Shokofeh Banaei, Vahid Asghariazar, Faraz Mahdizadeh, Mohammad Ghasem Golmohammadi, Elham Safarzadeh
{"title":"Oleuropein attenuates cardiac and lung injury induced by 5-fluorouracil via modulating oxidative stress and TNF-α/IL-6 signaling pathway","authors":"Shokofeh Banaei, Vahid Asghariazar, Faraz Mahdizadeh, Mohammad Ghasem Golmohammadi, Elham Safarzadeh","doi":"10.1007/s10735-025-10437-z","DOIUrl":"10.1007/s10735-025-10437-z","url":null,"abstract":"<div><p>The cardiac and lung damage are considered a serious risk associated with the administration of chemotherapy agents like 5-fluorouracil (5-FU). Oleuropein (OLE) is valuable medicinal plant that has diverse pharmacological properties with remarkable antioxidant activities. This research aimed to evaluate the impact of OLE on cardiac and pulmonary toxicity induced by 5-FU. 24 adult rats were randomly assigned to four groups (N = 6), which included a control group, a group receiving 5-FU at a dosage of 100 mg/kg, a group administered OLE at 200 mg/kg, and a group treated with both 5-FU and OLE (5-FU + OLE). Following the treatment, blood samples were obtained for the assessment of biochemical parameters, and the cardiac and pulmonary tissues were removed for the measurement of oxidative stress and inflammatory cytokines and histological alterations. 5-FU elevated lipid profiles (triglyceride, low-density lipoprotein (LDL), and cholesterol), glucose serum levels, and myocardial injury markers (CK-MB and LDH), malondialdehyde (MDA), interleukin‐6 (IL-6) and tumor necrosis factor alpha (TNF-α) expression. Additionally, the histopathological analysis of 5-FU revealed dystrophic calcification (DC) in the cardiac tissues and neutrophil infiltration in the lung tissues. However, the administration of OLE reduced lipid profiles, glucose, lactate dehydrogenase (LDH), creatine kinase-myocardial band (CK-MB) levels and inflammation, improved antioxidant capacity, and pathological alterations. It seems that OLE exerts cardio-pulmonary protective effects against 5-FU toxicity through the decrease of oxidative stress and inflammatory cytokines.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143925681","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}
Fikriye Yasemin Ozatik, Yasemin Teksen, Orhan Ozatik, Cigdem Çengelli Unel, Suna Karadeniz Saygili
{"title":"The effects of the GLP1 analog liraglutide on allodynia and motor coordination in peripheral neuropathy induced by a chemotherapeutic agent, cisplatin","authors":"Fikriye Yasemin Ozatik, Yasemin Teksen, Orhan Ozatik, Cigdem Çengelli Unel, Suna Karadeniz Saygili","doi":"10.1007/s10735-025-10440-4","DOIUrl":"10.1007/s10735-025-10440-4","url":null,"abstract":"<div><p>Peripheral neuropathy is one of the dose-limiting side effects of cisplatin (CIS) and still has no effective treatment. In this study, we aimed to investigate the potential protective effects of liraglutide, a Glucagon-like peptide-1 (GLP-1) analogue against CIS-induced peripheral neuropathy. For this purpose, female Sprague Dawley rats (<i>n</i> = 32) were randomly allocated into 4 groups: control, CIS, CIS + liraglutide (once weekly) and CIS + liraglutide (daily). Neuropathic pain was induced by CIS 3 mg/kg/week for 5 weeks. The potential effects of liraglutide were investigated by behavior tests (von Frey, tail flick and footprint analysis), biochemical analysis and histopathological analyses of sciatic nerves and dorsal root ganglions. In the von Frey and tail flick tests, liraglutide demonstrated anti-neuropathic effects. Liraglutide also ameliorated motor coordination which was impaired by CIS. Liraglutide was shown to have beneficial effects against CIS-induced peripheral neuropathy by parameters demonstrating reduction of histopathological damage (stained by toluidine blue) of the sciatic nerves and dorsal root ganglions, suppression of oxidative stress parameters (SOD, CAT and GPx), and inflammatory load (NO, IL-6 and IL-10). Weekly dosing regimen was more effective than daily administration of liraglutide in this study. As a result, liraglutide seems to be the candidate agent for the effective treatment of CIS-induced peripheral neuropathy.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143925680","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}
Wenzi Liang, Chang Mai, Yuandong Yuan, Xiuwen Chen, Bozhi Cai, Na Ni, Chutong Zhuang, Changmin Lin, Keng Huang
{"title":"Autografted hair follicles with dermal papilla removed promote wound repair and regeneration in Bama mini-pigs","authors":"Wenzi Liang, Chang Mai, Yuandong Yuan, Xiuwen Chen, Bozhi Cai, Na Ni, Chutong Zhuang, Changmin Lin, Keng Huang","doi":"10.1007/s10735-025-10420-8","DOIUrl":"10.1007/s10735-025-10420-8","url":null,"abstract":"<div><p>Autologous free flap transplantation is the most economical and effective method for clinical treatment of large-area trauma, but the shortage of flap donors prevents widespread use of this method. Hair follicle stem cells have great potential to repair wounds, but wound repair by hair follicle stem cells has not yet met expectations. We used a wound model of Bama mini-pigs and treated the wound with autologous hair follicles or flaps. The wound healing was observed on days 7, 14, and 21 post-surgery and wound healing rates were analyzed using Image J software. Hematoxylin and eosin staining was performed to evaluate re-epithelialization of the wound. Immunofluorescence staining was used to detect the expression of hair follicle stem cell markers (CK15, Sox9) and explore the mechanism of wound repair. This research found that autologous hair follicles can accelerate wound healing. The efficiency of hair follicles in wound repair is related to their structure. Dermal papilla acts as a biological barrier to hair follicle-mediated wound repair. Dermal papilla removal enhances wound healing efficiency, likely by relieving dermal papilla-imposed restrictions on hair follicle stem cell migration. Autologous hair follicles for wound repair has the advantages of minimal damage, simple fabrication, and abundant source, which may be able to replace the flap transplantation as a therapeutic strategy in the future. This study is helpful to elucidate the regulatory mechanism of hair follicles involved in wound repair, and has important academic and clinical value for solving the problem of shortage flap donor.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143925699","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}
Yin Shu, Xiaohui Cai, Xinhui Yang, Yuping Yang, Lei Ge
{"title":"Demethylated miR-184 regulates EPB41L5 and downregulates Notch signaling to inhibit metastasis in colorectal cancer","authors":"Yin Shu, Xiaohui Cai, Xinhui Yang, Yuping Yang, Lei Ge","doi":"10.1007/s10735-025-10434-2","DOIUrl":"10.1007/s10735-025-10434-2","url":null,"abstract":"<div><p>Colorectal cancer (CRC) remains a leading cause of cancer-related mortality worldwide, with metastasis being a major contributor to poor prognosis. MicroRNA-184 (miR-184) has been implicated in the progression of various cancers, but its role in CRC metastasis remains poorly defined. This study investigated the effects of miR-184 promoter demethylation on EPB41L5 expression and Notch signaling in CRC. SW620 human colon carcinoma cells were treated with the DNA methylation inhibitor 5-Aza for 96 h. Methylation status was assessed via bisulfite sequencing, and gene expression was evaluated using qRT-PCR and Western blotting. Functional assays were conducted to assess cell proliferation, apoptosis, migration, and invasion. 5-Aza treatment significantly decreased miR-184 promoter methylation, leading to increased miR-184 expression. This upregulation suppressed CRC cell migration and invasion, induced G2/M cell cycle arrest, and promoted apoptosis. Mechanistically, miR-184 inhibited EPB41L5 expression, thereby downregulating the Notch signaling pathway and modulating epithelial–mesenchymal transition markers. High EPB41L5 expression in CRC tissues was associated with worse prognosis. These findings suggest that demethylated miR-184 inhibits CRC metastasis by targeting the EPB41L5/Notch signaling axis. This regulatory pathway may serve as a novel prognostic biomarker and therapeutic target, with potential clinical implications for the prevention and treatment of metastatic colorectal cancer.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143925700","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":"Protective effects of lupeol on pesticides induced testicular and oxidative damage of male rats","authors":"Pınar Koroglu, Ismet Burcu Turkyılmaz Mutlu, Huseyin Us, Melis Coremen, Ayca Sezen Us, Omur Karabulut Bulan, Refiye Yanardag","doi":"10.1007/s10735-025-10425-3","DOIUrl":"10.1007/s10735-025-10425-3","url":null,"abstract":"<div><p>Pesticides are used as insecticides in agriculture. Lupeol (LUP) is a dietary triterpene with antioxidant effects. This experiment aimed to investigate the effects of LUP against testicular pesticides toxicity via histological and biochemical findings. Wistar albino rats were used. Control, corn oil, malathion (MAL), chlorpyrifos (CPF), tebuconazole (TEB), LUP, MAL + LUP, CPF + LUP, and TEB + LUP group. Control group rats were given physiological saline. Corn oil is used as a solvent in the preparation of pesticide agents. MAL 50 mg/kg, CPF 10 mg/kg, TEB 50 mg/kg (first 4 days) and 25 mg/kg (last 4 days), LUP 20 mg/kg were given via oral gavage. After 10 days, rats were dissected, and testes were taken for histological analysis. Oxidative stress parameters were determined spectrophotometrically in testicular tissue specimens. In the pesticide group, histological and biochemical damage score increased, morphological sperm smear defects were also detected. These defects were reversed upon the administration of LUP. LUP demonstrated an ameliorative effect on histopathological and biochemical parameters in pesticide induced testicular damage.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://link.springer.com/content/pdf/10.1007/s10735-025-10425-3.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143925701","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":"Ameliorative effects of chitosan on fluoride-induced kidney injury in rats: a stereological and immunohistochemical study","authors":"Fikret Altındağ, Uğur Özdek","doi":"10.1007/s10735-025-10428-0","DOIUrl":"10.1007/s10735-025-10428-0","url":null,"abstract":"<p>The present study aimed to investigate the possible protective effects of chitosan (CS) on fluoride-induced nephrotoxicity. 28 rats were divided into four groups (n = 7). The Control group received drinking water. Sodium fluoride (NaF) group received 100 mg/L NaF in drinking water. NaF + CS group received 100 mg/L NaF and 250 mg/kg/day CS by gastric gavage. CS group was given 250 mg/kg/day CS by gavage. The study period lasted 12 weeks. Total kidney volume, Bowman’s capsule volume, Bowman’s space volume, Tubular volume and Glomerulus volume were measured by stereological methods. Immunohistochemically, caspase-3 and TNF-alpha expressions were evaluated. Biochemically, levels of urea and creatinine were measured. In addition, a histopathological evaluation of the kidney was performed. According to the control group, an increase was observed in all stereological parameters except glomerulus volume in the NaF group. CS treatment inhibited the increase in stereological parameters. Fluoride increased expressions of caspase-3 and TNF-α in the kidney, and serum urea and creatine levels, but CS decreased these parameters. In addition, pathological changes in the kidney caused by fluoride such as tubular dilatation, enlargement of the Bowman’s space, and deterioration in tubular epithelial cells were restored with CS treatment. The conclusions of the current study reveal that fluoride can cause nephrotoxicity and CS treatment can prevent fluoride-induced nephrotoxicity.</p>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143888767","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":"Forsythoside A inhibited inflammatory response by inhibiting p38 JNK/MAPK/ERK and NF-κB signaling in Staphylococcus aureus pneumonia","authors":"Liangmin Song, Yu Lei","doi":"10.1007/s10735-025-10418-2","DOIUrl":"10.1007/s10735-025-10418-2","url":null,"abstract":"<div><h3>Background</h3><p><i>S. aureus</i> pneumonia, one of the most common <i>S. aureus</i>-induced diseases, is characterized by infectious inflammation in alveoli, distal airway, and lung interstitial. Forsythiaside A possesses anti-inflammatory, anti-infective, and other pharmacological properties in several diseases. The role of forsythiaside A remains unclear in <i>S. aureus</i> pneumonia.</p><h3>Aim of the study</h3><p>We aimed to figure out the role of forsythiaside A in <i>S. aureus</i> pneumonia.</p><h3>Methods</h3><p>RAW264.7 cells and C57BL6 mice were infected with <i>S. aureus</i> to construct <i>S. aureus</i> pneumonia cell model and animal model, respectively. A series of experiments including MTT, ELISA, Western blot, H&E staining and EBD staining were operated to figure out the role of forsythiaside A in <i>S. aureus</i> pneumonia.</p><h3>Results</h3><p>In RAW264.7 cells, forsythiaside A did not induce cell toxicity but triggered cytokines (TNF-α, IL-6 and IL-1β) release in a dose-dependent manner. Moreover, forsythiaside A inhibited p38 JNK/MAPK/ERK and NF-κB pathways by repressing phosphorylation of p38, JNK, ERK and p65 proteins. For in vivo study, forsythiaside A improved survival rate of <i>S. aureus</i> pneumonia mice by alleviating lung injury. In addition, forsythiaside A protected from air-blood barrier destruction and pulmonary edema. At last, forsythiaside A inhibited neutrophils infiltration and inflammatory response in bronchoalveolar lavage fluid.</p><h3>Conclusions</h3><p>Forsythoside A inhibited inflammatory response by inhibiting p38 JNK/MAPK/ERK and NF-κB signaling in <i>S. aureus</i> pneumonia, which provided a novel insight for <i>S. aureus</i> pneumonia treatment.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143879742","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}
Chenfei Wang, Yuyuan Su, Jinlong Shi, Guijuan Feng
{"title":"KIF2C promotes oral squamous cell carcinoma progression via PLK1 upregulation: implications for biomarker development and therapeutic targeting","authors":"Chenfei Wang, Yuyuan Su, Jinlong Shi, Guijuan Feng","doi":"10.1007/s10735-025-10415-5","DOIUrl":"10.1007/s10735-025-10415-5","url":null,"abstract":"<div><p>Oral squamous cell carcinoma (OSCC) is a highly aggressive malignancy with poor prognosis due to late detection, rapid progression, and frequent metastasis, underscoring the urgent need for novel therapeutic targets. This study investigates the roles of kinesin family member 2C (KIF2C) and Polo-like kinase 1 (PLK1) in OSCC progression and their functional interplay. Immunohistochemical and western blot analyses revealed marked upregulation of KIF2C and PLK1 in human OSCC tissues and cell lines (SCC9, SCC25, Cal27). Functional characterization in Cal27 cells (selected for highest KIF2C expression via qPCR/WB) demonstrated that KIF2C knockdown via siRNA transfection suppressed proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while inducing apoptosis and G0/G1 cell cycle arrest. Mechanistically, KIF2C silencing downregulated PLK1 expression, concomitantly reducing EMT markers (N-cadherin, vimentin), matrix metalloproteinases (MMP-2/9), and angiogenesis factors (VEGF, α-SMA). Complementary assays (CCK-8, EdU, Transwell, wound healing) and flow cytometry confirmed that KIF2C-PLK1 axis promotes tumor growth by enhancing matrix degradation, angiogenesis, and S-phase proliferation while inhibiting apoptosis. These findings establish KIF2C as a pivotal regulator of OSCC progression through PLK1-mediated signaling, highlighting their dual potential as prognostic biomarkers and therapeutic targets for OSCC management.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143879743","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":"STAT3/FoxO3a/Sirt1 pathway inhibition by ginsenoside Rc ameliorates cardiomyocyte damage in septic cardiomyopathy by altering macrophage polarization","authors":"M. S. Jinzhong Wang, M. S. Jian Fu","doi":"10.1007/s10735-025-10417-3","DOIUrl":"10.1007/s10735-025-10417-3","url":null,"abstract":"<div><p>This study explored the role and mechanism of action of ginsenoside Rc in treating septic cardiomyopathy. Ginsenoside Rc mitigated LPS-induced oxidative stress, inflammation, apoptosis, and mitochondrial dysfunction in cardiomyocytes and inhibited M1 polarization in macrophages. Ginsenoside Rc reduced the stimulating effect of M1-polarized macrophages on LPS-induced cardiomyocyte injury. Network pharmacological analysis suggested that ginsenoside Rc may play a role in septic cardiomyopathy through modulation of the STAT3/FoxO3a/Sirt1 pathway, which was validated in in vitro experiments. Ginsenoside Rc suppressed the expression of STAT3/FoxO3a pathway proteins and upregulated Sirt1. Moreover, influences of ginsenoside Rc on LPS-induced cardiomyocyte injury and macrophage polarization were abolished by ML115, a STAT3 agonist. In vivo, ginsenoside Rc notably improved myocardial injury and attenuated macrophage activation and inflammation in septic mice. Collectively, Ginsenoside Rc can ameliorate septic cardiomyopathy by modulating the STAT3/FoxO3a/Sirt1 pathway and altering macrophage polarization.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143883694","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}
Amna Khalid, Shazia Khurshid, Maliha Uroos, Jahangir Khan, Abid Sarwar, Ehsan ul Haq, Tariq Aziz, Fatma Alshehri, Fahad Al-Asmari, Bandar K. Baothman, Fakhria A. Al-Joufi, Maher S. Alwethaynani
{"title":"Green synthesis of silver and gold nanoparticles using seeds extract of Cichorium intybus and their comparative analysis with commercially available ointment for wound healing activity","authors":"Amna Khalid, Shazia Khurshid, Maliha Uroos, Jahangir Khan, Abid Sarwar, Ehsan ul Haq, Tariq Aziz, Fatma Alshehri, Fahad Al-Asmari, Bandar K. Baothman, Fakhria A. Al-Joufi, Maher S. Alwethaynani","doi":"10.1007/s10735-025-10426-2","DOIUrl":"10.1007/s10735-025-10426-2","url":null,"abstract":"<div><p>Wound healing is a complicated physiological process that involves several stages including hemostasis, inflammation, proliferation and repair to rebuild the integrity of the skin and subcutaneous tissue. Millions of people around the world are affected by poor wound healing, causing increased mortality rates and related costs. Immedicable wounds are a health problem because they directly affect the person’s standard of living and produce an ultimatum to the health of people and the international economy because of the expensive medical treatment. Other schemes/approaches must be designed to achieve productive and therapeutic results. In this context, the emergence of Nano biotechnology may provide another manifesto to produce latest drugs for long-term treatment processes. This article shows that the implementation of metal nanoparticles (Au and Ag) has unbolted a brand-new gateway in the discipline of eco-friendly medicine due to their unique properties such as medicine transportation, antimicrobial activity and quick recovery. Moreover, metal nanoparticles (NPs) manufactured by green synthesis not only add the effects of nanoparticles and plant extracts but also reduce toxicity to tissues and make their use safer. In the present work, Ag and Au nanoparticles were synthesized using an aqueous seed extract of <i>Cichorium intybus</i> and their wound healing ability was assessed by performing in-vivo wound healing activity on albino mice. Till now there is no study available on the in-vivo wound healing potential of Ag and Au nanoparticles using <i>Cichorium intybus</i>. This is the first study ever to assess the ability of <i>Cichorium intybus</i> seed extract and its metal nanoparticles (AgNPs & AuNPs) to promote wound healing in animals which shows its uniqueness and novelty. The results displayed augmented and quicker wound closure with Ag as compared to the Au nanoparticles, polyfax and simple plant extract in a 21-day research work. These results illustrated that eco-friendly prepared nanoparticles provide a prominent approach to fight with the bacteria resistant against combination therapy without any lethal affair. Environment-friendly NPs declared to be the low-cost best treatment for the faster recovery of wounds. The main goal of this research is to provide aid in the creation of plant-based, durable and affordable Nano medicine for wound care, lowering dependency on synthetic techniques and encouraging environmental friendly biomedical applications.</p></div>","PeriodicalId":650,"journal":{"name":"Journal of Molecular Histology","volume":"56 3","pages":""},"PeriodicalIF":2.9,"publicationDate":"2025-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143875313","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}