Journal of Physiology and Pharmacology最新文献

{"title":"Unraveling the complexity of <i>Helicobacter pylori</i>: Virulence factors, biofilm formation, and antibiotic resistance.","authors":"A Zurawik, M Pobiega, T Kasperski, A Chmielarczyk","doi":"10.26402/jpp.2026.1.04","DOIUrl":"https://doi.org/10.26402/jpp.2026.1.04","url":null,"abstract":"&lt;p&gt;&lt;p&gt;&lt;i&gt;Helicobacter pylori&lt;/i&gt; infection remains one of the most common chronic bacterial infections worldwide and represents a major etiological factor in diseases of the upper gastrointestinal tract, including chronic gastritis, peptic ulcer disease, and gastric cancer. Despite continuous refinement of eradication regimens based on antibiotics and proton pump inhibitors, treatment efficacy has progressively declined, primarily due to increasing antimicrobial resistance and the ability of &lt;i&gt;H. pylori&lt;/i&gt; to form biofilm structures. Accumulating evidence indicates that biofilm formation, bacterial virulence, and modulation of host immune responses constitute an interconnected network of mechanisms that collectively promote bacterial persistence and therapeutic failure. This review outlines an integrated pathogenic framework for &lt;i&gt;H. pylori&lt;/i&gt;, focusing on the functional interplay between key virulence determinants - including CagA, VacA, neutrophil-activating protein (NAP), high-temperature requirement A (HtrA), IceA, DupA, urease, catalase, and adhesins - and their contribution to biofilm development, epithelial barrier disruption, and sustained gastric inflammation. Biofilm formation is highlighted as a central adaptive strategy that not only limits antibiotic penetration but also induces metabolic dormancy, enhances efflux pump activity, and increases tolerance to oxidative stress and immune-mediated clearance, thereby significantly reducing the effectiveness of standard eradication therapies. In addition, the review incorporates novel insights derived from recent high-throughput omics approaches, including genomics, transcriptomics, proteomics, and metabolomics, which have advanced the understanding of &lt;i&gt;H. pylori&lt;/i&gt; pathogenicity, adaptive responses, and resistance mechanisms at a systems level. A major emphasis is placed on recent advances in therapeutic strategies that extend beyond conventional antibiotic-based regimens. The review summarizes current pharmacological approaches, including the use of more potent acid-suppressive agents such as vonoprazan, susceptibility-guided and personalized eradication therapies, and emerging anti-biofilm interventions, including antimicrobial peptides, phytochemicals, small-molecule inhibitors, and enzymatic degradation of the extracellular polymeric matrix. In addition, nanotechnology-based drug delivery systems are discussed as promising tools to improve antibiotic stability, bioavailability, and targeted release within the hostile gastric environment. In conclusion, effective management of &lt;i&gt;H. pylori&lt;/i&gt; infection requires a mechanistically informed and multidisciplinary approach that integrates bacterial virulence, biofilm biology, host immune modulation, and regional antimicrobial resistance profiles. The combination of established pharmacological therapies with innovative anti-biofilm and nanomedicine-based strategies represents a promising direction for improving eradication outcomes and","PeriodicalId":50089,"journal":{"name":"Journal of Physiology and Pharmacology","volume":"77 1","pages":"xxx"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147616971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of minerals in ischaemic heart disease.","authors":"D Selvan, K Skrypnik, J Suliburska","doi":"10.26402/jpp.2026.1.03","DOIUrl":"https://doi.org/10.26402/jpp.2026.1.03","url":null,"abstract":"<p><p>This review focuses on analysing existing research to offer a comprehensive understanding of the complex role minerals play in the pathophysiology of ischaemia. By examining changes in mineral levels, we aim to uncover the mechanisms by which these elements influence the onset and severity of ischaemic heart disease (IHD). Imbalances in key minerals (biologically active metal ions present in blood plasma and/or cells in dissolved form) such as calcium, magnesium, zinc, manganese and copper have been closely associated with the onset and progression of IHD. Disrupted calcium and magnesium levels, particularly altered calcium/magnesium ratios, contribute to vascular calcification and elevated blood pressure. Deficiencies in magnesium have been linked to greater risks of arrhythmias and poorer outcomes following cardiac events. Additionally, abnormal zinc and copper levels, along with their ratio, affect oxidative balance and lipid metabolism, suggesting that proper mineral regulation is essential for cardiovascular protection and reducing IHD risk. Elevated manganese levels may contribute to oxidative damage, potentially increasing the risk of IHD. As a conclusion this review emphasizes the significant role of minerals in IHD, noting their potential to support pharmacological treatments by reducing oxidative stress and improving heart health. While minerals like magnesium and calcium show protective effects, excess iron and zinc may increase risk. Despite promising findings, further large-scale studies are needed to confirm their therapeutic value and to guide evidence-based dietary strategies for IHD management.</p>","PeriodicalId":50089,"journal":{"name":"Journal of Physiology and Pharmacology","volume":"77 1","pages":"xxx"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147616954","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MiR-210-5p inhibits the proliferation and migration of colorectal cancer cells by down-regulating aquaporin 1.","authors":"B Kong, S P Zhao, Q Chen, B Wang, P F Zhang","doi":"10.26402/jpp.2026.1.10","DOIUrl":"https://doi.org/10.26402/jpp.2026.1.10","url":null,"abstract":"<p><p>The development of colorectal cancer (CRC) results from the progressive accumulation of genetic and epigenetic alterations, leading to the inactivation of tumor suppressor genes and activation of oncogenes. Aquaporin 1 (AQP1) has been shown to promote tumor angiogenesis; however, its specific role in CRC proliferation and migration remains unclear. This study aims to investigate the functions of miR-210-5p and AQP1 in CRC cell proliferation and migration. Using online datasets from the Cancer Genome Atlas (TCGA) and ten clinical samples, we examined AQP1 expression in CRC. Bioinformatic analysis was conducted to identify miRNAs potentially regulating AQP1. The effects of miR-210-5p and AQP1 on invasion and migration were further assessed <i>in vivo</i> in xenograft Balb/c nu/nu mice. Results showed that dysregulated AQP1 expression in CRC was correlated with advanced clinical stage and venous invasion. miR-210-5p was predicted to bind AQP1 and may target its expression. <i>In vitro</i> experiments revealed that miR-210-5p inhibits CRC proliferation and invasion by downregulating AQP1, which subsequently reduces the expression of vascular endothelial growth factor (VEGR), Wnt-7a, Matrix metallopeptidase 2 (MMP2), MMP9, and β-catenin. Targeting AQP1 led to suppressed proliferation and migration of CRC cells. In summary, AQP1 is upregulated in CRC and regulated by miR-210-5p. Downregulation of AQP1 by miR-210-5p attenuates CRC proliferation and migration through decreasing VEGR, Wnt-7a, MMP2, MMP9, and β-catenin expression.</p>","PeriodicalId":50089,"journal":{"name":"Journal of Physiology and Pharmacology","volume":"77 1","pages":"127-138"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147616976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bioactive compounds from Psilocybe cubensis mycelial cultures with transient anxiolytic effects in mice.","authors":"K Kala, D Bederska-Lojewska, J Lazur, K Gasior, A Maslanka, A Szewczyk, K Sulkowska-Ziaja, J Turek, B Szewczyk, A Pilc, B Muszynska","doi":"10.26402/jpp.2026.1.07","DOIUrl":"https://doi.org/10.26402/jpp.2026.1.07","url":null,"abstract":"<p><p>The growing percentage of people suffering from drug-resistant depression increases interest in alternative therapies, particularly the usage of psychedelics such as psilocybin. The main source of psilocybin is the Psilocybe cubensis species. Due to the potential therapeutic benefits of psilocybin and the legal restrictions on its possession and use in the form of fungal fruiting bodies, this research work documents an attempt to obtain <i>in vitro</i> <i>P. cubensis</i> mycelium in which psilocybin and other biologically active substances acting on the central nervous system would be present. It was hypothesized that chronic microdosing with whole <i>in vitro</i> - cultured <i>P. cubensis</i> mycelium, containing psilocybin together with other neuroactive secondary metabolites, could exert anti-anxiety and antidepressant effects through their combined action. For this purpose, the anti-anxiety and antidepressant activity of mycelium microdosing in male C57BL/6J mice was investigated. The tail suspension test (TST), novelty suppressed feeding test (NSFT), sucrose preference test (SPT), locomotor activity (LA), and female urine sniffing test (FUST) were used to examine animal behavior. The chemical analysis was performed using high-performance liquid chromatography (HPLC) and thin-layer chromatography (TLC) method. Analysis of the studied extracts showed that psilocybin was present only in the mycelium of the Cambodian strain, at a concentration of 20.78 mg per 100 g dry weight. The experiment showed that mycelium supplementation significantly reduced anxious behavior in mice on day 22 but did not affect locomotor activity, depressive, anxiety-related, or anhedonic behaviors at later stages of the experimental protocol. Although the results suggest the potential of <i>P. cubensis</i> mycelial cultures in anxiety prevention, further studies using higher doses or alternative models are needed to confirm and extend these findings.</p>","PeriodicalId":50089,"journal":{"name":"Journal of Physiology and Pharmacology","volume":"77 1","pages":"89-101"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147616676","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Bone marrow mesenchymal stem cells-derived exosomes repair degenerative intervertebral discs by modulating macrophage M1/M2 phenotype.","authors":"J Liang, J Mao, Z Tan, J Li","doi":"10.26402/jpp.2026.1.06","DOIUrl":"https://doi.org/10.26402/jpp.2026.1.06","url":null,"abstract":"<p><p>The effect of bone marrow mesenchymal stem cell-derived exosomes (BMSC-Exos) on intervertebral disc degeneration (IVDD) repair and healing and its possible mechanism were investigated. Tail IVDD puncture was performed on mice, and BMSC-Exos were injected into the joint cavity. The disc morphology was observed by HE staining, apoptosis rate of nucleus pulposus (NP) tissues was determined by TUNEL, and polarization of macrophages and NP cell damage were detected by Western Blot. An in vitro experimental model was established by co-culture of nucleus pulposus (NP) cells and M1 macrophages in a conditioned medium, and the improvement effect of BMSC-Exos on the proliferation of damaged NP cells was detected by CCK-8 assay. NP cell apoptosis was determined by flow cytometry. Inflammatory factors in NP cell supernatant was measured by ELISA. In results: BMSC-Exos reversed the degenerative changes of IVDD in mice. BMSC-Exos promoted the transformation of THP-1 cells from M1 to M2 and inhibited the release of inflammatory cytokines. BMSC-Exos inhibited matrix metallopeptidase 13 (MMP-13), matrix metallopeptidase 3 (MMP-3), and Cleaved caspase-3 expression in damaged NP tissues. BMSC-Exos significantly increased NP cell proliferation and blocked apoptosis. The concentration of inflammatory factors in the supernatant of NP cells treated with BMSC-Exos was significantly down-regulated. Conclusion: BMSC-Exos have a regenerative effect on IVDD, encourage macrophages to transform from M1 to M2, suppress NP cell apoptosis and inflammatory responses, and improve degenerative alterations in the intervertebral disc.</p>","PeriodicalId":50089,"journal":{"name":"Journal of Physiology and Pharmacology","volume":"77 1","pages":"77-88"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147616683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Baicalin alleviates doxorubicin-induced nephrotic syndrome by regulating the tumor necrosis factor-β/Smad signaling pathway and NOD-like receptor family, pyrin domain-containing protein 3 inflammasome.","authors":"Y Yang, J H Liu, D K Gui","doi":"10.26402/jpp.2026.1.05","DOIUrl":"https://doi.org/10.26402/jpp.2026.1.05","url":null,"abstract":"<p><p>Adriamycin (ADR)-induced nephrotic syndrome (NS) is a common renal disease model characterized by proteinuria, glomerular damage, and inflammatory responses. Baicalin, a bioactive flavonoid derived from Scutellaria baicalensis, demonstrates anti-inflammatory and anti-fibrotic properties. This study aims to investigate whether baicalin alleviates ADR-induced NS by regulating the transforming growth factor-beta (TGF-β)/Smad signaling pathway and the NOD-like receptor family, pyrin domain-containing protein 3 (NLRP3) inflammasome. A murine NS model in vivo was established by administering 10 mg/kg ADR to male C57BL/6J mice. Experimental groups were treated orally with 20 mg/kg or 40 mg/kg baicalin for 6 weeks. The following parameters were measured in each group: 24-h urinary protein, serum creatinine (Scr), blood urea nitrogen (BUN), total protein, albumin, total cholesterol, and triglycerides. In vitro, a cellular NS model was established by treating mouse podocyte cells (MPC5) with 0.75 µmol/L ADR, and the protective effects of baicalin were evaluated. Protein expression levels of the TGF-β/Smad signaling pathway and NLRP3 inflammasome were analyzed by Western blot. The secretion levels of interleukin-4 (IL-4), interleukin-8 (IL-8), interleukin-1β (IL-1β), and interleukin-18 (IL-18) were assessed by enzyme-linked immunosorbent assay, and the activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) were measured in cells. ADR reduced MPC5 cell viability to below 50% and increased MDA levels (≥6 nmol/mg prot). The expression of NLRP3 (upregulated by 4-fold), α-smooth muscle actin (upregulated by 3-fold), N-cadherin (upregulated by 3-fold), and IL-8/IL-1β/IL-18 (all upregulated by more than 1-fold) was significantly elevated. Treatment with 12.5 µmol/L baicalin markedly reversed these changes, restoring cell viability to over 85% and bringing pathway protein and cytokine levels close to those of the control group. <i>In vivo</i>, ADR-induced NS mice exhibited doubled 24-h urinary protein, Scr, and BUN levels, along with renal interstitial inflammatory infiltration and a 60% downregulation of podocin expression. Treatment with 40 mg/kg of baicalin restored these indicators to levels comparable to those in untreated mice, with effects similar to irbesartan (<i>P</i><0.05). We concluded that baicalin demonstrated significant renoprotective effects in both <i>in vivo</i> and <i>in vitro</i> models of ADR-induced NS by regulating the TGF-β/Smad pathway and NLRP3 inflammasome, mitigating renal injury and inflammation. These results offer experimental support for the potential use of baicalin as a therapeutic agent for NS.</p>","PeriodicalId":50089,"journal":{"name":"Journal of Physiology and Pharmacology","volume":"77 1","pages":"63-76"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147615764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Periodontal ligament cells regulate macrophage polarization <i>via</i> CCL7/CCR1 signaling.","authors":"K Yang, H Wang, X Y Zeng, S X Yang, C C Duan, Y W Guo, S J Zou, P P Duan","doi":"10.26402/jpp.2026.1.09","DOIUrl":"https://doi.org/10.26402/jpp.2026.1.09","url":null,"abstract":"<p><p>Orthodontically induced root resorption (OIRR), a common complication of orthodontic treatment exacerbated by excessive force application, is linked to pro-inflammatory M1 macrophage polarization. This study investigates whether periodontal ligament cells (PDLCs) under heavy compression force regulate macrophage polarization <i>via</i> the CCL7/CCR1 axis to exacerbate OIRR. In the animal experiment, male Wistar rats were subjected to heavy orthodontic force to establish the orthodontic tooth movement model, with the inhibitor group receiving CCR1 antagonist BX471. Histological and immunohistochemical analyses were conducted to assess root resorption and RAW 264.7 polarization <i>in vivo</i>. In the <i>in vitro</i> cell culture study, human PDLCs subjected to heavy compression force were analyzed <i>via</i> RNA-seq, RT-PCR, and Western blot for CCL7 and inflammatory markers. Conditioned media from force-loaded hPDLCs were applied to RAW 264.7 cells, with and without CCR1 inhibition. As a result, heavy compression force significantly increased CCL7 expression in hPDLCs, promoting M1 polarization (TNF-α, iNOS) and inhibiting M2 polarization (Arg-1). CCR1 inhibition reversed this imbalance, restoring the M1/M2 ratio. <i>In vivo</i>, BX471 treatment attenuated root resorption and macrophage polarization. The CCL7/CCR1 signaling pathway mediates the interaction between PDLCs and macrophages, promoting M1 polarization and OIRR under orthodontic force. Targeting CCL7/CCR1 may offer a promising therapeutic approach to mitigate OIRR during orthodontic treatment.</p>","PeriodicalId":50089,"journal":{"name":"Journal of Physiology and Pharmacology","volume":"77 1","pages":"113-125"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147617002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cellular senescence: Between protection and pathologies.","authors":"I Klak, A Ptak-Belowska, G Krzysiek-Maczka","doi":"10.26402/jpp.2026.1.01","DOIUrl":"https://doi.org/10.26402/jpp.2026.1.01","url":null,"abstract":"<p><p>Cellular senescence is a stable and irreversible state of proliferative arrest triggered by diverse stressors, inclh3uding DNA damage, oncogenic signaling, oxidative stress, and metabolic imbalance. Once regarded as a culture artifact, senescence is now recognized as a fundamental biological program that governs tissue homeostasis, development, aging, and disease. Based on its origin, senescence can be divided into two principal categories: damage-induced, encompassing replicative, oncogene-induced, and therapy-induced forms, and developmentally programmed, which orchestrates tissue patterning and remodeling during embryogenesis. These processes converge on the activation of p53/p21 and p16/RB tumor suppressor axes, sustained DNA damage response (DDR), and the establishment of the senescence-associated secretory phenotype (SASP). Acute senescence serves beneficial roles in tumor suppression, wound healing, and embryonic morphogenesis by transiently activating SASP-mediated immune clearance. However, persistent senescence becomes detrimental, promoting chronic inflammation, tissue dysfunction, and cancer progression. Within the tumor microenvironment, chronic SASP signaling driven by nuclear factor kB (NF-κB), CCAAT/enhancer-binding protein beta (C/EBPβ), and Signal Transducer and Activator of Transcription 3 (STAT3) fosters epithelial-to-mesenchymal transition (EMT), invasion, and therapy resistance. Therapy-induced senescence (TIS) often leads to polyploidization and the emergence of polyploid giant cancer cells (PGCCs) that can escape arrest, regenerate proliferative progeny, and drive tumor relapses. Thus, senescence represents a biological paradox: a protective, transient process that maintains tissue integrity but, when unresolved, transforms into a driver of aging and malignancy. Understanding the molecular determinants, distinguishing beneficial from pathological senescence is crucial for developing targeted senotherapies.</p>","PeriodicalId":50089,"journal":{"name":"Journal of Physiology and Pharmacology","volume":"77 1","pages":"3-14"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147616659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Craniosacral therapy and the pathophysiology of the craniosacral system: Mechanisms, controversies, and proposed future research directions.","authors":"M Bis, A S Tarnawski","doi":"10.26402/jpp.2026.1.02","DOIUrl":"https://doi.org/10.26402/jpp.2026.1.02","url":null,"abstract":"<p><p>Craniosacral therapy (CST) is a non-invasive, alternative therapeutic approach based on the concept of the craniosacral system and its inherent rhythm. This rhythm is a subtle, cyclical expansion and contraction of the dural membranes and cerebrospinal fluid (CSF), which regulates intracranial pressure and the physiological function of the craniosacral system (CS). The CS constitutes a semi-closed, physiological hydraulic network comprising the skull (cranium), the sacrum (tailbone), the associated membranes, and the circulating CSF. Within this system, CSF provides both protection and nourishment to the brain and spinal cord - the body's most vital organs. The craniosacral rhythm (CSR) refers to the physiological rhythm of expansion and contraction within the CS that regulates CSF pressure. Magnetic resonance imaging (MRI) studies have demonstrated the pulsatile nature of intracranial and spinal CSF circulation of approximately 6 to 12 cycles per minute. Experienced CST practitioners palpate this rhythm and assess it for abnormalities that may indicate dysfunction in the fascia, dural membranes, or CSF flow. CST techniques involve gentle manual palpation to release restrictions in dural and fascial structures and restore homeostasis. Some studies suggest that CST may provide therapeutic benefits for a range of conditions, including migraine headaches, non-specific low back pain, depression, anxiety, fibromyalgia, chronic pain, and improved overall quality of life. However, its efficacy for many other conditions remains controversial, and the scientific evidence supporting its physiological mechanisms is limited. This review presents a balanced overview of CST, highlighting its current clinical status, established and hypothesized mechanisms, and emerging directions for future research into both CST and the underlying pathophysiology of the craniosacral system. Notably, recent high-quality basic research has begun to elucidate potential neurophysiological pathways and pathophysiology relevant to CS. For example, new studies have revealed direct anatomical and functional connections between the dura mater and the brain. Furthermore, they demonstrated that in migraine models, trigeminal ganglion neurons are directly activated by CSF influx. Meningeal lymphatic calcitonin gene-related peptide (CGRP) signaling has been implicated in pain induction through CSF efflux and neuroinflammation. These findings opened new avenues for understanding the physiological underpinnings of CST and its potential impact on neural and autonomic regulation.</p>","PeriodicalId":50089,"journal":{"name":"Journal of Physiology and Pharmacology","volume":"77 1","pages":"15-24"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147616761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Matrine inhibits the proliferation, migration, invasion, and stemness of thymoma cells by regulating the Wnt3a/Β-catenin pathway.","authors":"G N Chen, J P Liu, M M Li, P Lu, B G Dai, Q Z Zhang","doi":"10.26402/jpp.2026.1.08","DOIUrl":"https://doi.org/10.26402/jpp.2026.1.08","url":null,"abstract":"<p><p>Matrine (MAT), a commonly employed Chinese botanical, has a long-standing history of application in the treatment of inflammation and cancer. Nevertheless, the precise molecular mechanism underlying MAT's impact on thymoma remains unresolved. Consequently, the objective of this investigation was to assess the influence of MAT on thymomas and ascertain the potential mechanisms through which it modulates the Wnt3a/β-catenin pathway. Thy0517 cells were treated with different doses of MAT to construct a thymoma cell therapy model <i>in vitro</i>, and given Wnt3a/β-catenin pathway agonist Laduviglusib for follow-up experiments. The effect of different doses of MAT on the proliferation, colony formation ability, apoptosis, migration, invasion, and stemness of Thy0517 cells was determined by MTT, colony formation assay, flow cytometry, wound healing assay, Transwell assay, and spheroid formation assay, respectively. Genes and proteins were evaluated by RT-qPCR and/or Western blot. High-dose MAT significantly inhibited the proliferation, migration, invasion, and stemness of Thy0517 cells, which also proved the anti-tumor effect of MAT. The suppressive impact of MAT on cellular function could potentially be augmented through the blockade of the Wnt3a/β-catenin pathway, thereby providing additional evidence for the pivotal role of MAT as a signaling pathway in governing the migratory and invasive capabilities of thymoma cells. We found that MAT has anti-tumor effects, inhibiting the proliferation, migration, invasion, and stemness of thymoma cells by regulating the Wnt3a/β-catenin pathway.</p>","PeriodicalId":50089,"journal":{"name":"Journal of Physiology and Pharmacology","volume":"77 1","pages":"103-112"},"PeriodicalIF":1.7,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147616765","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}