Journal of Molecular Histology最新文献

{"title":"Evaluation of anti-obesity effects of ethanolic extract of Hydrocotyle sibthorpioides and its phytosomal formulation in high-fat diet-induced obesity in Wistar rats","authors":"Vaishnavi G. Tirthe,&nbsp;Onkar V. Nikam,&nbsp;Nimisha S. Solas,&nbsp;Shaista S. Shaikh,&nbsp;Sonali S. Nipate","doi":"10.1007/s10735-026-11016-6","DOIUrl":"10.1007/s10735-026-11016-6","url":null,"abstract":"<div><p>Obesity is a chronic metabolic disorder characterised by dyslipidemia, hyperglycemia, oxidative stress, inflammation and organ dysfunction. The anti-obesity drugs available are effective but adverse effects often limit their long-term use. <i>Hydrocotyle sibthorpioides</i> is a medicinal plant rich in flavonoid and phenolic compounds, with reported antioxidant and metabolic regulatory properties. The present study was aimed at investigating the anti-obesity potential of ethanolic extract of <i>Hydrocotyle sibthorpioides</i> (EEHS) and its phytosomal formulation in a high-fat diet (HFD)-induced obesity model. EEHS was characterised by phytochemical screening, thin-layer chromatography and determination of total phenolic and flavonoid contents. Obese male Wistar rats induced by HFD were treated with EEHS (100–400 mg/kg), EEHS phytosomes (400 mg/kg) or orlistat (25 mg/kg) for seven weeks. Physiological, biochemical, and histopathological parameters were assessed. EEHS exhibited significant anti-obesity effects in a dose-dependent manner, with the phytosomal formulation being the most significant efficacy. Treatment resulted in marked improvement in body weight, fasting blood glucose, lipid profile, liver enzyme levels, liver lipid accumulation, total body fat, TNF-α, antioxidant status and organ weights. Histopathological analysis confirmed reduced hepatic and vascular damage, inflammatory cell infiltration and adipocyte hypertrophy. The phytosomal formulation showed effects similar to those of orlistat and was more effective than the traditional extract. EEHS, especially as a phytosomal preparation, exhibited a potent anti-obesity effect. It ameliorated metabolic, inflammatory, oxidative, and histopathological alterations associated with HFD-induced obesity. The present findings suggest that EEHS may be a promising natural approach for the management of obesity.</p><h3>Graphical abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149338651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of Tongqiao Huashuan decoction regulating neuroinflammation and its effect on intestinal flora in vascular dementia rats","authors":"Jing Cai,&nbsp;Xiaoqu Jiang,&nbsp;Shuyao Yu,&nbsp;Zhongsheng Tang,&nbsp;Shijie Zhu,&nbsp;Wenjing Huang,&nbsp;Yuan Huang,&nbsp;Yuanhua Wu","doi":"10.1007/s10735-026-11039-z","DOIUrl":"10.1007/s10735-026-11039-z","url":null,"abstract":"<div><p>To investigate molecular changes associated with the protective effect of Tongqiao Huashuan Decoction (THD) in vascular dementia (VD), focusing on the NF‑κB‑related inflammatory response, and to observe its influence on intestinal flora. The components of THD were identified using Liquid chromatography‑quadrupole time‑of‑flight tandem mass spectrometry (LC‑Q‑TOF‑MS/MS) with electrospray ionization in positive/negative modes, a methanol‑0.1% formic acid gradient mobile phase, and a C18 column (1.7 μm, 2.1 × 100 mm). Sprague‑Dawley rats were divided into four groups: Sham, VD, VD + TCM (THD), and VD+Donepezil (donepezil hydrochloride). Spatial learning and memory were assessed using the Morris Water Maze. Transmission electron microscopy (TEM) analyzed the ultrastructure of hippocampal CA1 neurons. Enzyme‑linked immunosorbent assay (ELISA) detected interleukin‑1β (IL‑1β), tumor necrosis factor‑α (TNF‑α), macrophage inflammatory protein‑2 (MIP‑2), and IL‑6 in the hippocampus and serum. Immunohistochemistry (IHC) and Western blotting (WB) measured the expression of sirtuin 1 (SIRT1), NF‑κB, caspase‑1, and NOD‑like receptor protein 3 (NLRP3). Fecal flora was analyzed via 16S rRNA sequencing. LC‑Q‑TOF‑MS/MS detected 998 chemical constituents in THD extract. Among them, 24 high‑signal‑intensity constituents with mass‑spectrometry response values &gt; 100 000 were tentatively annotated based on exact‑mass and MS/MS fragmentation matching against public databases and published literature. Compared with the Sham group, VD rats exhibited longer escape latency, hippocampal neuronal damage, elevated proinflammatory factors, upregulated caspase‑1/NLRP3/NF‑κB, and downregulated SIRT1/IκBα. THD treatment reversed these VD‑induced pathological abnormalities. In addition, THD restored intestinal flora dysbiosis observed in VD model rats. THD ameliorates VD‑related cognitive dysfunction, accompanied by altered expression of SIRT1/IκBα/NF‑κB‑related proteins and reduced pro‑inflammatory cytokines. Meanwhile, THD can restore disturbed gut microbiota in VD rats. Changes in the SIRT1/IκBα/NF‑κB signaling cascade are therefore associated with THD‑mediated protective outcomes.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-026-11039-z.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149338588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative effects of mesenchymal stem cell- and platelet-rich plasma-derived extracellular vesicles on peripheral nerve regeneration following sciatic nerve crush injury","authors":"Ayat Abdelnaby,&nbsp;Sara Abdel Gawad Elsebay,&nbsp;Ghada Galal Hamam,&nbsp;Abeer A. Abd El Samad","doi":"10.1007/s10735-026-11024-6","DOIUrl":"10.1007/s10735-026-11024-6","url":null,"abstract":"<div><h3>Background</h3><p>Mesenchymal stem cells (MSCs) and platelet-rich plasma (PRP) exert neuroregenerative effects partly through extracellular vesicle (EV)-mediated paracrine signaling. This study directly compared MSCs-derived EVs and PRP-derived EVs following sciatic nerve crush injury (SNCI).</p><h3>Materials and methods</h3><p>Fifty-six adult male albino rats were randomly allocated to sham, phosphate-buffered saline (PBS)-treated SNCI, MSCs-EVs-treated SNCI, and PRP-EVs-treated SNCI groups. The Sciatic Functional Index (SFI) was assessed on postoperative days 7, 14, 21, and 28. Histological, S100β immunohistochemical, and ultrastructural assessments evaluated nerve-tissue organization, Schwann-cell-associated immunoreactivity, axonal regeneration, and myelin organization on days 14 and 28. Morphometric analysis of myelinated axon number, axon and nerve-fiber diameters, myelin thickness, and G-ratio was performed on day 28.</p><h3>Results</h3><p>Both EVs-treated groups demonstrated improved SFI compared with the PBS-treated SNCI group. Both treatments were associated with improved tissue organization, reduced residual myelin debris, higher myelinated axon counts, larger axon and nerve-fiber diameters, and greater myelin thickness than PBS-treated SNCI group. On day 28, the MSCs-EVs-treated SNCI group exhibited greater S100β immunoreactivity and a higher myelinated axon count than the PRP-EVs-treated group, whereas the PRP-EVs-treated group had a lower G-ratio.</p><h3>Conclusion</h3><p>Both EV preparations were associated with improved functional and morphological outcomes following SNCI. MSCs-EVs were associated with greater Schwann-cell-related immunoreactivity and more myelinated axons, whereas PRP-EVs were associated with a lower G-ratio.</p><h3>Graphical abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149338617","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"E3 ubiquitin ligase WWP1 aggravates intestinal inflammation in CD‑like colitis: insights into KLF5 ubiquitination‑mediated NF‑κB signaling regulation","authors":"Xiaoli Fang,&nbsp;Heng Deng,&nbsp;Ming Li","doi":"10.1007/s10735-026-11040-6","DOIUrl":"10.1007/s10735-026-11040-6","url":null,"abstract":"<div><p>The expression and function of E3 ubiquitin ligase WWP1, as well as the post-translational modification of transcription factor KLF5, have rarely been systematically characterized in Crohn’s disease (CD). We established a TNBS-induced CD-like colitis mouse model and an LPS-stimulated intestinal epithelial cell model. Histopathological staining, Western blot, qPCR and immunofluorescence were used to detect the expression and distribution of WWP1, KLF5 and NF-κB pathway-related proteins in colon tissues. Co‑immunoprecipitation (Co‑IP) and ubiquitination‑related signal assays were performed to examine protein co‑precipitation and ubiquitin‑associated signals for KLF5. CCK-8, ELISA, qPCR and Western blot were applied to assess cell viability, inflammatory cytokine secretion and NF-κB activation. A KLF5 overexpression rescue experiment was conducted to indicate the regulatory relationship between WWP1 and KLF5. In colonic tissues of colitis mice, WWP1 expression was increased to 3.46-fold, while KLF5 expression was decreased to 0.47-fold compared with controls. The levels of pro-inflammatory TNF-α and IL-6 were elevated to 2.81-fold and 3.06-fold, accompanied by noticeable NF-κB pathway activation. Co‑IP assays detected both proteins within immunoprecipitated complexes. WWP1 overexpression was accompanied by altered KLF5 ubiquitination signals, changes in KLF5 protein abundance, and exacerbated LPS‑induced inflammation, whereas ectopic KLF5 overexpression partially mitigated this pro‑inflammatory phenotype. Immunofluorescence suggested the co-localization of WWP1 and KLF5 in colonic mucosal cells of mouse colon tissues. This study suggests that WWP1 may aggravate intestinal inflammation in CD‑like colitis through potential modulation of KLF5, accompanied by downstream changes in NF‑κB signaling activation. This work provides additional mechanistic insights into CD‑like colitis and identifies a potential mediator for further pre‑clinical exploration.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149338650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Inhibition of RBM25 preserves cardiac mitochondrial homeostasis and attenuates ischemic heart failure","authors":"Shu Liu,&nbsp;Hong Ding,&nbsp;Kejuan Li,&nbsp;Xiaowei Zhang","doi":"10.1007/s10735-026-11034-4","DOIUrl":"10.1007/s10735-026-11034-4","url":null,"abstract":"","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149338618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ZhiXie capsule mitigates ionizing radiation-induced intestinal injury by inhibiting PI3K/AKT signaling pathway","authors":"Shimei He,&nbsp;Zheng Cai,&nbsp;Xiaolin Wang,&nbsp;Wenjun Zhang,&nbsp;Zhaochao Zhang,&nbsp;Zhongxing Fu,&nbsp;Ruixue Wang,&nbsp;Qinyun Yang,&nbsp;Ying Shi","doi":"10.1007/s10735-026-11015-7","DOIUrl":"10.1007/s10735-026-11015-7","url":null,"abstract":"<div><p>This study aimed to investigate the therapeutic effects of Zhixie Capsule (ZXC) on ionizing radiation (IR)-induced intestinal injury (radiation enteritis, RE) and to elucidate the underlying molecular mechanisms, focusing on the PI3K/AKT signaling pathway. A rat model of RE was established by 12 Gy abdominal IR. ZXC was administered daily for 7 days, and its effects were evaluated by monitoring body weight, disease activity index (DAI), colon length, histopathology (H&amp;E), and intestinal barrier integrity (Alcian blue staining, FITC-dextran permeability assay, and immunofluorescence for ZO-1 and occludin). Network pharmacology was used to predict key pathways. Inflammatory cytokines (IL-1β, IL-6, TNF-α, IL-10) were measured by ELISA, and pathway protein expression (p-PI3K, p-AKT, p-IKKβ, p-p65) was analyzed by Western blot. A rescue experiment using the PI3K activator YS49 was performed to confirm pathway specificity. In terms of results, ZXC dose-dependently alleviated RE manifestations, including weight loss, colonic shortening, and histological damage, and improved intestinal barrier integrity, as evidenced by increased goblet cell numbers and upregulated expression of tight junction proteins. Network pharmacology predicted the potential involvement of the PI3K/AKT axis. Mechanistically, ZXC suppressed IR-induced PI3K/AKT phosphorylation and downstream NF-κB activation, reducing pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and increasing IL-10 levels. These protective effects were partially reversed by YS49, suggesting that ZXC mitigates RE by inhibiting PI3K/AKT-mediated inflammation and improving mucosal barrier integrity, highlighting its potential as a radiomitigative strategy.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-026-11015-7.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149338688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DJ1 attenuates iron accumulation and ferroptosis-associated lung injury in association with SAHH activity and glutathione homeostasis","authors":"Jing Tang,&nbsp;Wenzhu Dong,&nbsp;Dan Wang,&nbsp;Qin Deng,&nbsp;Yiqiao Li,&nbsp;Guibao Xiao","doi":"10.1007/s10735-026-11033-5","DOIUrl":"10.1007/s10735-026-11033-5","url":null,"abstract":"<div><p>Iron-dependent ferroptosis has emerged as an important pathological mechanism in acute lung injury, but the endogenous mechanisms that limit iron accumulation and lipid peroxidation during lung injury remain incompletely understood. We investigated whether DJ1 (Parkinson disease protein 7, encoded by PARK7), a cytoprotective protein induced by oxidative stress, limits iron accumulation and ferroptosis in lipopolysaccharide (LPS)-induced acute lung injury. Experiments were performed in male C57BL/6J mice challenged with intratracheal LPS and in Beas-2B human bronchial epithelial cells treated with the ferroptosis inducer erastin. LPS challenge in mice and erastin treatment in cells increased total iron content and produced changes consistent with ferroptosis, including glutathione depletion, malondialdehyde accumulation, and reduced expression of glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (SLC7A11). C11-BODIPY analysis directly confirmed erastin-induced lipid peroxidation, and among the regulated cell death inhibitors tested, only ferrostatin-1 (Fer-1) substantially restored cell viability. DJ1 expression rose under both conditions. Adeno-associated virus-mediated DJ1 overexpression, delivered three weeks before LPS challenge, attenuated iron accumulation and lung injury, whereas DJ1 knockdown worsened both. Co-immunoprecipitation showed that DJ1 was associated with <i>S</i>-adenosylhomocysteine hydrolase (SAHH), an enzyme linked to methionine metabolism and glutathione synthesis. Higher DJ1 levels were accompanied by lower AHCYL1-SAHH association and higher SAHH activity. After treatment with adenosine periodate-oxidized (AdOx), the protection associated with DJ1 overexpression was no longer observed. Fer-1 produced protection similar to that associated with DJ1 overexpression. These findings support a role for DJ1 in limiting iron accumulation and ferroptosis-associated lung injury and are consistent with a contribution of SAHH activity. The precise contribution of the DJ1-SAHH-AHCYL1 relationship requires further mechanistic validation.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149338616","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulatory effects of alpha-lipoic acid on cardiac tissue alterations associated with 2.45 GHz radiofrequency electromagnetic radiation exposure","authors":"Nese Colcimen,&nbsp;Seda Keskin,&nbsp;Fikret Altindag,&nbsp;Tahir Cakir,&nbsp;Kenan Yildizhan","doi":"10.1007/s10735-026-11030-8","DOIUrl":"10.1007/s10735-026-11030-8","url":null,"abstract":"<div><p>The widespread use of devices emitting electromagnetic radiation (EMR) at 2.45 GHz has raised concerns regarding their potential impact on biological systems, particularly the cardiovascular system. This study aimed to characterize cardiac tissue alterations associated with repeated 2.45 GHz EMR exposure and to evaluate whether ALA administration modulated these alterations. EMR exposure was generated using a voltage-controlled oscillator and a low-noise RF amplifier, and the electric-field intensity within the exposure cage was measured using a calibrated electromagnetic field meter. The EMR and ALA + EMR groups were exposed to 2.45 GHz EMR at 2 h per day for 30 days. The ALA and ALA + EMR groups received ALA (30 mg/kg/day) by oral gavage for 30 consecutive days; in the ALA + EMR group, ALA was administered 1 h before each RF-EMR exposure session. Histopathological and histomorphometric evaluations revealed significant lymphocytic infiltration, collagen deposition, and increased mast cell area fraction in the EMR group compared to controls. These alterations were markedly alleviated in the ALA + EMR group. Furthermore, 2.45 GHz EMR exposure significantly increased the immunoreactivity of TNF-α, NF-κB, IL-6, iNOS, and S100A4, as well as serum cTnI and CK levels. ALA administration significantly attenuated these alterations. Stereological analysis further showed increased myocardial volume density in the EMR group, which ALA + EMR significantly attenuated. Collectively, these findings indicate that ALA administration attenuated cardiac structural, inflammatory, and biochemical alterations observed under the present 2.45 GHz RF-EMR exposure conditions; however, the experimental design does not establish a causal RF-EMR-specific effect.</p><h3>Graphical abstract</h3><div><figure><div><div><picture><source><img></source></picture></div></div></figure></div></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149332015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Taurine protects against cadmium-induced neurocardiac injury by modulating inflammatory and apoptotic pathways","authors":"Abdullah Coğuplugil,&nbsp;Münevver Nazlıcan Kaplan,&nbsp;Bedriye Çiftçi,&nbsp;Özlem Özmen,&nbsp;Recep Kiliç,&nbsp;Osman Çiftçi","doi":"10.1007/s10735-026-11029-1","DOIUrl":"10.1007/s10735-026-11029-1","url":null,"abstract":"<div><p>Cadmium (Cd) is a highly toxic environmental pollutant that induces multi-organ damage, through inflammation and apoptosis, including the brain and heart. Taurine (Tau), a sulfur-containing amino acid, is known to regulate inflammatory signaling and maintain cellular homeostasis. In this study, the protective effects of taurine against cadmium-induced brain and cardiac toxicity were investigated in rats. Adult male Sprague–Dawley rats (3–4 months old, 250–300 g; n = 6/group, 24 rats in total) were divided into four groups<b>:</b> control, cadmium, taurine, and cadmium + taurine. Cadmium chloride (administered intraperitoneally) and taurine (administered orally by gavage) were given for 50 days, at doses of 1 mg/kg and 200 mg/kg/day, respectively. To evaluate cadmium-induced toxicity, serum cytokine levels (TNF-α, IL-6, IL-1β), gene expression of apoptosis- and inflammation-related markers (Bax, Bcl-2, NF-κB), and histopathological alterations were assessed. Cadmium exposure significantly increased serum cytokine levels and upregulated pro-apoptotic and inflammatory gene expression (<i>p</i> &lt; 0.05). These molecular changes were accompanied by marked histopathological alterations in both organs, including, edema, gliosis, and neuronal damage in the brain, as well as myocardial degeneration and structural disruption in cardiac tissue. In contrast, taurine treatment, the taurine treatment significantly reversed the effects of cadmium by reducing serum inflammatory cytokine levels and suppressing both pro-inflammatory and pro-apoptotic gene expression (<i>p</i> &lt;0.05). Similarly, it ameliorated histopathologic damage in both the brain and heart caused by cadmium toxicity. Consequently, taurine treatment significantly protected both the brain and heart tissues by modulating inflammatory and apoptotic pathways induced by cadmium toxicity. These findings indicate that taurine therapy may be used as a potential therapeutic agent in cadmium-induced brain and heart damage.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149332016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Xianfang Huoming Decoction ameliorates hidradenitis suppurativa-like pathology by restoring NCSTN/Notch signaling homeostasis in NcstnΔKC mice and NCSTN-knockdown HaCaT cells","authors":"Qiuxia Mao,&nbsp;Xuling Wu,&nbsp;Zixi Wang,&nbsp;Yingying Zhou,&nbsp;Zhen Fang,&nbsp;Hongliu Zhu,&nbsp;Yihong Gao,&nbsp;Feng Shi,&nbsp;Yuegang Wei","doi":"10.1007/s10735-026-10990-1","DOIUrl":"10.1007/s10735-026-10990-1","url":null,"abstract":"<div><p>Hidradenitis suppurativa (HS) is a chronic inflammatory skin disorder characterized by follicular occlusion, hyperkeratosis, epidermal hyperplasia, and persistent inflammation. Dysregulation of NCSTN/Notch signaling, often associated with loss-of-function variants, contributes to impaired epidermal differentiation and inflammatory amplification. Xianfang Huoming Decoction (XFHMD), a traditional Chinese herbal formula, has shown therapeutic potential in inflammatory skin conditions; however, its mechanism of action in HS remains unclear. This study aimed to investigate the therapeutic effects and underlying mechanisms of XFHMD in HS, with a particular focus on the restoration of NCSTN/Notch signaling homeostasis. Keratinocyte-specific <i>Ncstn</i> knockout (<i>Ncstn</i>^ΔKC) mice were used as an HS-like model to evaluate the in vivo effects of XFHMD. <i>NCSTN</i>-knockdown HaCaT keratinocytes were employed for in vitro mechanistic studies. The activity of NCSTN/Notch signaling and related downstream pathways, including PI3K/AKT and EGFR-associated signaling, was assessed using molecular and biochemical approaches. XFHMD significantly ameliorated follicular hyperkeratosis and epidermal hyperplasia in <i>Ncstn</i>^ΔKC mice, accompanied by restoration of NCSTN/Notch signaling. In <i>NCSTN</i>-knockdown HaCaT cells, XFHMD similarly reactivated NCSTN/Notch signaling and promoted normalization of dysregulated downstream pathways, including EGFR and PI3K/AKT signaling. XFHMD exerts therapeutic effects in HS primarily through restoration of NCSTN/Notch signaling homeostasis, accompanied by coordinated regulation of multiple downstream pathways. These findings provide mechanistic support for the development of XFHMD as a multi-target therapeutic strategy for HS.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 6","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-11-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149316963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}