Histology and histopathology, Vol.40, Nº11, (2025)

Ir a Estadísticas

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    Histological and transcriptomic analysis of paravaginal and central defects in anterior vaginal wall prolapse: Insights from DeLancey's pelvic floor theory
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Zhang Chun; Tang Qingxia; Zhou Yan; Fu Xuemei; Hu Pan; Liu Lubin; Biología Celular e Histología
    Background. This study aimed to pre-liminarily explore the differences between paravaginal and central defect types of anterior vaginal wall prolapse based on DeLancey's pelvic floor theory. Methods. Seventy-eight patients with normal, paravaginal, or central defect vaginal wall tissues were collected and stained using hematoxylin and eosin (HE) and immunofluorescence staining to analyze and identify the expression of vimentin and phosphohistone H3 (PH3). Ribonucleic acid from fresh tissues was extracted for transcriptome sequencing to analyze differences between paravaginal and central defect types of anterior vaginal wall prolapse. Results. Significant differences were found in age, menopausal status, body mass index, pregnancy, and delivery among the control, paravaginal, and central defect groups. Histological analysis revealed that the distribution of interstitium in the normal HE staining group was compact and continuous. In the paravaginal defect interstitium, fiber morphology was altered, while central defect interstitial fibers were fragmented. PH3 expression was significantly lower in the central defect type than in the normal and paravaginal defect groups, suggesting degenerative lesions in the vaginal mucosa with central defects. Vimentin distribution in the normal group was tightly packed and continuous, whereas, in the paravaginal defect interstitium, vimentin filaments were fragmented into small spots and micro-aggregates. In the central defect interstitium, vimentin micro-aggregates exhibited altered coalescence and cell shape, appearing punctate. These findings indicated degenerative lesions in the anterior vaginal interstitium of both paravaginal and central defect types. KEGG enrichment analysis of differential genes revealed their involvement in proteinaceous extracellular matrix (ECM)-related signaling pathways, with increased expression of matrix metalloproteinase 13 (MMP13), MMP3, MMP12, and MMP7 in the paravaginal defect type compared with the central defect type. Conclusion. The differences between paravaginal and central defect types of anterior vaginal wall prolapse may be related to the expression of MMP-related proteins; KEGG enrichment analysis of differential genes indicated that they were closely related to the protein ECM pathway. Moreover, delineative lesions appeared in the paravaginal defect interstitium, and degenerative lesions appeared in the central defect mucosa and interstitium, which further enriched the DeLancey three-level theory
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    Sheng-Jiang-Yi-You decoction inhibits the inflammatory response by down-regulating the p38MAPK signaling pathway to alleviate Helicobacter pylori-associated gastritis
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Li Ze; Chen Ruirui; Tang Weihong; Zheng Xiaoya; Jin Xuefeng; Wang Zhongmin; Wu Qiao; Biología Celular e Histología
    Background. Helicobacter pylori (HP)-associated gastritis is an important factor in development of stomach cancer. Components of Sheng-Jiang-Yi-You decoction (SJYYD) exert gastroprotective effects. However, the effects and mechanism of SJYYD in HP-associated gastritis remain uncertain. Methods. HP bacterial solution (1×109 CFU/mL) was gavaged every other day for 14 days to construct an HP-associated gastritis mouse model. Male BALB/c mice were randomized into Sham, HP, HP+Standardized triple therapy (HP+Triplet), HP+SJYYD (0.4 mL/20 g), HP+Triplet+SJYYD, HP+anisomycin (ANI) (2.5 mg/kg/d, p38MAPK agonist, HP+ANI), and HP+ SJYYD+ANI groups (n=6). Gastric mucosal injury detection and rapid urease test for HP infection were conducted. HE staining for pathological damage and ELISA for pro-inflammatory factors and immuno-globulin G (IgG) content were performed. Measurement of p38 mitogen-activated protein kinase (p38MAPK) pathway-related factor expression was performed by qRT-PCR and western blot. Results. The increased IgG content and HP colonization rate indicated successful modeling. SJYYD caused attenuated gastric mucosal damage, with decreased ulcer index (UI), HP colonization rate, inflammatory cell infiltration, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β levels in HP-associated gastritis mice. Moreover, SJYYD reduced p38MAPK, c-Jun N-terminal kinase (JNK), and extracellular regulated protein kinase (ERK) mRNA expression, as well as p-p38MAPK/p38MAPK, p-JNK/JNK, and p-ERK/ERK protein expression in gastric mucosa tissues of HP-associated gastritis mice. The above effects were reversed by further ANI treatment. Conclusion. SJYYD may attenuate HP-associated gastritis by inhibiting inflammatory response by down-regulating p38MAPK pathway, providing scientific evidence for clinical application of SJYYD in HP-associated gastritis treatment and promoting the development of therapeutic approaches in HP-associated gastritis
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    Venous vasculature drives neovascularization and stroma formation in pancreatic neuroendocrine tumors via intussusceptive angiogenesis and vein intravasation
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Díaz-Flores Lucio; Gutiérrez Ricardo; Pino García Maria; González-Gómez Miriam; Carrasco Jose Luis; Madrid Juan Francisco; Díaz-Flores Varela Lucio; Biología Celular e Histología
    The microenvironment of pancreatic neuroendocrine tumors (PanNETs) has been extensively studied; however, research on their venous vasculature has largely focused on tumor invasion and metastasis. This study aims to (a) evaluate the role of veins/venules in PanNET neovascularization, tumor intravasation, and stromal tract (trabecula) formation, including the potential involvement of intussusceptive angiogenesis (IA); and (b) compare the trabeculae observed in PanNETs with those found in hepatic cavernous hemangiomas (HCHs) where IA in veins plays an important role. To achieve these objectives, we conducted an integrated morphological approach encompassing primary PanNETs (n=42), hepatic metastases of PanNETs (n=4), and HCHs (n=11). Our findings in both primary and metastatic PanNETs reveal (a) the involvement of veins/venules in tumor neovascularization, with IA acting synergistically with sprouting angiogenesis, through the formation of pillars, meshes, and complex meshes (vessels that encapsulate tumor clusters-endothelium-coated tumor clusters); (b) the development of connective tissue around the neo-vasculature, potentially involving adventitial CD34-positive stromal cells/telocytes; and (c) a notable architectural resemblance between the trabeculae of PanNETs and those of HCHs. In conclusion, this work highlights the pivotal role of the preexisting venous vasculature in PanNET neovascularization, tumor intravasation, and stroma formation, with active participation of IA. These findings provide a pathophysiological foundation for future in-depth molecular investigations and may pave the way for new studies on therapeutic strategies targeting angiogenic mechanisms
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    Chelerythrine-mediated targeting of NF-κB and Nrf2 pathways alleviates liver injury in a carbon tetrachloride-induced liver fibrosis mouse model
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Ding Yisong; Li Xiaoming; Qi Ruixing; Su Yingshi; Wang Xiaoli; Biología Celular e Histología
    Background and Aims. This study aimed to investigate the mechanism and efficacy of chelerythrine (CHE) in treating carbon tetrachloride (CCl4)-induced liver fibrosis, with a particular focus on the nuclear factor-erythroid-related factor-2 (Nrf2) and nuclear factor-kappa-B (NF-κB) signaling pathways. Methods. Mice were induced with CCl4 for eight weeks and categorized into the control group, CCl4 model group, and CHE low (7 mg/kg/d, ig,), medium (14 mg/kg/d, ig), and high-dose (28 mg/kg/d, ig) groups with 10 animals in each group. Following CHE treatment, liver sample morphology was assessed using multiple immunohistochemistry, and serum biochemical indicators were measured. ELISA was used to determine IL-10, IL-1β, and TNF-α contents. Western blotting and RT-PCR were employed to analyze protein and mRNA levels of α-SMA, Col-I, fibronectin, Nrf2, HO-1, NQO1, GCLc, GCLm, NF-κB, p-NF-κB, IκBα, and p-IκBα. Nrf2 knockout mice were used to assess the impact of CHE on the Nrf2 signaling pathway. Results. The findings demonstrated that CHE significantly ameliorated oxidative damage, inflamma-tory response, and liver fibrosis in CCl4-induced mice. CHE treatment increased Nrf2 expression and its target proteins, including HO-1 and GCLc, an effect not observed in Nrf2 knockout mice. In addition, CHE reduced NF-κB expression levels. Conclusions. These results suggest that CHE can alleviate liver fibrosis in CCl4-induced mice by modulating NF-κB/IκBα and Nrf2 signaling pathways. These findings propose CHE as a potential novel anti-liver fibrosis drug
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    Pinocembrin ameliorates non-alcoholic fatty liver disease by activating Nrf2/HO-1 and inhibiting the NF-κB signaling pathway
    (Universidad de Murcia, Departamento de Histología e Histopatología, 2025) Chen Weina; Xue Diming; Feng Xia; Zhong Yinhang; Li Quanqing; Zhang Weihang; Jiang Guojun; Biología Celular e Histología
    Objectives. The high intake of high-fat diets and changes in sedentary lifestyles have led to an increase in non-alcoholic fatty liver disease (NAFLD). This study aimed to investigate the effect and mechanism of Pinocembrin (Pin) on NAFLD in vivo and in vitro. Methods. The pharmacodynamics of Pin alone or in combination with ML385 was assessed in high-fat diet (HFD)-mediated NAFLD mice. HepG2 cells were treated with palmitic acid (PA)/oleic acid (OA) (1:2) as an in vitro model to study the effect of Pin on lipid deposition and oxidative stress. The roles of Pin in glucose and lipid metabolism, inflammation, oxidative stress, and the Nrf2/HO-1/NF-κB pathway were measured. Results. Pin alleviated lipid deposition, inflam-matory response, and oxidative stress in HFD-induced NAFLD mice and PA/OA-induced HepG2 cells. Moreover, ML385 partly attenuated the protection of Pin on inflammatory response and oxidative stress in vivo and in vitro. More importantly, feeding with an HFD significantly decreased the expression of Nrf2 and HO-1, but treatment with Pin increased their expression, accompanied by an increased nuclear transposition of Nrf2. Conclusion. Taken together, these results indicated that Pin alleviated glucose and lipid metabolism disorders, inflammation, and oxidative stress in NAFLD by activating the Nrf2/HO-1 signaling pathway and restraining the NF-κB pathway