Histology and histopathology, Vol.41, Nº2, (2026)

Ir a Estadísticas

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http://hdl.handle.net/10201/183569

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    Amygdalin improves ovarian function by inhibiting oxidative stress and inflammation in premature ovarian failure mice
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Jintao Han; Jianyuan Li; Jin Yao; Wenwei Jiang; Biología Celular e Histología
    Background. Menstrual stoppage, follicular dysplasia, and hypergonadotropic hypoestrogenism in women under forty are among the symptoms of premature ovarian failure (POF). This study aimed to explore the role and mechanism of amygdalin on ovarian function in a POF mouse model. Methods. A POF mouse model was established via injection of D-galactose (D-gal), followed by amygdalin treatment. Histological staining of ovarian tissues was applied to determine follicular development and granulosa cell apoptosis. Levels of malondialdehyde (MDA), glutathione peroxidase (GSH-px), and superoxide dismutase (SOD) were measured in ovarian tissues. Enzyme-linked immunosorbent assay was used to detect levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), progesterone (P), estradiol (E2), anti-Müllerian hormone (AMH), and reactive oxygen species (ROS) in serum, and tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 levels in ovaries. Results. D-gal increased levels of FSH, LH, ROS, MDA, TNF-α, IL-1β, IL-6, Bax, atretic follicles, and granulosa cell apoptosis, and decreased P, E2, AMH, SOD, GSH-px, Bcl-2, and primordial, primary, secondary, and total follicles (p<0.01). Amygdalin with different concentrations reversed the effects of D-gal on mice (p<0.05). Conclusion. Amygdalin improved ovarian function in POF mice through inhibiting oxidative stress, inflammation, and granulosa cell apoptosis. These results suggested that amygdalin may be a potential antioxidant for POF treatment.
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    Local amifostine administration mitigates chemotherapy-induced esophageal mucosal damage: A novel approach for targeted treatment in a rabbit model
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Junqin Zhang; Bin Wang; Yaxing Li; Biología Celular e Histología
    Objective. Effective preventive measures for radiotherapy and chemotherapy-induced esophagitis are currently lacking. This study aims to investigate the local impact of chemotherapeutic agents on normal esophageal tissue and assess the cytoprotective effects of amifostine against chemotherapy-induced esophageal injury. Methods. Twenty-four New Zealand white rabbits were randomly assigned to the control group, which only received saline; the cisplatin (DDP) group, which received 0.25 mg/ml of the chemotherapeutic drug (DDP); and the combined treatment group, which received pre-treatment with 0.8 mg/ml amifostine followed by 0.25 mg/ml DDP. Each group consisted of eight rabbits. A custom-made balloon device for targeted esophageal drug delivery was inserted into the esophagus, followed by the infusion of DDP and/or amifostine into the created space. After six days, rabbits were euthanized, and esophageal specimens were examined for mucosal damage. Results. Macroscopically, compared with the control group, the DDP group exhibited significant thickening, edema, mucosal ulceration, and congestion in the infused esophageal region. Conversely, the combined treatment group showed mild thickening and a smooth or mildly congested mucosal surface. Microscopically, the DDP group displayed extensive mucosal detachment, edema, dilated submucosal blood vessels, and substantial infiltration of inflammatory cells. The combined treatment group exhibited partial mucosal detachment and moderate inflammatory cell infiltration in the submucosal and muscular layers, with few inflammatory cells in the muscle layer. Conclusion. This study provided evidence that damage caused by the local infusion of DDP might be reduced by pre-treatment of the cytoprotective agent amifostine.
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    PU.1 aggravates hepatic sinusoidal obstruction syndrome by upregulating PTBP1 and activating the Wnt/β-catenin pathway
    (2026) Yang, Li; Ju, Honglin; Chen, Zhiyuan; Cheng, Siqi; Liu, Ya; Wang, Xiangyang; Biología Celular e Histología
    Objective. Hepatic sinusoidal obstruction syndrome (HSOS) is a disease characterized by damage to hepatic sinusoidal endothelial cells (HSECs). This research investigates the role and regulatory pathway of PU box-binding protein (PU.1) in the progression of HSOS. Methods. We established an in vivo HSOS model through peritoneal administration of monocrotaline (MCT). Primary murine HSECs were isolated and treated with various concentrations of MCT to establish an in vitro HSOS model. PU.1 knockdown was achieved using lentiviral shRNA constructs, and its impact on oxidative stress, PTBP1 expression, β-catenin mRNA stability, and Wnt/β-catenin signaling was evaluated through kits, RT-qPCR, and western blot. Dual-luciferase and chromatin immunoprecipitation assays were conducted to assess the interaction between PU.1 and the PTBP1 promoter. The molecular association between PTBP1 and β-catenin mRNA was confirmed through RNA pull-down and RIP assays. Results. PU.1 was upregulated in MCT-induced HSOS, contributing to elevated oxidative stress and activation of the Wnt/β-catenin pathway. PU.1 directly enhanced PTBP1 transcription, which stabilized β-catenin mRNA and sustained Wnt/β-catenin signaling. PU.1 knockdown alleviated oxidative stress, reduced liver damage, and disrupted the PTBP1-β-catenin interaction, leading to Wnt/β-catenin activity inhibition. Overexpression of PTBP1 reversed the protective effects of PU.1 knockdown, reinstating oxidative stress and reactivating Wnt/β-catenin signaling. Conclusion. PU.1 facilitated HSOS pathogenesis by promoting the transcriptional activity of PTBP1 and activating the Wnt/β-catenin pathway. Targeting PU.1 can serve as a promising therapeutic strategy for reducing oxidative stress and liver damage in HSOS.
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    Empagliflozin protected kidney function in CKD rat through suppressing hypoxic and fibrotic signalings mediated inflammation and EMT
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Jui-Ning Yeh; Tsuen-Wei Hsu; John Y. Chiang; Ben-Chung Cheng; Pei-Hsun Sung; Shun-Cheng; Chi-Ruei Huang; Pei-Lin Shao; Hon-Kan Yip; Chih-Chao Yang; Biología Celular e Histología
    Background. This study tested the hypothesis that PI3K/Akt/GSK3β and TGF-β/Smad2/3 signaling play essential roles in mediating the epithelial-mesenchymal transition (EMT) and fibrosis, resulting in the deterioration of renal function and parenchyma in chronic kidney disease (CKD) rats, which is reversed by early empagliflozin treatment. Methods and results. NRK-52E cells were divided into the A1 (NRK-52E), A2 (NRK-52E + 200 μM p-Cresol), A3 (NRK-52E + 200 μM p-Cresol + 50 μM empagliflozin), B1 (NRK-52E), B2 (NRK-52E + 5 ng/mL TGF-β1) and B3 (NRK-52E + 5 ng/mL TGF-β1 + 50 μM empagliflozin) groups. Compared with those in the A1 group, the expression levels of proteins related to the EMT (TGF-β1/p-Smad2/p-Smad3/α-SMA), extracellular matrix (MMP2/9) and EMT (IGF-1) activators were significantly higher in the A2 group, but these changes were significantly reversed in the A3 group, whereas the protein expression levels of antifibrotic markers (TIMP1/TIMP2) exhibited the opposite pattern to the EMT-related proteins among the groups (all p<0.001). The expression of these proteins, along with the other EMT markers (snail, fibronectin, and vimentin) related to cellular function/protein expression, also exhibited an identical pattern to the A1 to A3 groups among Groups B1 to B3 (all p<0.001). Adult male SD rats were categorized into Groups 1 (sham-operated control), 2 (CKD) and 3 (CKD + empagliflozin). On Day 56 after CKD induction, the renal artery resistive index (RARI) was significantly higher in Group 2 than in Groups 1 and 3 and significantly higher in Group 3 than in Group 1 (all p<0.0001). The expression of EMT (Snail/α-SMA/ fibronectin/vimentin/TGF-β1/p-Smad2/3), apoptotic (cleaved caspase-3/cleaved-PARP), inflammatory (HIF-1α/IL-1β/TNF-α/MPO/MMP-2/MMP-9), and cell stress signaling (p-PI3K/p-Akt/GSK-3β) proteins and the cellular kidney injury score, expression of fibrosis and EMT markers (Snail/vimentin)/glomerular-hyper-cellularity/fibrocellular crescent formation displayed an identical pattern, whereas the cellular expression of podocyte components (podocin/synaptopodin/ZO-1) displayed the opposite pattern to the RARIs among the groups (all p<0.0001). Conclusions. Empagliflozin protected kidney function and architecture mainly by suppressing fibrosis, cellular oxidative stress signaling, the EMT and inflammation.
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    The effects of polysaccharides from Schizophyllum commune (Fr.) on amyloid-β and GFAP-induced neuronal injury in hippocampal regions of hyperlipidemia-affected rats
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2026) Wanida Chuaikhongthong; Uraporn Vongvatcharanon; Manaras Komolkriengkrai; Udomlak Matsathit; Wipapan Khimmaktong; Natyamee Thipthong; Biología Celular e Histología
    Aims. The hippocampal region is an essential area for memory. Alzheimer's disease (AD) continues to impact this brain region. It is caused by the accumulation of amyloid-β (Aβ) along with neurofibrillary tangles, together with glial fibrillary acidic protein (GFAP) expression, which causes loss of synapses, resulting in memory problems. Consuming a high-fat diet (HFD) causes the abnormal production of certain neuro-transmitters through the gut-brain axis system, resulting in hippocampal neuron damage. Therefore, this study examined the effects of polysaccharides from Schizophyllum commune (Fr.) or split-gill mushroom (SG) in rats induced with an HFD. Methods. The Y-maze test assessed spontaneous alternation percentages and short-term memory in all rat groups, while H&E and Cresyl violet staining revealed alterations in the characteristics of neurons across treatment groups. Immunofluorescence was employed to identify the expressions of neurodegenerative and inflammatory proteins. Results. The short-term memory was evaluated using the Y-maze test, which found that the spontaneous alternation percentage was lower in the HFD group and higher in the HFD+SG group compared with the control group. Alterations in neuron characteristics were revealed by Cresyl violet and H&E staining. The HFD group was found to have necrotic neurons; however, the HFD+SG group had less damage than the HFD group. Immunofluorescence observations indicated the expression of Aβ and GFAP proteins; the HFD group showed an increase in Aβ and GFAP accumulation, whereas in the HFD+SG group, these were significantly reduced. Conclusions. The study demonstrated improvements in hippocampal neurons, suggesting that polysaccharides from SG may be able to lessen the harm caused to the brain by consuming an HFD.