BACKGROUND:Impaired efferocytosis is a key driver of plaque instability during atherosclerosis progression. Efficient clearance of apoptotic cells through efferocytosis relies on the coordinated action of multiple regulatory factors. METHODS:PubMed, Web of Science, ScienceDirect, OVID MEDLINE, and Scopus were searched for studies published up to February 7, 2026. Eligible preclinical studies were systematically reviewed to identify endogenous factors that regulate efferocytosis in atherosclerosis. Clinical evidence was also incorporated to enable a preliminary translational assessment of these regulatory factors. RESULTS:Thirty-five endogenous regulatory factors were identified from 36 included studies, and their functional roles across distinct stages of efferocytosis were characterized. Notably, metabolic regulators such as PKM2, PFKFB3, GLS1, and Drp1 were involved in distinct efferocytosis stages. This suggests that metabolic reprogramming may provide the metabolic support require for efficient efferocytosis and inflammation resolution. Ten factors were supported by preliminary clinical evidence consistent with preclinical data. PKM2 was the only candidate biomarker with prospective observational data. However, its independent predictive value still requires validation in multicenter prospective studies. CONCLUSIONS:This review provides a systematic synthesis of 35 endogenous efferocytosis regulators and elucidates their regulatory network in atherosclerosis based on a functional stage framework. Metabolic reprogramming is identified as a central hub linking efferocytosis efficiency to inflammation resolution. This review offers a new theoretical basis for efferocytosis-targeted intervention strategies.

This study aimed to investigate the effect of miRNAs differentially expressed in serum exosomes on endothelial cells after myocardial infarction. Specific pathogen-free male Sprague–Dawley rats with acute myocardial infarction (AMI) were established by ligating the anterior descending branch of the left coronary artery. Hematoxylin–eosin staining was used to detect myocardial histopathological changes during model evaluation. The differentially expressed miRNAs carried by the serum exosomes were detected using the Agilent Rat miRNA Gene Chip on the Illumina platform. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses were performed using the Database for Annotation, Visualization, and Integrated Discovery. The culture supernatant of hypoxic H9c2 cells was collected and centrifuged to obtain exosomes. The expression of miR-484 was verified using real-time fluorescence quantitative PCR (qRT‒PCR). miR-484 mimics were transfected into human umbilical vein endothelial cells (HUVECs) to construct cell models of miR-484 overexpression. Cellular proliferation, scratch wound, and tube formation assays were conducted with HUVECs. A dual-luciferase reporter assay was used to validate the target gene of miR-484. Serum exosomes were sequenced on an Illumina sequencing platform, and 22 differentially expressed miRNAs between the model and sham groups were detected (P < 0.05). Among them, miR-484 was prioritized for further evaluation, and its downregulation in MI serum exosomes was confirmed through both gene chip analysis and animal experiments. miR-484 expression increased in HUVECs after culture with exosomes from hypoxia-exposed H9c2 cells. miR-484 expression upregulation suppressed proliferation, migration, and vascular formation in HUVECs, indicating that miR-484 plays an antiangiogenic role. Bioinformatics analyses showed that rno-miR-484 and the VEGFA 3’UTR possess base binding sites. The dual-luciferase reporter assay showed that rno-miR-484 could significantly downregulate the expression of luciferase in r-Vegfa-3UTR-WT (P < 0.01). VEGFA expression was downregulated after miR-484 mimic transfection in HUVECs. Our study revealed that miR-484 may inhibit angiogenesis after myocardial infarction by targeting VEGFA, providing a novel focal point for the diagnosis and treatment of this disease.

ETHNOPHARMACOLOGICAL RELEVANCE:Xiaoqinglong Decoction (XQLD), a classic herbal formula for respiratory diseases, is clinically effective against chronic obstructive pulmonary disease (COPD). However, whether its anti-inflammatory effects involve modulation of macrophage immunometabolism remains unknown. AIM OF THE STUDY:This study investigated whether XQLD suppresses M1 macrophage polarization in COPD by modulating glycolysis-related pathways. MATERIALS AND METHODS:COPD was induced in rats by alternate intratracheal instillation of papain (Papa) and lipopolysaccharide (LPS). After modeling, the rats received XQLD at high, medium, and low doses, while a separate group received dexamethasone as the positive control. Therapeutic effects on pulmonary function and lung pathology were evaluated, along with M1 polarization by immunofluorescence and other assays. Core pathways were identified through transcriptomic-metabolomic integration. In vitro, XQLD-containing serum was used to treat THP-1-derived M1 macrophages, and M1 polarization, glycolytic indicators, and MET/AKT/HK2 pathway proteins were assessed following treatment with 2-DG, HK2 overexpression, or HGF. RESULTS:XQLD dose-dependently improved pulmonary function and lung pathology, and reduced M1 infiltration. Multi-omics identified MET and HK as central nodes; XQLD reversed aberrant MET/AKT/HK2 expression in vivo. In vitro, XQLD-containing serum inhibited M1 polarization, glycolytic flux, and HGF-induced MET/AKT/HK2 signaling, with its effects partially reversed by HK2 overexpression. CONCLUSION:XQLD attenuates M1 macrophage-driven airway inflammation by normalizing the MET/AKT/HK2 signaling-metabolic axis and suppressing, at least in part, HK2-dependent glycolysis. These findings provide a novel immunometabolic mechanism for the traditional anti-inflammatory efficacy of XQLD in COPD.

OBJECTIVE:This study aimed to investigate the therapeutic mechanisms of CY in treating UC using an integrated metabolomics and proteomics approach. METHODS:A murine UC model was induced using dextran sulfate sodium (DSS). The therapeutic efficacy of CY was evaluated via histological examination (H&E staining) of colon tissues to assess inflammation, epithelial necrosis, and crypt abscesses. Serum and colon tissues were collected for ELISA, immunofluorescence, Western blotting, metabolomics, and proteomics analyses. Additionally, an in vitro intestinal epithelial barrier model was established using LPS-induced Caco-2 cells. Cell viability, barrier function (TEER and FITC-Dextran permeability), cell damage (LDH), and inflammatory cytokine levels (IL-6 and IL-1β) were measured. The expression and distribution of tight junction proteins (ZO-1 and occludin) and signaling proteins (FAK, p-FAK, paxillin, and p-paxillin) were analyzed via immunofluorescence and Western blotting. RESULTS:CY treatment significantly reduced the Disease Activity Index (DAI) and suppressed the levels of pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α) in UC mice. Proteomic analysis identified Caveolin-1 (CAV1) and the focal adhesion pathway as key therapeutic targets and signaling pathways. Metabolomic profiling revealed 17 endogenous metabolites, highlighting tryptophan metabolism and butyrate metabolism as critical pathways. Furthermore, CY intervention modulated arachidonic acid and linoleic acid metabolism. Mechanistically, CY upregulated the expression of CAV1 and FAK while downregulating AKT and paxillin phosphorylation. In vitro experiments demonstrated that CY-containing serum restored the barrier function of LPS-induced Caco-2 cells by regulating FAK/paxillin phosphorylation, upregulating tight junction proteins, and mitigating inflammatory responses. CONCLUSION:CY involvement in colonic mucosal healing attenuates inflammation and enhances intestinal barrier function in DSS-induced colitis, likely through the modulation of the CAV1/FA axis. These findings provide a theoretical basis for the clinical application of CY and offer novel insights for the development of therapeutic agents for UC.

The cardiometabolic index (CMI) serves as a significant marker of diabetes mellitus (DM) and may predict the potential for cardiovascular disease development. Nevertheless, the correlation between CMI and atherosclerotic cardiovascular disease (ASCVD) among individuals exhibiting varying glucose metabolism statuses (GMS) continues to be unclear. Overall, 24,006 individuals aged 20 and above were enrolled in the research, drawn from the National Health and Nutrition Examination Survey (NHANES) database. Individuals in the study was classified into three distinct categories according to the level of fasting plasma glucose or glycated haemoglobin: normal glucose regulation, prediabetes, and DM. Multivariate logistic regression models and smoothed curve-fitting techniques were applied to investigate the correlation between CMI and ASCVD risk across varying GMS. Additionally, subgroup analyses stratified by relevant factors were performed to identify potential effect modifiers in this relationship. Overall, 2352 participants (9.8

ETHNOPHARMACOLOGICAL RELEVANCE:Ulcerative colitis (UC) is a chronic, relapsing inflammatory bowel disease primarily characterised by persistent disruption of the colonic epithelial barrier. Despite the proven clinical efficacy of the traditional Chinese medicine formulation Wumei Wan (WMW), its pharmacological mechanisms remain inadequately understood. AIM OF THE STUDY:This study aims to elucidate the therapeutic mechanisms through which WMW promotes the repair of colonic epithelial barrier damage in UC. METHODS:UC was induced in rats via dextran sulfate sodium (DSS), followed by treatment with low- and high-dose WMW or the positive control 5-ASA. Therapeutic effects of WMW on colonic barrier damage were assessed using conventional indices and serum biomarkers. Mechanistic insights were derived through network pharmacology analysis and transcriptome sequencing (RNA-seq), with experimental validation performed using reverse transcription quantitative PCR, Western blot analysis, and immunofluorescence (IF). RESULTS:Both high- and low-dose WMW improved serum biomarkers associated with intestinal barrier function (endotoxin, diamine oxidase, and D-lactate), alongside conventional metrics such as disease activity index, ZO-1, and MUC2 expression. Network pharmacology and RNA-seq analyses identified key therapeutic mechanisms, including modulation of pyroptosis, regeneration of LGR5+ intestinal stem cells (ISCs), and regulation of inflammatory signalling pathways. Experimental validation confirmed that WMW inhibited pyroptosis-associated proteins (NAIP5, NAIP6, NLRC4, GSDMD-N, caspase-1 p20, IL1β, and IL18) while promoting ISC regeneration via upregulation of LGR5, ASCL2, and IL11RA1, with co-localisation of LGR5 and IL11RA1-a novel finding. Additionally, WMW suppressed phosphorylation of JAK2/STAT3 pathway components (p-JAK2 and p-STAT3) and elements of the STING1/IRF3 pathway (p-STING1, p-IRF3, and p-NF-κB p65), offering moderate complementary regulation of inflammatory pathways in UC. CONCLUSIONS:WMW mitigates UC-associated epithelial barrier dysfunction through a multifaceted mechanism involving inhibition of NAIP5/6-NLRC4 pathway-mediated epithelial pyroptosis, enhancement of ASCL2/IL11RA1-dependent LGR5+ ISC regeneration, and suppression of JAK-STAT and STING1/IRF3 inflammatory signalling. This polypharmacological action, driven by WMW's complex phytochemical composition, underscores therapeutic potential of multi-target herbal medicines in addressing the multifactorial pathogenesis of UC.

OBJECTIVES:This study was designed to investigate the pharmacological activity and therapeutic mechanism of Mahuang Xixin Fuzi decoction (MXFD) on migraine.METHODS:Migraine model rats induced by nitroglycerin were established, and then orally administered with MXFD for 7 days. Blood and urine samples were collected to identify differential metabolites with metabolomics. To integrate the findings from network pharmacology and metabolomics analysis, the metabolites and targets related to MXFD therapy for migraine were filtered.KEY FINDINGS:MXFD was found to alleviate the symptoms of migraines in rats. After treatment with MXFD, nine metabolites were found to be regulated and returned to normal levels. MXFD acted directly on nine key targets including MAOB, MAOA, ADRB1, ADRB2, ADRB3, ADORA2A, ADORA2B, DRD5, and HTR4 and regulated two out of nine metabolites, namely deoxycholic acid and 5-methoxyindoleacetate.CONCLUSIONS:The study found that MXFD can alleviate migraines through multitarget and multicomponent interaction networks.

As open substructures of fullerenes, aromatic p-bowls are promising candidates as new organic semiconductors, as well as attractive hosts for fullerenes. We demonstrate herein the synthesis and characterization of a novel C-2v symmetric p-bowl, pyracyleno [6,5,4,3,2,1-pqrstuv]pentaphene (3). Bowl 3 was equipped with two distinctive reactive sites, allowing for bromination and cross-coupling reactions to readily yield functionalized bowls with two 2,4,6trimethylphenyl (5) and triethylsilyl (TES)-ethynyl (6) substituents, respectively. Variable-temperature H-1 NMR analysis and density functional theory (DFT) calculations indicated bowl-to-bowl inversions of 3, 5, and 6 at room temperature. By alternating the substituents, the crystal structures of the three p-bowls 3, 5, and 6 could be controlled from 1D linear to 1D slipped to 2D herringbone packing motifs, providing insight into the packing behavior of p-bowls. H-1 NMR titration study indicated that the TES-ethynyl substituent enhanced the ability of p-bowl to bind C-70 with an association constant of 2485 M-1. The C-70 molecules with p-bowls 3 and 6 formed 1:1 complexes, in which C-70 molecules aggregated into zig-zag and 1D linear arrays, respectively. The hole mobility of 2.3 cm(2) V-1 s(-1) and electron mobility of 0.16 cm(2) V-1 s(-1) of pbowl 3 and its complex with C-70 were demonstrated, respectively, which proved a great value for the development of aromatic p-bowl semiconductors with tunable properties for organic electronic devices.

Sample preparation based on extraction techniques plays a crucial role in the entire analytical process, as it ensures accurate and reliable analysis of analytes by eliminating matrix interferences. However, conventional sample preparations are considered the labor-intensive, time-consuming part of analysis, relying on the extensive use of harmful organic solvents. In line with green analytical chemistry concepts, implementing sustainable green solvents in microextraction techniques for sample preparation contributes significantly to the development of green analytical methodologies. Taking advantages of the solvation properties and greenness merits, these sustainable green solvents can be tailored as promising extractants for specific microextraction tasks, facilitating an efficient and environmental-friendly sample preparation prior to instrumental analysis. In this review, we provide a concise summary of recent advances in the prominent sustainable green solvents (such as ionic liquids, deep eutectic solvents, natural deep eutectic solvents, amphiphilic solvents, switchable solvents, sub-/supercritical fluids, and bio-based solvents) utilized in microextraction techniques, and their applications coupled with various mass spectrometric approaches for highly selective and sensitive analysis. Finally, we discuss the potential future outlooks in this field.

Ethnopharmacological relevance: The process of atherosclerosis (AS) is complicated. Transcriptomics technology can assist in discovering the underlying mechanisms and exploring the key targets of Traditional Chinese Medicine (TCM) against atherosclerosis. Aim: This study aimed to investigate targets and signaling pathways significantly related to AS and the potential intervention targets of Xuefu Zhuyu decoction by transcriptomics. Materials and methods: AS models were established by subjecting ApoE(-/-)mice to an 8-week high-fat diet. Structural changes and plaque formation in the aortic root were observed using hematoxylin-eosin staining (HE staining), while Oil Red O staining was employed to visualize lipid deposition within the aortic root plaque. Movat staining and immunohistochemical staining were conducted to examine the components present in the aortic root plaque. Macrophage content within the plaque was observed through immunofluorescence. Additionally, mRNA sequencing was performed on aortic tissues to identify differentially expressed genes. Enrichment analysis was performed using GO and KEGG analysis. Visualization of the protein-protein interaction (PPI) network was achieved using Cytoscape 3.7.1 and STRING. Western blotting (WB) was employed to assess the protein expression of major differentially expressed genes in the aortic tissue. The drug freeze-dried powder of Xuefu Zhuyu decoction was prepared and the RAW264.7 cells were induced by lipopolysaccharide (LPS) to build an in vitro model. Real-time quantitative PCR was employed to measure the mRNA expression of major differential genes. Results: After ApoE(-/-) mice were fed with an 8-week high-fat diet, observable changes included the thinning of the aortic root wall, the accumulation of foam cells within the plaque, and the formation of cholesterol crystals in the model group. Treatment with Xuefu Zhuyu (XFZY) decoction for 12 weeks significantly reduced the lipid deposition and the number of macrophages (P < 0.05) and significantly increased the collagen content within the plaque (P < 0.01). Enrichment analysis revealed a high enrichment of the Cytokine-cytokine receptor interaction pathway and Chemokine signaling pathway. Noteworthy genes involved in this response included Ccl12, Ccl22, Cx3cr1, Ccr7, Ccr2, Tnfrsf25, and Gdf5. Xuefu Zhuyu decoction significantly downregulated the expression of CX3CL1 and CX3CR1 (P < 0.05) and upregulated the expression of GDF5 (P < 0.01). Compared with control group, in cell models, the mRNA expressions of Ccl12, Ccl22, and Ccr2 were significantly upregulated (P < 0.05 or P < 0.01). Xuefu Zhuyu decoction significantly downregulated the expression of Ccl12, Ccl22, Cx3cr1, Ccr7 and Ccr2 (P < 0.05 or P < 0.01). Conclusion: Xuefu Zhuyu decoction demonstrates effective regulation of plaque components, retarding plaque progression and preserving plaque stability by modulating lipid metabolism and inflammatory responses. Subsequent transcriptome analysis identified the Cytokine-cytokine receptor interaction and Chemokine signaling pathway as potential key pathways for the therapeutic effects of Xuefu Zhuyu decoction. This insight not only provides crucial avenues for further exploration into the mechanisms underlying Xuefu Zhuyu decoction but also offers valuable perspectives and hypotheses for enhancing disease prevention and treatment strategies.

Ethnopharmacological relevanceThe traditional Chinese medicine (TCM) formula Banxia Xiexin decoction (BXD) has definite therapeutic effect in treating stress-induced gastric ulceration (SIGU) and many other gastrointestinal diseases, but its effect on gastric lymphatic pumping (GLP) remains unclear.Aim of the studyElucidating the role of GLP in SIGU and BXD treatment, and exploring the molecular mechanisms of GLP regulation.Materials and methodsIn vivo GLP imaging were performed on SIGU rat model, and the lymphatic dynamic parameters were evaluated. Gastric antrum tissues and serum were collected for macroscopic, histopathological and ulcerative parameters analysis. Gastric lymphatic vessel (GLV) tissues were collected for RNA-Seq assays. Differentially expressed genes (DEGs) were screened from RNA-Seq result and submitted for transcriptomic analysis. Key DEGs and their derivative proteins were measured by qRT-PCR and WB.ResultsGLP was significantly suppressed in SIGU rats. BXD could recover GLP, ameliorate stomach lymphostasis, and alleviate the ulcerative damage. Transcriptome analysis of GLV showed the top up-DEGs were concentrated in smooth muscle contraction signaling pathway, while the top the down-DEGs were concentrated in energy metabolism pathways especially fatty acid degradation pathway, which indicated BXD can promote lymphatic smooth muscle contraction, regulate energy metabolism, and reduce fatty acid degradation. The most possible target of these mechanisms was the lymphatic smooth muscle cells (LSMCs) which drove the GLP. This speculation was further validated by the qRT-PCR and WB assessments for the level of key genes and proteins.ConclusionsBy activating the smooth muscle contraction signaling pathway, restoring energy supply, modulating energy metabolism program and reducing fatty acid degradation, BXD effectively recovered GLP, mitigated the accumulation of inflammatory cytokines and metabolic wastes in the stomach, which importantly contributes to its efficacy in treating SIGU.

C1q/tumor necrosis factor-related protein-6 (CTRP6) has multiple protective effects against cardiovascular diseases. Myofibroblast differentiation plays a critical role in cardiac fibrosis under various cardiac pathological conditions. The aim of the present study was to determine the effects of CTRP6 on cardiac fibrosis, and to identify the possible mechanisms of action. Toward this end, we measured the expression of fibrotic markers, including collagen I, collagen III, CTGF, and TGFβ1, and assessed the effects of CTRP6 on cardiac fibroblast differentiation into myofibroblasts. CTRP6 inhibited the expression of the angiotensin II (Ang II)-induced myofibroblast markers α-SMA and SM22, and of profibrotic molecules, including collagen I, collagen III, CTGF, TGFβ1, MMP2, MMP9, and TIMP1. Furthermore, CTRP6 significantly attenuated the proliferation and migration of cardiac fibroblasts incubated with Ang II and activated the phosphorylation of AMP-activated protein kinase (AMPK). Incubation with an AMPK inhibitor reversed the subsequent inhibitory effects of CTRP6 on Ang II-induced myofibroblast differentiation. Therefore, CTRP6 suppresses cardiac fibrosis by inhibition of myofibroblast differentiation via AMPK pathway activation, suggesting CTRP6 as a target for the treatment of cardiac fibrosis.

Ethnopharmacological relevance: Qiwei Tiexie capsule (QWTX) is an improved form of a classical prescription of Tibetan medicine-Qiwei Tiexie pill. It has been employed in the treatment of a variety of chronic liver disorders, including liver fibrosis. Uncertainty still exists regarding the mechanism of QWTX action in liver fibrosis.Aim of the study: Confirm the anti-liver fibrosis effect of QWTX and reveal its mechanism from the perspective of NOD-like receptor protein 3 (NLRP3) inflammasome activation. Materials and methods: In vivo experiment: A rat model of carbon tetrachloride-induced liver fibrosis was con-structed. All rats were randomly divided into six groups: a control group, a model group, a group receiving the positive drug (Biejia Ruangan tablet), and three groups receiving QWTX at high, medium, and low doses. The contents of aspartate aminotransferase (AST), alanine aminotransferase (ALT), and total bilirubin (TBil) were detected in serum. Hematoxylin and eosin staining and Masson's staining were used to assess the histo-morphological alteration of the liver. The levels of glutathione peroxidase, hydroxyproline, tumor necrosis factor alpha (TNF-alpha), and interleukin 1 beta (IL-18) in the liver were determined using the corresponding detection kits. Real-time polymerase chain reaction, immunofluorescence, and western blotting were used to determine the expression levels of NLRP3, adaptor protein (ASC), caspase-1, and alpha-smooth muscle actin (alpha-SMA). In vitro experiment: Four groups of rat hepatic stellate cell line (HSC-T6) cells were created: the control group, the low -dose QWTX group (0.05 mg/mL), the medium-dose QWTX group (0.1 mg/mL), and the high-dose QWTX group (0.2 mg/mL). Cell viability was assessed using a cell counting kit, and the amounts of collagen type I (Col I) and IL-18 in the cell lysate were measured using an enzyme-linked immunosorbent assay kit. The mRNA and protein expression of NLRP3, ASC, caspase-1, and alpha-SMA were also estimated.Results: QWTX had an inhibitory effect on liver fibrosis and a negative effect on HSC activation, while it improved liver histopathological injury and abnormal liver function and increased hydroxyproline content and glutathione peroxidase activity in vivo. QWTX decreased the expression of alpha-SMA, NLRP3, caspase-1, ASC, and IL-18 both in vitro and in vivo.Conclusions: Tibetan medicine QWTX had a significant anti-liver fibrosis effect that was related to the inhibition of NLRP3 inflammasome activation in vivo and in vitro.

慢性胰腺炎是发生胰腺癌的独立危险因素,高度重视慢性胰腺炎"炎-癌转化"并进行干预具有重要意义.基于李东垣的阴火理论,认为阴火主要是指脾胃气虚所致的气郁郁火及湿热之邪,是慢性胰腺炎"炎-癌转化"的关键.从阴火理论出发探讨中医药干预慢性胰腺炎"炎-癌转化",需把握其动态变化,紧扣阴火这一核心环节,健脾益气、因势利导、攻伐有道,才能取得临床效益的最大化.

Due to the lack of classic estrogen receptors, there has been a shortage of targeted therapy for triple-negative breast cancer (TNBC), resulting in a poor prognosis. However, the newly discovered G protein-coupled estrogen receptor (GPER) has been found to be expressed in TNBC cells. Salvia miltiorrhiza (Danshen) is an essential Chinese medicine for gynecological disorders, and its component tanshinone IIA (Tan IIA) exerts an anticancer effect. Therefore, this study attempted to investigate whether GPER is involved in the inhibitory effect of Tan IIA on TNBC. We applied various databases and GO pathway analysis to predict the possible mechanism of Tan IIA. We identified 39 overlapping targets, including c-Jun, c-Fos, and caspase-3, and enriched cell cycle-related pathways. Next, we demonstrated the strong binding ability of Tan IIA to GPER by molecular docking assay. In the subsequent validation tests, Cell Counting Kit-8 (CCK8) assay showed that Tan IIA inhibited proliferation of MDA-MB-231 cells time and dose dependently without affecting normal cells. Using Transwell plate, flow cytometry, and Western blot assays, we showed that Tan IIA inhibited migration and induced apoptosis of MDA-MB-231 dose dependently. Importantly, protein expressions of GPER, epidermal growth factor receptor (EGFR), extracellular regulated protein kinases (ERK), c-Fos, and c-Jun were all decreased by Tan IIA dose dependently. Administration of GPER inhibitor partly abolished these effects. Furthermore, nuclear translocation of c-Fos and c-Jun as well as cell cycle-related proteins was downregulated by Tan IIA dose dependently. In summary, Tan IIA could inhibit the proliferation and migration of MDA-MB-231 cells and induce apoptosis, and the possible mechanism may be the regulation of GPER-mediated pathways, suggesting that GPER could be a therapeutic target for TNBC.

The incorporation of nonbenzenoid rings into the hexagonal networks of graphenoid nanostructures is of immense importance for electronic, magnetic, and mechanical properties, but the underlying mechanisms of nonbenzenoid ring fusion are rather unexplored. Here, we report the synthesis and characterization of a rippled C84 molecular carbon, which contains 10 nonbenzenoid rings (five-, seven-, and eight-membered rings) that are contiguously fused to give a cyclic geometry. The fused nonbenzenoid rings impart high solubility, configurational stability, multiple reversible redox behaviors, unique aromaticity, and a narrow band gap to the system. Moreover, this carbon nanostructure allows for further functionalization via electrophilic substitution and metalation reactions, enabling access to finely tuned derivatives. Interestingly, both the bowl-shaped and planar conformations of the core in molecular carbon are observed in the solid state. Additionally, this molecular carbon displays ambipolar transport characteristics.

The term of "Water Scope" comes from Jin Gui Yao Lue. "Water" refers to body Fluid, and "Scope" has the meaning of range.Therefore, "Water Scope" refers to the area where body Fluid is located, including the movement and location of body Fluid.Therefore, the body Fluid theory and the corresponding channel theory of it constitute the main body of Water Scope.Water is a system that integrates structure, function, and information, encompassing physiological and pathological categories, with body Fluid as the core and waterways, striae, and six organs as the framework as well as the generation, distribution and metabolism of body Fluid as the network.It is a system that aggregates structure, function, and information, including physiological and pathological categories.In the pathological state of the human body, Water is the intermediate stage between Qi and blood, and it is also an important link for diseases transition from Qi to blood.It is a key turning point from easy to difficult in treatment.

胆石症是胆道系统常见疾病,腹腔镜胆囊切除术(LC)是治疗症状性胆结石的"黄金标准"手术,但术后仍有一些患者继续出现临床症状.中医药因其具有整体调节,辨证论治的优势在临床发挥独特作用.综合国内外有关文献,对胆囊切除术后综合征的中医发病机制及辨证论治进行探讨.期许为胆囊术后综合征的中医药治疗提供新思路.

中医五脏系统中,脾的主要功能被概括为"脾主运化"和"脾主统血".在解剖实体上,中医"脾"与现代医学的脾脏存在巨大差异."运脾"是中医"脾"最初、最核心的内涵,其解剖实体对应胰腺,负责水谷的消化、吸收和转运.从《黄帝内经》时期"脾为胃行其津液"到宋以后"脾主运化",胃、小肠、大肠的一部分功能被让渡于脾,最终形成以脾为核心的消化、转运系统.

现今中医药治疗颈椎病多从气血、肝肾出发,或从经络、六经辨证,而鲜少提及津液.本文从津液角度,论述津液对阴阳平衡、筋骨平衡的影响,并从流体结构与固体结构论证了津液病变是形成颈椎病的关键点.津液既可化生精、髓、血、液,是调补气血、肝肾的关键;又能内滋脏腑,节制阳气,维持五脏元真通畅、阴平阳秘的生理状态;还能润养筋脉肌肉,濡养关节骨骼,维系筋骨平衡.若津液不通、不和,难以润养,则易导致病变.在治疗方面,本文从桂枝汤类、柴胡汤类与承气陷胸类三组类方分析出经方治疗颈椎病重在调津液.桂枝汤类方重在平衡阴阳,调和津液;柴胡汤类方善于疏利三焦,畅达津液;承气陷胸类方则可开水热结,急下存阴.总而言之,津液以"通""和"为用,津液不足者当以调和阴阳,补充津液为主要治法;津液不利者则应随其所得而攻之,以令津气通行.津液充沛,运行正常,则阴平阳秘,筋骨得养;筋柔骨正,则邪去正安.基于津液探析颈椎病的形成机理与治疗方案,能够为临床提供更多思路与参考.