{"title":"Phytoextract-loaded bioinspired PLGA nanofibrous scaffold promotes diabetic wound healing via anti-inflammatory and antioxidant effects in in vitro and in vivo experimental models.","authors":"Garima Sahu, Mukul Maurya, Satyam Sharma, Virendra Kumar Kushwaha, Alok Mukerjee, Brahmeshwar Mishra","doi":"10.1007/s10735-026-10903-2","DOIUrl":"https://doi.org/10.1007/s10735-026-10903-2","url":null,"abstract":"<p><p>Diabetic wounds pose significant healing challenges due to persistent inflammation, oxidative stress, and impaired tissue regeneration. This study developed bioinspired PLGA-gelatin nanofibrous scaffolds encapsulating Vitex negundo (VN) and Jatropha multifida (JM) phytoextracts to mimic the extracellular matrix, enhance drug release, and promote wound healing via anti-inflammatory and antioxidant mechanisms in in vitro (HUVEC cells) and in vivo (streptozotocin-induced diabetic rat) models. VN-JM nanofibers exhibited uniform nanoscale morphology (255-280 nm) with successful phytoconstituent incorporation, while XRD analysis confirmed crystalline-to-amorphous transformation, indicating enhanced solubility. The nanofibers demonstrated high porosity (83.6 ± 0.9%), excellent swelling capacity (450 ± 18% at 24 h), and controlled biodegradation (63.5 ± 4.5% weight loss at 28 days), supporting their suitability as bioresorbable wound dressings. Furthermore, the formulation provided sustained drug release over 168 h, achieving approximately 90% cumulative release, thereby ensuring prolonged therapeutic availability at the wound site. At optimal doses, nanofibers enhanced HUVEC viability, reduced ROS (DCFH intensity, boosted colony formation, and enhances migration wound closure. In diabetic rats, daily topical application for 21 days yielded better wound closure at day 21, markedly lowered TNF-α, IL-6, and diminished lipid peroxidation, DCF, nitrite levels compared to gels and extracts. Histology showed complete re-epithelialization, fibroblast proliferation, neovascularization, and organized collagen in nanofiber-treated groups, outperforming diabetic controls and matching standard groups. These findings demonstrate VN+JM-loaded nanofibers could be taken as a promising regenerative scaffold for diabetic wounds by mitigating oxidative stress and inflammation.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896333","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":"Identification of STAT1 as a biomarker for lymph node metastasis in esophageal squamous cell carcinoma.","authors":"Guoli Lv, Haoyu Li, Youming Lei, Jungao Peng, Fanghao Liu, Wei Zhao","doi":"10.1007/s10735-026-10914-z","DOIUrl":"https://doi.org/10.1007/s10735-026-10914-z","url":null,"abstract":"<p><p>Lymph node metastasis in esophageal squamous cell carcinoma (ESCC) is associated with poor prognosis, and screening for potential biomarkers of metastasis is significant for improving the prognosis of ESCC. After batch effect removal and integration of two ESCC transcriptome datasets (GSE157804, GSE118493), differentially expressioned gene analysis was performed. The intersection of differentially expressed genes was obtained to identify characteristic genes associated with lymph node metastasis in ESCC. GO/KEGG enrichment analyses were conducted for the characteristic genes. The top 10 pathways and pathway genes based on q-value were selected to construct a PPI network. Hub genes were identified and intersected with the characteristic genes to determine key genes. GO/KEGG enrichment, expression level analysis, and immune infiltration analysis were performed for the key genes. Immunohistochemistry was used to validate the expression levels of key genes in clinical samples. A cell model with regulated expression of key genes was established to verify their impact on the invasive and migratory capabilities of ESCC cells and epithelial-mesenchymal transition (EMT), as well as ECM‑related gene expression. A total of 542 characteristic genes associated with lymph node metastasis in ESCC were identified through differential gene analysis, which were mainly enriched in extracellular matrix-related pathways. PPI network analysis identified 63 hub genes, and the intersection with characteristic genes resulted in 20 key genes, which were also primarily enriched in extracellular matrix-related pathways. Expression level analysis showed that key genes such as STAT1, STAT2, IFIT1, and IFIT3 were highly expressed in metastatic ESCC tissues compared to primary sites and adjacent non-tumor tissues. Immune infiltration analysis revealed a significant positive correlation between IFIT3, STAT1, STAT2, and M1 macrophage polarization. Immunohistochemical analysis indicated high expression of STAT1 in ESCC patient samples with lymph node metastasis. Upregulation of STAT1 in ESCC cells enhanced cell invasion, migration, EMT levels and ECM‑related gene expression, while downregulation of STAT1 expression suppressed these processes. Consistently, an additional gain‑of‑function experiment further confirmed these promoting effects. STAT1 serves as a biomarker for lymph node metastasis in ESCC. The expression level of STAT1 is positively correlated with the degree of lymph node metastasis in ESCC clinical samples. Overexpression of STAT1 promotes the invasion, migration, EMT and ECM‑related gene expression of ESCC cells, while the downregulation of STAT1 inhibits these effects.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148896271","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":"Exosomal miR-22-3p targets p53 to regulate endometrial epithelial cell function in the pathogenesis of endometriosis.","authors":"Congxiang Yu, Yuefei Li, Gele Qi, Qiao Qiao","doi":"10.1007/s10735-026-10966-1","DOIUrl":"10.1007/s10735-026-10966-1","url":null,"abstract":"<p><p>Endometriosis (EMs) is a widespread gynecological disease, affecting approximately 6-10% of females of child-bearing age. Despite its significant influence on women's health, the specific pathophysiology remains unclear. The enrichment of miR-22-3p in exosomes has been implicated in cellular proliferation and migration. This study aimed to elucidate the mechanisms by which exosomal miR-22-3p affects endometrial epithelial cell function in the etiology of endometriosis. The patient samples and clinical data were acquired from the Affiliate Hospital of Inner Mongolia Medical University. Quantitative reverse transcription‒polymerase chain reaction (qRT‒PCR), a miRNA microarray and Western blotting were used to confirm that the level of miR-22-3p was specifically elevated in peripheral blood exosomes from EMs patients. The influence of miR-22-3p on EMs-derived exosomes was determined by Transwell and cell counting kit-8 (CCK-8) assays. Luciferase reporter assays, RNA pull-down assays, and fluorescence in situ hybridization (FISH) were performed to determine whether exosomal miR-22-3p binds to p53. miR-22-3p expression was significantly elevated in peripheral blood exosomes (p < 0.001) from patients with endometriosis. ROC curve analysis demonstrated the high sensitivity (93.55%) and specificity (84.85%) of this correlation, suggesting that miR-22-3p is a promising diagnostic biomarker. Endometrial epithelial cell proliferation, migration, and invasion are regulated by exosomal miR-22-3p, which targets and inhibits p53, a crucial tumor suppressor related to cell cycle regulation and apoptosis. Exosomal miR-22-3p regulates endometrial epithelial cell proliferation, migration, and invasion by targeting and inhibiting p53. Combining standard endometriosis treatments with exosome-mediated miR-22-3p targeting of p53 could restore p53 function, induce apoptosis, and reduce disease recurrence, providing a promising therapeutic strategy for endometriosis management.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13541819/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148885951","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}
Yibin Li, Qinglin Li, Jun Liu, Juncen Li, Huaman Geng, Genke Li, Huilin Huang, Chen Jin, Jie Luo, Zhihong Zhang
{"title":"Exploring the mechanism of Panax notoginseng injection in the treatment of skin wound based on network pharmacology and experimental verification.","authors":"Yibin Li, Qinglin Li, Jun Liu, Juncen Li, Huaman Geng, Genke Li, Huilin Huang, Chen Jin, Jie Luo, Zhihong Zhang","doi":"10.1007/s10735-026-10969-y","DOIUrl":"https://doi.org/10.1007/s10735-026-10969-y","url":null,"abstract":"<p><p>Prolonged healing of skin wounds remains a major clinical challenge. This study employed network pharmacology combined with in vivo experimental validation to investigate the mechanisms of Panax notoginseng (PN) in treating skin wounds. Network pharmacology identified 156 targets and 115 signaling pathways, with top core targets (TNF, IL-6, IL-10) enriched in NF-κB, MAPK, and JAK-STAT pathways. Molecular docking showed favorable binding affinities between PN components (Ginsenoside Rb₁, Rd, Re, Rg₁, Notoginsenoside R₁) and key target proteins. In vivo, 48 SD rats were randomly divided into a PN group and a control group with a full-thickness skin excision model. The PN group showed significantly smaller wound areas at days 4 and 7 (P < 0.05), with reduced inflammatory cell infiltration and enhanced fibroblast proliferation at day 7. qRT-PCR and ELISA demonstrated that TNF-α was significantly lower in the PN group at days 4 and 7 (P < 0.01), IL-6 was lower at all time points (P < 0.01), and IL-10 was lower at days 1 and 7 (P < 0.01). These findings suggest that PN modulates the inflammatory cytokine network (TNF-α, IL-6, IL-10) in a time-dependent manner, consistent with the regulation of the \"inflammation initiation → repair transition\" temporal sequence, representing a promising natural agent for regulating the inflammatory phase of skin wound healing.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890694","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}
Shaofeng Chen, Jie Wang, Yuhong Feng, Chunxu Li, Fu Wang, Lin Miao, Yaojun Li, Yangyang Lei, Qiang Geng, Zhong Li, Feng Zhao, Yuan Sun, Lijian Du
{"title":"Mechanism of Kushen Tongguan Pill on benign prostatic hyperplasia: roles of TLR4/NF-κB pathway and macrophage M1 polarization.","authors":"Shaofeng Chen, Jie Wang, Yuhong Feng, Chunxu Li, Fu Wang, Lin Miao, Yaojun Li, Yangyang Lei, Qiang Geng, Zhong Li, Feng Zhao, Yuan Sun, Lijian Du","doi":"10.1007/s10735-026-10945-6","DOIUrl":"https://doi.org/10.1007/s10735-026-10945-6","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the therapeutic effect of Kushen Tongguan Pill (KSTG) on benign prostatic hyperplasia (BPH) induced by castration combined with testosterone propionate in rats, and to explore its underlying mechanism associated with the Toll-like receptor 4/nuclear factor κB (TLR4/NF-κB) signaling pathway.</p><p><strong>Methods: </strong>A rat BPH model was established by castration combined with subcutaneous injection of testosterone propionate. Rats were randomly divided into sham group, BPH group, and low-, medium-, and high-dose KSTG groups (2.52, 5.04, and 10.08 g/kg). After 4 weeks of intervention, prostate wet weight was weighed and prostate index was calculated; histopathological changes were observed by hematoxylin-eosin (HE) staining; collagen deposition and fibrosis were evaluated by Masson's trichrome staining; the expression of α-smooth muscle actin (α-SMA) was detected by immunohistochemistry; serum testosterone (T), estradiol (E2), and dihydrotestosterone (DHT) levels were measured by enzyme-linked immunosorbent assay (ELISA); peripheral white blood cell and neutrophil counts were measured using an automated hematology analyzer; toluidine Blue staining was performed to observe mast cell infiltration in prostate tissue to assess local chronic inflammation. RT-qPCR was used to detect the mRNA expression of key pathway molecules including TLR4, NF-κB p65, IKKα, and IKKβ, as well as inflammatory markers TNF-α, IL-1β, MCP-1, and iNOS in prostate tissue. Western blotting was performed to analyze the protein expression of key pathway molecules including TLR4, MyD88, IκBα, p-IκBα, NF-κB p65, and p-NF-κB p65, as well as the inflammatory marker iNOS in prostate tissue. For in vitro experiments, KSTG-containing serum was used to treat LPS/IFN-γ-induced THP-1-derived macrophages. The mRNA expression of M1 polarization markers (CD86, TNF-α, IL-6) in macrophages was determined by RT-qPCR. Subsequently, the conditioned medium from each macrophage group was collected, and its effect on WPMY-1 cell proliferation was evaluated by CCK-8 assay.</p><p><strong>Results: </strong>Compared with the BPH group, KSTG dose-dependently reduced prostate volume, wet weight, and prostate index (P < 0.05) and improved the pathological morphology of glandular hyperplasia and interstitial thickening. KSTG dose-dependently reduced serum E2 levels and the E2/T ratio, and significantly decreased the abnormally elevated serum DHT levels (P < 0.05). KSTG also reduced peripheral white blood cell and neutrophil counts, downregulated the mRNA expression of TNF-α and IL-1β, and decreased the protein expression of iNOS in prostate tissue (P < 0.05). Toluidine blue staining further revealed that KSTG treatment reduced mast cell infiltration in the prostate, corroborating the alleviation of local inflammation (P < 0.05). Western blotting showed that KSTG significantly inhibited the protein expression of TLR4 and MyD88 in prostate tissue and suppress","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148890650","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}
M J Macedo, I L Lemos, I M U Rossetto, F R Santos, F Montico, V H A Cagnon, M R J Maróstica
{"title":"Annona crassiflora seed extract modulates histological and molecular markers associated with prostate cancer progression in TRAMP mice.","authors":"M J Macedo, I L Lemos, I M U Rossetto, F R Santos, F Montico, V H A Cagnon, M R J Maróstica","doi":"10.1007/s10735-026-10948-3","DOIUrl":"10.1007/s10735-026-10948-3","url":null,"abstract":"<p><p>Prostate cancer ranks second among the most common malignant neoplasms in men worldwide. Fruit extracts with potential anti-prostate cancer properties have gained increasing attention, with the most notable belonging to the Annonaceae family, including Araticum (Annona crassiflora Mart). In this study, we aimed to evaluate the chemopreventive and anti-inflammatory potential of Araticum seed extract (Annona crassiflora Mart) on the ventral prostate lobe of Transgenic Adenocarcinoma of the Mouse Prostate (TRAMP) model. Sixty male TRAMP mice, aged 8 and 12 weeks, were divided into four groups: two groups received the extract at a dose of 100 mg/kg body weight, and two control groups received equivalent volumes of water and DMSO (Dimethyl Sulfoxide). After 30 days, animals were euthanized and ventral prostate samples were collected for morphological evaluation by light microscopy, immunohistochemistry, and Western blotting. Treatment with Araticum seed extract delayed the progression of premalignant and malignant lesions (HGPIN and adenocarcinoma) and preserved healthy tissue. The extract showed antiproliferative activity, reducing PCNA, IGFR-1, and AR protein levels. Inflammatory signaling was suppressed via Toll-like receptor pathways, with decreased NFκB, TNF-α, and other inflammatory markers. Moreover, the extract reduced BCL-2 expression and promoted caspase activation, suggesting pro-apoptotic protection. In conclusion, treatment with Araticum seed extract demonstrated promising chemopreventive activity, effectively reducing the progression of epithelial lesions in the ventral prostate lobe of TRAMP mice and may be suggested as a potential chemopreventive agent in combined prostate cancer therapies.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534168/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148872570","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}
Jianliang Li, Yanhuai Ma, Jiale Mai, Fanchen Wang, Hao Wang
{"title":"Correction: Myricitrin as a potent inhibitor of osteoclast differentiation via RAW264.7 Cells, BMMs and ovariectomized mouse model.","authors":"Jianliang Li, Yanhuai Ma, Jiale Mai, Fanchen Wang, Hao Wang","doi":"10.1007/s10735-026-10954-5","DOIUrl":"https://doi.org/10.1007/s10735-026-10954-5","url":null,"abstract":"","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148872579","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":"Anti-LCN2 antibody treatment is associated with attenuated hearing loss and blood-labyrinth barrier disruption in a mouse model of chronic kidney disease.","authors":"Ye Ding, Xin Jiang, Xiangming Ye","doi":"10.1007/s10735-026-10963-4","DOIUrl":"https://doi.org/10.1007/s10735-026-10963-4","url":null,"abstract":"<p><p>Chronic kidney disease (CKD) is associated with sensorineural hearing loss, but the mechanisms linking renal injury to cochlear dysfunction remain incompletely defined. Because lipocalin-2 (LCN2/NGAL) is markedly increased in CKD and has been implicated in endothelial dysfunction and barrier injury, we investigated whether LCN2 contributes to cochlear damage in a mouse model of CKD. Male C57BL/6J mice underwent 5/6 nephrectomy, and CKD mice received either an anti-LCN2 monoclonal antibody or an isotype control three times weekly for seven weeks beginning one week after completion of surgery. Auditory function, cochlear morphology, blood-labyrinth barrier integrity, cochlear perfusion, and LCN2-associated signaling were assessed using auditory brainstem responses, distortion product otoacoustic emissions, whole-mount immunofluorescence, FITC-dextran extravasation, Western blotting, quantitative PCR, and laser Doppler flowmetry. CKD mice developed elevated auditory brainstem response thresholds, reduced distortion product otoacoustic emission amplitude at a single primary tone pair with f2 = 8.0 kHz, outer hair cell loss, and a reduction in the number of CtBP2-positive presynaptic ribbon puncta per inner hair cell. These changes were accompanied by increased serum and cochlear LCN2, upregulation of 24p3R/SLC22A17 and NLRP3, increased blood-labyrinth barrier permeability, reduced claudin-5 and ZO-1 expression, impaired cochlear blood flow, stria vascularis atrophy, and decreased expression of strial ion-transport genes. Anti-LCN2 antibody treatment improved auditory thresholds and otoacoustic emission responses, attenuated outer hair cell and synaptic injury, reduced vascular leakage, partially restored tight junction and ion-transport gene expression, and improved cochlear perfusion, without measurably lowering serum blood urea nitrogen or creatinine. These findings support a possible contribution of LCN2 to CKD-associated cochlear vascular dysfunction and hearing loss. Targeting LCN2 may represent a therapeutic strategy for preserving hearing in CKD, although validation in additional CKD models, both sexes, and human tissues is required.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148860393","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}
Nusaiba Nujhat, Inun Nahar Payel, Md Liakot Ali, Rowshan Akter Mukta, S M Moazzem Hossen, Mohammad Helal Uddin
{"title":"Anti-inflammatory, wound healing, and hepatoprotective effects of Acampe papillosa (Lindl.) Lindl. seed in wistar rats: insights from biochemical, histopathological, and in silico investigations.","authors":"Nusaiba Nujhat, Inun Nahar Payel, Md Liakot Ali, Rowshan Akter Mukta, S M Moazzem Hossen, Mohammad Helal Uddin","doi":"10.1007/s10735-026-10958-1","DOIUrl":"https://doi.org/10.1007/s10735-026-10958-1","url":null,"abstract":"<p><p>Acampe papillosa (Lindl.) Lindl. has long been used to cure a variety of illnesses, including rheumatism and traumatic tissue injuries. Nevertheless, there is a dearth of comprehensive information on its phytochemical composition and pharmacological actions. Therefore, here, we present the first thorough pharmacological and histopathological analysis of Acampe papillosa seed methanolic extract (ME-APS), together with in silico molecular docking studies, hepatoprotective, wound-healing, and anti-inflammatory properties. Before pharmacological evaluations, safety was assessed through oral and dermal toxicity studies. The anti-inflammatory activity of ME-APS was tested using carrageenan and formalin-induced paw oedema models, and the wound healing potential was observed using incision and excision wound models. Hepatoprotective activity was studied in the CCl<sub>4</sub>-induced hepatotoxicity model in rats. In oral (up to 5000 mg/kg) and dermal (10% ointment formulation) toxicity studies, ME-APS was found to be safe with no visible signs of toxicity. In the study on anti-inflammatory properties, ME-APS significantly reduced paw oedema in carrageenan and formalin models of inflammation. Wound healing assays showed that the extract significantly improved wound contraction, tensile strength, epithelialization, collagen deposition, and fibroblast proliferation in a dose-dependent way. The hepatoprotective study showed that ME-APS treatment significantly restored the altered biochemical parameters, such as ALT, AST, TC, TG, and LDL levels, and ameliorated CCl<sub>4</sub>-induced histopathological liver damage. Further, the molecular docking study showed that the major phytochemicals in the extract, such as squalene, cholesta-4,6-dien-3-ol (3β), stigmasterol, and γ-sitosterol, showed significant binding affinities for COX-2 and TGF-β-related targets involved in inflammation, wound healing, and hepatoprotection. Additionally, a high probability of biological efficacy was predicted using PASS (Prediction of Activity Spectra for Substances) analysis. Overall, the findings suggest that ME-APS has possible anti-inflammatory, wound healing, and hepatoprotective activities that support its traditional medicine use and imply that it is a potential source of therapeutic phytochemicals.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"57 5","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-08-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148860390","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}