Histology and histopathology, Vol.41, Nº5, (2026)
Ir a Estadísticas
Permanent URI for this collection
Browse
Recent Submissions
- PublicationOpen AccessCardioprotective mechanisms of Jiangfu Decoction against myocardial ischemia may involve regulation of the AMPK/PINK1/ Parkin mitochondrial autophagy pathway(2026) Yiwei Hao; Chen Li; Haoying Li; Xue Han; Hefei Wang; Xi Chu; Zhiwei Su; Shijiang Sun; Yawei Zhao; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBackground. Jiangfu Decoction (JFD) is a classical traditional herbal medicine used to clinically treat ischemic heart disease (IHD). Nonetheless, the influence of JFD on myocardial ischemia (MI), along with its precise underlying mechanism, is still unclear. The objective of this research was to investigate the potential mechanisms by which JFD exerts cardio protective effects on MI induced by isoproterenol (ISO). Methods. An acute MI model was established by subcutaneous injection of ISO (85 mg/kg/d). To evaluate alterations in myocardial structure, electrocardiogram recordings and heart histology examinations were employed. The myocardial ultrastructure was observed by transmission electron microscopy (TEM). Using specific kits, the levels and activities of oxidative stress markers as well as inflammatory cytokines were separately assessed. Western blotting was employed to assess the expression levels of proteins related to adenosine monophosphate activated protein kinase (AMPK), PTEN-induced putative kinase 1 (PINK1), Parkin, Nod-like receptor protein 3 (NLRP3), and Caspase-1. Results. The findings show that JFD treatments markedly diminished heart rate, pathological alterations in cardiac tissue, chondriosome injury, and serum concentrations of creatine kinase, creatine kinasemyocardial band, lactate dehydrogenase, malon dialdehyde, interleukin-1β, and interleukin-18. Concurrently, these treatments augmented the activation of superoxide dismutase, catalase, and glutathione peroxidase in the serum of animals subjected to ISO treatment. Additionally, JFD also reversed the ISO induced changes in the levels of AMPK, PINK1, Parkin, NLRP3, and Caspase-1. Conclusion. JFD exhibits a notable safeguarding influence on MI via a mechanism that involves regulation of the AMPK/PINK1/Parkin mitochondrial autophagy pathway, inhibition of pyroptosis, and reduction of oxidative stress and inflammation.
- PublicationOpen AccessElectroacupuncture ameliorates learning and memory impairment by inhibiting inflammation and promoting synaptic plasticity via inhibition of the NF-KB/NLRP3 signaling pathway in cerebral ischemic rats(2026) Guoyuan Pan; Dan Lu1; Mingjin Zhu; Guifen Yang; Chenyi Huang; Yisu Shou; Xiong Jiangnan; Fang Luo; Sun Di; Chuchu Huang; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaObjective. Electroacupuncture (EA) has a protective effect on cerebral ischemic injury. However, the specific mechanism of action of EA has not been studied. In this study, we investigated whether EA was involved in the treatment of learning and memory impairment in rats with cerebral ischemia‒reperfusion injury (CIRI) through the NF-KB/NLRP3 signaling pathway. Methods. Ninety-five male Sprague–Dawley (SD) rats were randomly divided into five groups, each consisting of 19 rats. A rat model of cerebral ischemia was established using transient middle cerebral artery occlusion (tMCAO) combined with cerebral blood flow monitoring. Intervention treatments consisted of electroacupuncture and lipopolysaccharide (an NF-κB agonist) injection. The behavior, spatial learning, and memory ability of the rats were evaluated with the Morris water maze method. The degree of brain injury in the rats was observed via triphenyl tetrazolium chloride (TTC), hematoxylin-eosin (H&E), and Fluoro-Jade B (FJB) staining. The expression levels of proteins related to the inflammatory response, pyroptosis, and synaptic plasticity were determined via western blotting and immunofluorescence staining. Changes in dendrites and spines were observed via Golgi-Cox staining. Results. Compared with those of the tMCAO group, the neural function scores and escape latency of the EA+tMCAO group were reduced. The cerebral infarct volume and the number of denatured neurons decreased. NF-κB, caspase-1, NLRP3, and IL-18 expression levels were significantly decreased. PSD95, SYP, and BDNF expression levels were significantly increased. The total number of dendrite junctions and the total length of dendrites increased. Compared with the EA+tMCAO and NS+EA+tMCAO groups, the escape latency in the lipopolysaccharide (LPS)+EA+tMCAO group was significantly increased. NF-κB, IL-18, and cleaved caspase-1 expression levels were elevated. Conclusion. EA may inhibit NF-κB/NLRP3 pathway proteins; regulate the neuroinflammatory response; promote the expression of PSD-95, SYN, and BDNF; improve the structure of dendrites and dendritic spines; and alleviate cognitive impairment in rats with CIRI.
- PublicationOpen AccessPIP5K3 upregulation correlates with unfavorable prognosis in patients with nasopharyngeal carcinoma(2026) Hung-Chang Wu; Ching-Chieh Yang; Yun-Tzu Lin; Chien-Feng Li; Shih-Lun Chang; Yu-Hsuan Kuo; Szu-Chi Yao; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBackground. Nasopharyngeal carcinoma (NPC) is prevalent in East and Southeast Asia, with metastasis and recurrence leading to poor prognosis. Identifying prognostic biomarkers is essential. Methods. We analyzed differentially expressed genes involved in the phosphatidylinositol metabolic process (GO: 0046488) and tumorigenesis (GSE12452) in NPC. Associations between PIP5K3 expression and clinicopathological features were assessed using chi square tests and Cox proportional hazards models. Results. PIP5K3 was significantly upregulated in NPC tissues, correlating with advanced stage (p=0.001) and nodal metastasis (p<0.001). High PIP5K3 expression was associated with worse disease-specific survival (DSS), distant metastasis-free survival (DMeFS), and local recurrence-free survival (LRFS). Multivariate analysis confirmed its association with poor prognosis (DSS: HR=4.321, DMeFS: HR=2.883, LRFS: HR=2.249; all p<0.001). Conclusions. PIP5K3 upregulation is associated with unfavorable clinical outcomes in NPC and may serve as a novel prognostic biomarker and potential therapeutic target.
- PublicationOpen AccessHistologic evaluation of the effect of grape seed oil and ferric sulfate in pulpotomy applied to molar teeth of rats: An in vivo study(2026) Günay Yapici Yavuz; Ebru Elibol Annaç; Aydın Keskinrüzgar; Muhammed Baybatmaz; İlknur Öz; Mesut Tozar; Osman Küçükkelepçe; Kamile Nur Tozar; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaBackground. The objective of this study was to examine the healing potential of Grape Seed Oil (GSO) on the pulp tissue that remains following pulpotomy treatment. Materials and Methods. The upper first molars of 18 two-month-old male Wistar albino rats were divided into two groups according to the material used in pulpotomy treatment. In the pulpotomy treatment group, GSO was used, while ferric sulfate (FS) was used in the control group. The rats were euthanized at 24 hours, 15 days, and 30 days following treatment. Histopathological evaluation of the samples was conducted using the hematoxylin-eosin staining method. The evaluation was conducted to ascertain alterations in connective tissue, vascular changes (i.e., angiopathic findings), inflammation, and hemorrhagic findings in the pulp. The data obtained in this study were analyzed with the IBM SPSS Statistics Version 21 software program. Results. In the present study, it was observed that the inflammatory response in the GSO group was higher than that in the FS group at 24 hours. The investigation revealed that the vascular response exhibited a higher magnitude in the GSO group compared to the FS group at 24 hours and at day 15. However, this response exhibited a decline at day 30. Despite an increase in hemorrhaging on the 15th day in the GSO group, this phenomenon decreased over time. Conclusions. It has been observed that GSO is a biocompatible material that can be used as an alternative to FS in pulpotomy treatment.
- PublicationOpen AccessMorphological evidence of telocytes in DHEA-induced polycystic ovary syndrome model(2026) Mehmet Yüncü; Yurdun Kuyucu; Esma İşçel; Biología Celular e Histología; Universidad de Murcia, Departamento de Biologia Celular e HistiologiaPolycystic Ovary Syndrome (PCOS) is a condition causing histopathological alterations in the ovarian stroma. Telocytes (TCs) are specialized interstitial/stromal cells present in the connective tissue of various organs. In this study, we investigated the presence and spatial organization of TCs in the ovaries of a rat model of PCOS induced by dehydro epiandrosterone (DHEA). The ovarian tissues from both PCOS and control groups were stained using hematoxylin-eosin (H&E), Bielschowsky's silver stain, methylene blue, and toluidine blue for light microscopy analysis, and scanned digitally. Ovaries were marked with double-labeled immunofluorescence with CD34/estrogen receptor-α (ER-α) and vimentin/ progesterone receptor-A (PR-A) and evaluated with a confocal microscope. The ultrastructure and telopodes (TPs) of TCs were also examined by transmission electron microscopy. TCs were identified in both groups, localized within follicular walls, adjacent to follicles, in stromal regions distant from the follicles, and perivascular areas. CD34/ER-α and vimentin/PR-A cells were significantly increased in PCOS. In conclusion, TCs were preserved in the DHEA-induced PCOS model, and according to our quantitative analysis, their ultrastructural features were unaffected by the PCOS microenvironment. Our findings suggest a potential association between TCs and the pathophysiology of PCOS. Further studies are necessary to elucidate the functional relationship of TCs in the development and progression of PCOS.
- «
- 1 (current)
- 2
- 3
- »