Histology and histopathology Vol.40, nº4 (2025)
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- PublicationOpen AccessThe Lian-Dou-Qing-Mai formula activates the PPARγ-LXRα-ABCA1/ABCG1 pathway by regulating IL-10, leading to the promotion of cholesterol efflux and a reduction in atherosclerotic plaques(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Liao, Wenqi; Li, You; Zhao, Haoyan; Lu, ShuBackground. To observe the effect of the Lian-Dou-Qing-Mai (LDQM) formula on lipid metabolism in mice and explore its mechanism from the perspective of regulating the PPARγ/LXRα/ABCA1 signaling pathway. Methods. THP-1 cells were induced to transform into foam cells with ox-LDL. Atherosclerosis (AS) models were constructed using a high-fat diet in ApoE-/- mice. Detection kits were used to evaluate triglyceride (TG) and total cholesterol (TC) content; TNF-α, MCP-1, MMP-9, TMP-1, PPARγ, LXRα, ABCA1, and ABCG1 mRNA and protein expression were identified using real-time PCR and western blot. Aortic plaque development and lipid deposition were seen using hematoxylin and eosin (HE) and oil red O staining, respectively. Results. In the cell model, LDQM could inhibit the formation of THP-1 macrophage-derived foam cells and the expression of inflammatory factors, promote macrophage cholesterol efflux, increase the expression of IL-10, and activate the PPARγ-LXRα-ABCA1/ ABCG1 pathway. Additional IL-10 treatment further promotes LDQM-induced cholesterol efflux in THP-1 cells. In in vivo models, LDQM inhibited the area of atherosclerotic lesions, aortic lipid deposition, and inflammation levels in ApoE-/- mice through IL-10, and activated the expression level of the PPARγ-LXRα-ABCA1/ABCG1 pathway. Conclusion. LDQM may affect the PPARγ/LXRα/ ABCA1 signaling pathway through IL-10, regulate lipid metabolism, reduce serum inflammatory expression and lipid deposition, and improve the formation of atheroplaques.
- PublicationOpen AccessBaicalin promotes migration and angiogenesis of endothelial progenitor cells but impedes thrombus formation via SIRT1/NF-κB signaling in a rat model of deep vein thrombosis(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Xie, Jinfeng; Liao, Yonggui; Wang, DileBackground. Deep vein thrombosis (DVT) is the third most prevalent vascular disease worldwide, seriously threatening human health. Baicalin, a flavonoid isolated from the roots of Scutellaria baicalensis, has been identified to play a crucial role in various vascular diseases. The study aimed to explore the efficacy and underlying mechanisms of baicalin in DVT. Methods. Endothelial progenitor cells (EPCs) were differentiated from peripheral blood mononuclear cells isolated from rat bone marrow. Dil-ac-LDL/FITC-UEA-1 double staining and flow cytometry analysis were conducted for the identification of EPCs. The angiogenesis and migration of EPCs in vitro were tested by a tube formation assay and Transwell assay, respectively. DVT rat models were established by stenosis of the inferior vena cava (IVC). After the euthanasia of rats, thrombi in the IVC were collected and weighed, and histological alterations in IVC tissue were measured by H&E staining. The protein levels of SIRT1, p-P65, and p65 in rat IVC tissues were quantified via western blotting. Results. EPCs used in this study displayed a spindle-like shape and were positive for endothelial cell-specific markers, suggesting the phenotypic characteristics of EPCs. Baicalin enhanced the migratory and angiogenetic abilities of EPCs in vitro. For in vivo experiments, baicalin reduced thrombus weight and mitigated DVT formation in model rats. Moreover, baicalin activated SIRT but repressed NF-κB signaling in IVC tissues of DVT rats. Conclusion. Baicalin facilitates migration and angiogenesis of EPCs but impedes thrombus formation via regulation of SIRT1/NF-κB signaling in DVT model rats.
- PublicationOpen AccessExpression feature and prognostic function of a novel immune checkpoint Siglec-15 in human colorectal cancer(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Liang, Guodong; Zhou, Linyun; Fan, Yang; Ding, Run; Yang, Junrong; Xu, Li; Zhu, Yidan; Huang, WenBackground. Sialic acid-bound immuno-globulin lectin 15 (Siglec-15) plays an important role in the development of cancer. However, the association between Siglec-15 expression and clinicopathological characteristics of colorectal cancer (CRC) has not been fully investigated. Methods. In this present study, a number of bioinformatics analyses were performed to provide an overview and detailed characteristics of Siglec-15. Quantitative real-time polymerase chain reaction (qPCR), western blotting and immunohistochemistry analyses were conducted to characterize the expression of Siglec-15 in CRC. Kaplan-Meier survival and Cox regression analyses were performed to identify the prognostic parameters of CRC. Results. The results of bioinformatics analyses revealed the expression characteristics and prognostic roles of Siglec-15 in CRC. The data of qCPR, western blotting, and IHC analyses demonstrated that the expression of Siglec-15 in CRC tissues was significantly higher than that in non-cancerous tissues. Moreover, the expression level of Siglec-15 in CRC was significantly associated with lymph node metastasis (p=0.001), TNM stage (p=0.001), and overall survival (p=0.026). COX multi-factor analysis indicated that Siglec-15 expression (p=0.023) and tumor differentiation (p=0.003) were independent prognostic factors for CRC. Conclusions. Collectively, the data suggested that Siglec-15 expression may serve as a novel prognostic factor and Siglec-15 might be identified as an ideal candidate for immunotherapy in CRC treatment.
- PublicationOpen AccessClomiphene and dexamethasone inhibit apoptosis and autophagy via the ROS-JNK/MAPK-P21 signaling pathway in PCOS(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Liu, Ruxia; Tang, Yuxiang; Chen, Xiangjun; Shang, XintongBackground. Polycystic ovarian syndrome (PCOS) is a complicated endocrine and metabolic disease, which seriously affects women’s health. However, the etiology and genetic basis of PCOS are complex, and the pathogenesis remains unclear. In this study, we aimed to explore the effects of clomiphene and dexamethasone on PCOS and their potential mechanisms. Methods. Sprague-Dawley (SD) rats were injected with dehydroepiandrosterone (DHEA) to establish a PCOS model. After treatment with clomiphene, dexamethasone, and their combination, ovarian tissue of rats was collected. The morphological changes in the ovary were observed by hematoxylin and eosin (HE) staining and Electron microscopy. The levels of oxidative stress and hormones were determined by ELISA. Apoptosis was assessed by TUNEL assay. The mechanism of clomiphene and dexamethasone effects on PCOS was explored by Immunohistochemical staining, real-time PCR, and western blotting. Results. Clomiphene and dexamethasone could improve the morphology of the ovary in PCOS. TUNEL assay and ELISA showed that clomiphene, dexamethasone, and their combination could inhibit apoptosis and significantly reverse the levels of ROS, T-SOD, CAT, T, and E2 in the ovary. Immunohisto-chemical staining revealed that clomiphene and dexamethasone could remarkably reduce the protein levels of Bax, Caspase-3, LC3II, p-JNK, p-P38 MAPK, and P21, and increase P62 and Bcl-2 protein expression. The mRNA levels of Bax, Bcl-2, and Caspase-3 were also modulated in the PCOS model with clomiphene and dexamethasone treatment. Additionally, western blotting indicated that clomiphene and dexamethasone significantly regulated the levels of Bax, Bcl-2, Caspase-3, LC3I, LC3II, P62, p-JNK, JNK, p-P38 MAPK, P38 MAPK, and P21 in PCOS rats. Conclusions. Clomiphene and dexamethasone can not only reduce oxidative damage, and inhibit apoptosis and autophagy, but they can also regulate the ROS-JNK/MAPK-P21 signaling pathway in PCOS rats. It provides an experimental basis for the clinical application of clomiphene and dexamethasone in PCOS
- PublicationOpen AccessImpact of 6-OHDA injection and microtrauma in the rat substantia nigra on local brain amyloid beta protein concentrations in the affected area(Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2025) Roldán Kalil, Joshua A.; Vendrell Gonzalez, Sara E.; Espinosa Ponce, Natalia; Colón Vasques, Jadier; Ortiz Rivera, Jescelica; Tsytsarev, Vassiliy; Alves, Janaina M.; Inyushin, MikhailAmyloid beta peptides (Aβ) are key indicators of Alzheimer’s disease and are also linked to cognitive decline in Parkinson’s disease (PD) and other neurodegenerative disorders. This study explored the accumulation of Aβ in a standard 6-Hydroxydopamine (6-OHDA) model of PD. We unilaterally injected 6-OHDA into the substantia nigra of Wistar rats to induce dopaminergic cell degeneration and death, a characteristic of PD. The goal was to detect Aβ protein in tissues and blood vessels showing inflammation or degeneration from the 6-OHDA injection. Our results showed that 6-OHDA injection produced a statistically significant rise in Aβ concentration at the injection site 60 minutes after injection, which was slightly reduced 24 hours post-injection but still significantly higher than in controls. We also tried Gp120 injection in the same zone but it only produced effects comparable to control needle trauma. The presence of Aβ in tissues and blood vessel walls after injection was confirmed through ELISA tests and was supported by immunohistochemical staining of injection areas. We found that the increased Aβ concentration was visible in and around blood vessels and inside blood vessel walls, and also, to a lesser extent in some cells, most probably neurons, in the area. This research highlights the connection between dopaminergic cell poisoning and the accumulation of Aβ, offering insights into the progression of PD to cognitive disorders and dementia
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