 on tumor growth in vivo. Results: Circ_0004913 was downregulated in HCC, and its expression impeded cell proliferation, migration, and invasion, EMT, and glycolysis in HCC cells. miR-184 was identified as a target miRNA of circ_0004913, and their expression levels were negatively correlated. miR-184 overexpression could reverse the inhibitory effect of circ_0004913 on HCC cell progression. Moreover, as a target gene of miR-184, HAMP expression was positively correlated with circ_0004913 expression in HCC tissues, and repression of miR-184 could inhibit the progression of HCC cells by increasing HAMP expression. Circ_0004913 could inhibit JAK2/STAT3/AKT signaling pathway and tumor growth in vivo by regulating the miR-184/HAMP axis. Conclusion: Circ_0004913 inhibited the tumorigenesis of HCC by sponging miR-184 to regulate HAMP expression in vitro and in vivo.

Background Qinggan Huoxue recipe (QGHXR), a traditional Chinese medicinal formula, has a protective effect against liver fibrosis. However, the underlying mechanisms remain unclear. Objective This study investigated the antifibrotic role of QGHXR and its underlying mechanisms. Methods The composition of QGHXR was determined using ultra performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS). Female C57BL/6J mice were fed either a Lieber–DeCarli liquid diet or pair-fed control diet and intraperitoneally injected with CCl4 for 8 weeks (n = 8). In week 5, the mice were administered 100, 200, and 400 mg/kg QGHXR via oral gavage daily for 4 weeks. Results UPLC-MS result showed that QGHXR contained 45 compounds including salvianolic acid A, scutellarin, baicalin, rutin, and chai saponin D. QGHXR alleviated pathological alterations in the liver. The alanine aminotransferase (ALT) level was reduced to 44.88 ± 4.39 U/L, aspartate aminotransferase (AST) to 76.25 ± 4.17 U/L, alkaline phosphatase (ALP) to 60.75 ± 5.41 U/L, and acetaldehyde to 38.54 ± 1.01 U/L compared with that of the control group (ALT 72.38 ± 5.19 U/L, AST 119.63 ± 9.82 U/L, and ALP 98.63 ± 6.71 U/L and acetaldehyde 64.86 ± 4.70 U/L). QGHXR inhibited lipid overproduction and fibrotic gene expression. The serum concentration of chemokine C-X-C ligand 16 (CXCL16) was reduced to 62.83 ± 6.80 pg/ml compared with that of the control group (130.91 ± 13.72 pg/mL). QGHXR downregulated CXCL16 mRNA and protein expressions. Pharmacological CXCL16 treatment reversed the QGHXR-induced protective effects in ethanol plus CCl4 fed mice. QGHXR reduced CXCL16 levels (91.97 ± 5.86 pg/ml) in LPS-stimulated RAW264.7 cells compared with that of the control group (148.68 ± 8.62 pg/ml) and inhibited toll-like receptor 4 and nuclear factor-kappa B phosphorylation. Conclusions This study demonstrated that QGHXR mitigates experimental alcoholic liver fibrosis by CXCL16 inhibition, and may be considered a potential therapeutic agent for treating liver fibrosis.

Background:In lean individuals, nonalcoholic fatty liver disease (NAFLD) is not a benign disease, and these patients have long-term morbidity and mortality similar to those of their nonlean counterparts. Finding biomarkers for noninvasive and early detection is urgent and microRNAs (miRNAs) show potential. The aims of this study were to investigate the potential role of serum miRNAs in the detection of lean NAFLD and to explore the possible pathogenesis of lean NAFLD.Methods:A total of 498 patients with NAFLD and 98 healthy controls were included to compare the clinical characteristics of lean NAFLD patients [LNs: body mass index (BMI) <23 kg/m2], nonlean NAFLD patients (NLNs: BMI ≥23 kg/m2) and normal healthy individuals (HIs). A total of 14 serum samples were collected from 4 LNs, 6 NLNs and 4 HIs for high-throughput profiling to identify altered miRNA expression patterns in lean NAFLD. The candidate miRNA, miR-4488, was identified by filtering based on studies in a second independent cohort (31 LNs, 62 NLNs, 72 HIs) that included quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Gene Ontology (GO) enrichment, Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment, and protein-protein interaction network analyses were performed to investigate the potential molecular mechanism of miR-4488 in lean NAFLD.Results:LNs were older and had a smaller waist circumference, lower levels of alanine aminotransferase, glutamyl transpeptidase, fasting insulin, and uric acid, lower HOMA-IR score, and higher levels of total cholesterol, high-density lipoprotein cholesterol, and hemoglobin (P<0.05). The serum level of miR-4488 was increased in LNs compared with HIs (P<0.0001) and NLNs (P=0.025). miR-4488 had acceptable performance in predicting [area under the curve (AUC) =0.794, 0.698] lean NAFLD. Moreover, GO and KEGG enrichment analyses revealed that the differentially expressed target genes were mainly involved in choline metabolism in cancer, the tumor-necrosis factor (TNF) signaling pathway and the p53 signaling pathway. PPI analysis identified ARHGAP1, SLC10A1 and SIX5 as the hub genes.Conclusions:Taken together, our findings indicate that serum miR-4488 is a potential biomarker for diagnosing and predicting the pathogenetic mechanisms of lean NAFLD.

OBJECTIVE:To explore the therapeutic effect and mechanism of Dachengqi decoction on patients with mild acute pancreatitis (MAP).METHODS:A parallel randomized controlled trial was conducted. Sixty-eight patients with acute pancreatitis (AP) admitted to Shanghai Traditional Chinese Medicine (TCM)-Integrated Hospital from March 2018 to February 2021 were enrolled. Referring to the condition on admission of the patients and whether they agreed to receive the Dachengqi decoction or not, they were divided into conventional treatment group and Dachengqi decoction group according to the principle of 1:1 equal randomness. Meanwhile, 20 healthy volunteers were recruited as controls. Both groups of patients were treated with octreotide, fasting, gastrointestinal decompression, antipyretic and analgesic, anti-inflammatory, inhibition of gastric acid and pancreatic juice secretion, maintenance of electrolyte balance and other western conventional medicine. The patients in the Dachengqi decoction group received Dachengqi decoction orally on the basis of routine treatment, 100 mL each time, twice a day, for seven consecutive days. The inflammation parameters [white blood cell count (WBC), C-reactive protein (CRP), procalcitonin (PCT), interleukin-6 (IL-6)] before and after treatment and the recovery time of gastrointestinal function (first exhaust time, time to recover bowel sounds, first defecation time) of patients were recorded. 16S rRNA gene sequencing of stool samples was recorded, and normalized data were obtained after quality control and other related processing. The data were subjected to diversity analysis (Alpha diversity and Beta diversity) and linear discriminant analysis effect size analysis (LEfSe analysis) to observe changes in the gut microbiota of MAP patients. Spearman rank correlation coefficient was used to analyze the correlation between inflammatory indexes and microorganisms at the intestinal genus level. Blood, urine, stool samples, renal function, and electrocardiogram (ECG) during treatment of MAP patients were detected to assess the safety of the treatment.RESULTS:Of the 68 patients with AP, 16 were excluded from moderate-severe AP, 4 were not collected or voluntarily abandoned treatment. Finally, 48 patients with MAP were enrolled, 24 in the conventional treatment group and 24 in the Dachengqi decoction group. The inflammation parameters levels at 7 days of treatment in both groups were significantly lower than those before treatment. CRP, PCT and IL-6 levels in the Dachengqi decoction group were significantly lower than those in the conventional treatment group [CRP (mg/L): 8.50 (3.50, 13.00) vs. 16.00 (9.25, 29.75), PCT (μg/L): 0.06 (0.03, 0.08) vs. 0.09 (0.05, 0.11), IL-6 (ng/L): 6.36 (3.96, 10.79) vs. 13.24 (6.69, 18.87), all P < 0.05]. The first exhaust time, time to recover bowel sounds and first defecation time in the Dachengqi decoction group were significantly shorter than those in the conventional treatment group [first exhaust time (days): 1.62±0.65 vs. 2.80±0.65, time to recover bowel sounds (days): 1.13±0.58 vs. 2.31±0.76, first defecation time (days): 3.12±0.75 vs. 4.39±0.76, all P < 0.05]. The analysis of intestinal microflora diversity showed that both the diversity and abundance of microbial communities were the highest in the healthy control group and the lowest in the conventional treatment group. In addition, the coincidence degree of microbial communities in healthy controls and MAP patients was small, while the coincidence degree of MAP patients among different treatment methods was relatively large. LEfSe analysis showed that Dachengqi decoction reduced the relative abundance of Escherichia coli-Shigella and Clostridium erysipelae, and increased the relative abundance of three beneficial bacteria, namely Lactobacillus, Rombutzia and Brutella. In the intestines of MAP patients, Lactobacillus mucilaginus and Lactobacillus conjunctus were significantly enriched. Correlation analysis showed that positive correlations between Escherichia coli-Shigella and the four inflammatory indicators including WBC, CRP, PCT, IL-6 were statistically significant (r value was 0.31, 0.41, 0.57, 0.43, respectively, all P < 0.05). There was no significant correlation between other bacteria and inflammatory indicators. During the treatment, there was no obvious abnormality in blood, urine and feces, renal function and ECG of MAP patients.CONCLUSIONS:Dachengqi decoction could reduce inflammatory responses and promote recovery of intestinal microecological balance and gastrointestinal function in patients with MAP by regulating the composition of intestinal flora. No significant adverse effects were observed during the treatment period.

目的:研究慢性胃炎辨属肝胃不和证患者运用疏肝调中汤加减的疗效.方法:采用前瞻性研究,选择2019年1月-2020年12月就诊的60例慢性胃炎且辨证属肝胃不和证的患者,采用随机数字表法,分为对照组和治疗组,每组30例.对照组予胃苏颗粒治疗,治疗组予疏肝调中汤治疗.对照组30例予胃苏颗粒治疗,治疗组30例予疏肝调中汤治疗.连续治疗1个月后进行指标评价.结果:治疗后,治疗组中医证候积分、胃功能三项(胃泌素-17、胃蛋白酶原Ⅰ、胃蛋白酶原Ⅱ)、血清炎症因子(表皮生长因子、白细胞介素-32、转化生长因子-β1)低于对照组(P<0.05),一氧化氮高于对照组,慢性胃炎患者报告结局指标量表之慢性胃炎模块(SSDPRO-CG)评分优于对照组(P<0.05),总有效率高于对照组(P<0.05).结论:疏肝调中汤加减治疗肝胃不和证慢性胃炎可有效调节患者的胃功能及炎症因子水平,显著提升疗效,使患者的生活质量获得较大改善.

Nonalcoholic fatty liver disease (NAFLD) is a general term for a series of liver diseases including simple steatosis, non-alcoholic steatohepatitis, liver fibrosis, which is closely related to metabolic syndrome. The pathogenesis of NAFLD is relatively complex, which has gradually changed from the previous 'two-hit' hypothesis to the current "multiple hits" hypothesis. However, there is currently no approved treatment for NAFLD in clinic, highlighting the urgent need for drug development. Peroxisome proliferator activated receptors (PPARs) are members of the nuclear receptor superfamily, whose different subtypes have been proved to regulate different stages of NAFLD, thus becoming promising drug targets for NAFLD. As important sources of drug development, natural products have been proven to treat NAFLD through multiple pathways and multiple targets. In this paper, we outline the regulatory role of PPARs in NAFLD, and summarize some natural products that target PPARs to ameliorate NAFLD, in order to provide reference for drug development of NAFLD.

酒精性肝病(ALD)囊括了一系列由于长期、大量的酒精摄入所致的肝脏疾病,根据疾病发展的进程以及相应的临床特征、病理生理表现,主要分为酒精性脂肪肝、酒精性肝炎及肝纤维化、酒精性肝硬化,严重者可发展至肝细胞癌,大致可与中医学的"酒伤""酒癖""酒疸""酒臌"等病证相对应.目前ALD尚无确切有效的治疗方法,主要以患者禁欲戒酒、营养支持、皮质类固醇、乙酮可可碱、肝移植等为主[1].近年来,许多专家学者对该病的认识逐渐深入,同时也展开了大量的临床及实验研究,成果显著,现试进行梳理.