Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan最新文献

Objective: To eliminate ineffective or interfering compounds from the eight absorbed compounds (8ACs), identify the primary ACs that represent the multifunctional therapeutic effects of Zhiqiao (Fructus Aurantii Submaturus) and Houpo (Cortex Magnoliae Officinalis) (FM), along with elucidating their underlying mechanisms.

Methods: Key multifunctional ACs were screened through ex vivo-to-in vitro extrapolation (ex vivo dose = serum concentration) and validated in vivo, with efficacy assessed via contribution (dose = FM content). Functional magnetic resonance imaging analyzed brain regions's blood oxygen level-dependent (BOLD) changes, and the molecular mechanisms were analyzed by transcriptome of the dentate gyrus (DG).

Results: The results showed that representative 2ACs (Nobiletin + Magnolol) and 3ACs (Nobiletin + Magnolol + Meranzin hydrate) screened on ex vivo experiment by the criteria of contribution ranking contributed 80.72% -126.74% of the antidepressant and prokinetic effects of the FM (improvement of depressive-like behaviours, gastrointestinal disorder, monoamine neurotransmitters, ghrelin, endocrine hormones, pro-inflammatory factors, oxidative stress indicators). In addition, 3ACs demonstrated superiority over 2ACs in improving depression and levels of multiple stress mediators. Zhiqiao (Fructus Aurantii Submaturus) (FRA) reduced acute stress-induced hyperactivation of the cingulate cortex, thalamus, hypothalamus, and entorhinal cortex and elevated BOLD signaling in the insular cortex, temporal association cortex. Furthermore, FRA upregulated pathways of neurotransmitter receptor activity and serotonergic synaptic function and downregulated inflammation-related pathways at the genetic level.

Conclusion: 2ACs and 3ACs closely reflected FM's multifunctional effect in antidepressant and prokinetic. FRA restores stress-impaired neural connectivity in functional brain regions and improves synaptic plasticity and neurogenesis at the genetic level.

Objective: To investigate the pharmacological effects and underlying mechanisms of Pinggan Yuyin Qingre formula (, PGYYQR) in the treatment of meibomian gland dysfunction (MGD) through network pharmacology and in vivo validation.

Methods: A mouse model of MGD was induced using the stearoyl-coenzyme a desaturase 1 inhibitor, followed by PGYYQR treatment for 2 weeks. MGD sign scoring, hematoxylin and eosin (HE) staining, oil red o (ORO) staining, and serum inflammatory cytokine analysis were conducted to assess the effects of PGYYQR on meibomian gland (MG) function, histopathology, and associated inflammation. Network pharmacology was employed to identify the active compounds and potential targets of PGYYQR. Molecular mechanisms were further investigated using Western blotting, reverse transcription quantitative real-time polymerase chain reaction, and reactive oxygen species (ROS) assays.

Results: PGYYQR treatment significantly reduced the scores of MG orifice obstruction and meibum quality in MGD mice. HE and ORO staining further demonstrated that PGYYQR ameliorated glandular damage and lipid dysfunction. Enzyme-linked immunosorbent assay results revealed that PGYYQR markedly decreased the serum levels of key inflammatory cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor-α. Network pharmacology identified 162 active compounds and 598 target genes in PGYYQR. Among these, IL-6, IL-1β, matrix metalloproteinase-9, and C-X-C motif chemokine ligand 8 were recognized as core targets related to MGD and were mainly enriched in the IL-17/ nuclear factor kappa B (NF-κB) signaling pathway. Further molecular analyses confirmed that PGYYQR significantly inhibited the IL-17/NF-κB axis by downregulating IL-17 expression and reducing phos-phorylated NF-κB p65 levels at both the protein and mRNA levels in MG tissues. PGYYQR also effectively reduced ROS levels in the conjunctival tissues of MGD mice.

Conclusion: PGYYQR effectively improves MG function and preserves local tissue morphology in MGD model mice, primarily by suppressing the inflammatory response through coordinated modulation of the IL-17/NF-κB signaling pathway and oxidative stress.

Objective: To investigate the effects of Jinlida granules (, JLD) on body weight, glucose tolerance, intestinal inflammation and barrier function in high-fat diet (HFD)-induced obese rats and explore the regulation of the gut microbiota as a potential treatment mechanism.

Methods: Sprague-Dawley rats were divided into control, HFD, low-dose JLD (L-JLD), high-dose JLD (H-JLD), and sitagliptin groups. The rats, with the exception of those in the control group, were fed a HFD to establish an obesity model while simultaneously receiving 0.5% carboxymethyl cellulose, L-JLD, H-JLD or sitagliptin for 25 weeks. We assessed body weight, conducted oral glucose tolerance tests, and analysed faecal samples using metagenomic sequencing. Haematoxylin-eosin (HE), Masson and immunohistochemical (IHC) staining were employed to evaluate histological changes in the colon tissue. Immunofluorescence (IF) staining was used to measure the expression levels of Zonula occludens-1 (ZO-1) and Claudin-1 in colon tissue. The colon tissue was also subjected to transcriptomic evaluation.

Results: JLD treatment significantly reduced body weight and enhanced glucose tolerance in obese rats. It alleviated colonic tissue damage, decreased collagen deposition, inhibited macrophage infiltration, and increased the expression of the tight junction proteins ZO-1 and Claudin-1. Metagenomic analysis revealed JLD-induced shifts in the gut microbiota composition (increasing the abundance of Turicibacter, Faecalibaculum, Coriobacteriaceae and Lactobacillus reuteri), enriching beneficial bacteria and metabolic pathways (increasing the biosynthesis of various secondary metabolites, ascorbate and aldarate metabolism, oxidative phosphorylation, C5-branched dibasic acid metabolism and beta-alanine metabolism). Transcriptomic analysis revealed downregulation of inflammatory and immune pathways (inhibition of the tumour necrosis factor signalling pathway, advanced glycation end products-receptor for advanced glycation end products signalling pathway, toll-like receptor signalling pathway, and interleukin-17 signalling pathway), suggesting a comprehensive modulatory effect of JLD on intestinal health and metabolic function.

Conclusions: JLD granules effectively improve glucose tolerance and ameliorate obesity-related intestinal dysfunctions in HFD-induced obese rats. These benefits are likely mediated through the modulation of the gut microbiota, the suppression of intestinal inflammation, the enhancement of barrier function, and the attenuation of proinflammatory pathways. Our findings offer novel insights into the therapeutic potential of JLD, emphasizing its role in integrating gut microbiota management into the treatment of metabolic disorders.

Objective: To explore the bioactive constituents, key targets, signalling pathways, and molecular mechanisms of Lianshi Jianpi formula (, LSJPF) in the treatment of impaired glucose tolerance (IGT) through network pharmacology, molecular docking, and in vivo experiments.

Methods: The active ingredients and targets of LSJPF were identified using the Traditional Chinese Medicine Systems Pharmacology and HERB databases, whereas the IGT-related targets were sourced from GeneCards, DisGeNET, and PubMed. The overlap analysis identified potential targets of LSJPF. Protein-protein interaction networks and core targets were evaluated using the Search Tool for the Retrieval of Interacting Genes/Proteins and Cytoscape, and molecular docking confirmed the binding affinities. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed using Metascape. The therapeutic mechanisms were validated in an animal IGT model.

Results: LSJPF contained 229 compounds, with 15 active compounds and 77 potential target proteins. The phosphatidylinositol-3-kinase (PI3K)-protein kinase B (AKT) signalling pathway emerged as a key IGT pathway. The KEGG enrichment analysis revealed the pivotal genes RAC-alpha serine/threonine-protein kinase (AKT1), heat shock protein 90 kDa alpha B1, and B-cell lymphoma 2 family protein, which predominantly interact with beta-sitosterol and beta-carotene, the major constituents of Semen Euryales, Semen lablab Album, Semen sojae Atricolor in LSJPF. Molecular docking revealed strong binding affinities between LSJPF and IGT-related targets. In an animal IGT model, LSJPF treatment prevented weight loss; reduced food and water intake; decreased blood glucose levels; improved insulin resistance; decreased serum triglyceride, cholesterol, and low-density lipoprotein cholesterol levels; alleviated liver pathology; and significantly increased the levels of phosphorylated adenosine 5'-monophosphate-activated protein kinase (AMPK), PI3K, and AKT, suggesting its potential role in regulating glucose and lipid metabolism.

Conclusions: These findings reveal the potential of LSJPF as an IGT intervention that targets the AMPK/PI3K/AKT cascade, validating network pharmacology predictions and highlighting the role of multipathway mechanisms in metabolic diseases.

Objective: To assess the efficacy of point application therapy (PAT) in alleviating the exacerbation of chronic respiratory diseases represented by bronchial asthma.

Methods: In this multicenter randomized placebo-controlled trial, eligible bronchial asthma patients received placebo PAT on the dog days of the first summer to establish a baseline, and then patients who continued to participate in the trial and repassed the eligibility review were randomized to receive regular or placebo PAT in the next two consecutive summers. The primary outcome was the change from baseline in the number of asthma exacerbations at 24 months. Secondary outcomes included severity of asthma exacerbation, asthma control test (ACT) score, percentage of forced expiratory volume in 1 s (FEV₁) to the predicated value (FEV₁%pred), peak expiratory flow (PEF), ratio of FEV₁ to forced vital capacity (FEV₁/FVC), and use of palliative drugs during bronchial asthma exacerbations at 12 and 24 months. The adverse events (AEs) were also assessed.

Results: A total of 835 patients with bronchial asthma were randomized in this trial. Compared with the placebo control, the PAT significantly decreased the mean number of asthma exacerbations (1.42; 95% confidence interval, 0.69 to 2.14; P < 0.001), and increased the FEV₁%pred at 24 months (P = 0.039) and FEV₁/FVC at 12 months (P = 0.01) and 24 months (P = 0.01). There were no significant differences between the groups in PEF or ACT score at 12 and 24 months, or in FEV₁%pred at 12 months. Treatment-related AEs were mild and more common in the PAT group than in the placebo PAT group. No serious AEs were reported.

Conclusion: PAT conducted on dog days could reduce asthma exacerbations in patients with bronchial asthma.

Objective: To elucidate the anti-inflammatory mechanisms of modified Shoutai pills (, MSTP) in miscarriages, we performed transcriptome sequencing on the decidua and placental tissues of pregnancy mice.

Methods: The therapeutic effects and anti-inflammatory mechanisms of MSTP were studied in mice with lipopolysaccharide (LPS)-induced miscarriage. First, the effects of MSTP on pregnancy outcomes and the maternal-fetal interface, in LPS-induced miscarriage mice were examined. RNA sequencing was used to further investigate gene expression changes in LPS-induced miscarriage mice and to assess the effects of MSTP intervention. Finally, the expression levels of inflammation-related genes in the decidua and placental tissues were determined using quantitative real-time polymerase chain reaction (qRT-PCR).

Results: A high dose of MSTP significantly decreased the resorption rate (P < 0.05) and reduced apoptosis of the decidua and placental tissues in mice. Gene ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses showed that inflammatory and immune-related signals were enriched. qRT-PCR results confirmed that in decidual and placental tissues, MSTP reduced the gene expression levels of toll-like receptor 4 (TLR4), nuclear factor kappa-B (NF-κB), c-Jun N-terminal kinase 1, p38, and tumor necrosis factor-α.

Conclusions: In this study, we demonstrated that MSTP effectively prevented embryo loss with an anti-inflammatory mechanism through downregulation of the TLR4-NF-κB/ MAPK signaling pathway, in LPS-induced miscarriage mice model. To our knowledge, this is the first study to reveal the therapeutic mechanism of MSTP in LPS-induced miscarriage in mice.

Objective: To develop an expert consensus on kidney deficiency syndrome (KDS) in pregnant women and construct a validated self-reported KDS Patient-Reported Measures Pregnancy Scale (KDS-PRMs-Pregnancy Scale) for early identification and management.

Methods: The study was conducted in three phases. First, a comprehensive review of Traditional Chinese Medicine (TCM) literature and diagnostic criteria was performed, generating initial KDS symptoms for pregnancy. Second, a two-round Delphi survey, involving 21 experts from TCM, obstetrics, and gynaecology, assessed importance, relevance, and appropriateness of the items. Third, a psychometric evaluation was conducted, including exploratory factor analysis and internal consistency assessment.

Results: In the first Delphi round, 19 items were flagged for revision or removal due to expert variability, with 12 items deemed irrelevant. In the second round, consensus was reached, resulting in a 25-item scale. After psychometric evaluation, seven items were removed due to poor factor loadings, leaving an 18-item scale. Three factors-physiological discomfort, fatigue & weakness, and excretion abnormalities-accounted for 78.4% of the variance. The final scale demonstrated excellent internal consistency (Cronbach's alpha = 0.959).

Conclusion: The validated 18-item KDS-PRMs-Pregnancy Scale is a reliable tool for assessing KDS in pregnant women. Future research should focus on validation in diverse populations and exploring its predictive validity for pregnancy outcomes.

Berberine, an isoquinoline quaternary alkaloid, is a molecule with significant therapeutic adaptability. It has been identified, isolated, and measured in a wide range of plant families and species. Of these, Berberis stands out as a significant natural source of berberine, with Berberis vulgaris (B. vulgaris) bark being one of the most notable. The numerous health benefits associated with berberine include its potential use in the treatment of diseases, such as cancer, cardiovascular diseases, diabetes, and neurological disorders. The principal use of berberine has been for its antidiarrheal properties, which may have several modes of action. Its potent antioxidant and anti-inflammatory effects are responsible for its preventive action against stomach ulcers, and it has been found to kill dangerous gut bacteria while boosting the species and numbers of health-promoting bacteria. It protects the colon by influencing the production of several immune factors in addition to upregulating the Wnt-β creatinine signaling cascade. Berberine has shown its potential in regulating cholesterol metabolism by elevating the levels of low-density lipoprotein receptor in the liver. This review comprehensively examines the pharmacokinetics, multifaceted bioactivities, and gut-protective roles of berberine, providing a detailed analysis of its diverse physiological functions and potential clinical applications to advance the understanding and management of gastrointestinal diseases.

Objective: To elucidate the therapeutic efficacy and mechanism of action of Chaihu Guizhi Ganjiang decoction (, CGGD) in autoimmune hepatitis.

Methods: CGGD components and potential target genes were extracted from previously published databases. The autoimmune hepatitis (AIH)-related regulatory genes were obtained from the DisGeNET database. Intersections were taken, and enrichment analyses were performed on the extracted data. Concanavalin A (ConA)-induced AIH model mice were treated with CGGD via gavage. The results of network pharmacological analysis were experimentally validated.

Results: Network pharmacology revealed 228 genes at the intersection of AIH and CGGD. Kyoto Encyclopedia of Genes and Genomes analysis revealed that CGGD primarily regulates the phosphoinositide 3-kinase (PI3K)/ protein kinase B (AKT) signaling pathway and cellular metabolism in AIH. Gene Ontology enrichment analysis revealed that CGGD modulates inflammation through transcription factor-mediated signaling pathways. As predicted, CGGD attenuated ConA-induced AIH in a dose-dependent manner by activating the PI3K/AKT signaling pathway. Histopathological assessment confirmed the protective effects of CGGD against ConA-induced AIH. Further investigation revealed that CGGD regulated the T helper cell 17 (Th17)/regulatory T cell (Treg) balance by modulating the PI3K/Akt/ nuclear factor kappa-B (NF-κB) pathway.

Conclusions: This study demonstrated the therapeutic effect of CGGD on AIH through a combination of network pharmacological prediction and experimental validation. Its mechanism of action involves PI3K/Akt/ NF-κB-mediated regulation of Th17/Treg cells.

Objective: To compare the efficacy of Tongxie Yaofang (, TXYF) versus pinaverium bromide for the treatment of diarrheal irritable bowel syndrome (IBS-D) with liver depression and spleen deficiency.

Methods: A search of the China National Knowledge Infrastructure Database, China Science and Technology Journal Database, Wanfang Database, PubMed, EMBASE, Cochrane Library and Web of Science databases was conducted from database creation to the 28th of September 2022. Meta-analysis was performed using Revman 5.4 software.

Results: Twelve randomized controlled trials comprising 1058 patients were included in the analysis. TXYF was more efficacious in improving the clinical symptoms of patients. Comparison of the efficacy rate, Traditional Chinese Medicine Evidence Score (TCM-PES), self-rating anxiety scale anxiety score, self-rating depression scale depression score, adverse reaction rate and calcitonin gene-related peptide (CGRP) levels showed that TXYF was significantly superior to pinaverium bromide treatment (P < 0.05); there was no statistically significant difference in the plasma vasoactive peptide level between the two groups (P > 0.05). Funnel plots of the total efficacy rate and TCM-PES were asymmetrically distributed, suggesting publication bias. The GRADEpro Guideline Development Tool was also used to evaluate the studies, and the evidence rating of the included studies was not high.

Conclusions: Although the results of this study suggest that TXYF may be superior for the treatment of IBS-D with liver depression and spleen deficiency, as compared to pinaverium bromide, definitive conclusions are unable to be drawn at this time due to flaws in the overall design of the included trials. Therefore, more rigorous trials are needed to determine the benefit and safety of TXYF.