Histology and histopathology最新文献

Neonatal hypoxic-ischemic encephalopathy, an important cause of death as well as long-term disability in survivors, is caused by oxygen and glucose deprivation, and limited blood flow. Following hypoxic-ischemic injury in the neonatal brain, three main biochemical damages (excitotoxicity, oxidative stress, and exacerbated inflammation) are triggered. Mitochondria are involved in all three cascades. Mitochondria are the nexus of metabolic pathways to offer most of the energy that our body needs. Hypoxic-ischemic injury affects the characteristics of mitochondria, including dynamics, permeability, and ATP production, which also feed back into the process of neonatal hypoxic-ischemic encephalopathy. Mitochondria can be a cellular hub in inflammation, which is another main response of the injured neonatal brain. Some treatments for neonatal hypoxic-ischemic encephalopathy affect the function of mitochondria or target mitochondria, including therapeutic hypothermia and erythropoietin. This review presents the main roles of mitochondria in neonatal hypoxic-ischemic encephalopathy and discusses some potential treatments directed at mitochondria, which may foster the development of new therapeutic strategies for this encephalopathy.

Hepatic fibrosis is the basis of multiple liver diseases and may eventually develop into hepatocellular carcinoma. Hepatic stellate cell (HSC) activation is a driving factor of hepatic fibrogenesis. In the liver microenvironment, liver cells and others play a crucial role in HSC activation. The liver tissues of CCl4-induced rats show excessive fibrosis, inflammation, and cell apoptosis. Yin Yang 1 (YY1) was highly expressed in hepatic fibrosis rats and TGF-β1-treated liver cells. In animal experiments, YY1 knockdown effectively attenuated CCl₄-induced liver injury and pyroptosis-related IL-1β and IL-18 expression. In cellular experiments, NLRP3 inflammasome-mediated pyroptosis was activated by TGF-β1 treatment, while YY1 knockdown significantly inhibited the activation of the NLRP3 inflammasome, pyroptosis, and the secretion of IL-1β and IL-18. In addition, our data showed that TGF-β1-treated liver cell conditional medium markedly induced HSC activation, which was rescued by YY1 knockdown in liver cells. YY1 overexpression in liver cells contributed to the activation of TGF-β1-treated liver cell conditional medium in HSCs, however, this effect of YY1 was attenuated by NLRP3 inhibition. Overall, YY1 overexpression in liver cells contributed to HSC activation by facilitating IL-1β and IL-18 production via activating NLRP3 inflammasome-mediated pyroptosis, thus aggravating hepatic fibrogenesis. Our data indicate that YY1 may be a novel target for the treatment of hepatic fibrosis and associated liver diseases.

Hypoxia is characterized by a disparity between supply and demand of oxygen. The association between hypoxia and head and neck tumors is a topic of significant interest. Tumors frequently encounter areas with inadequate oxygen supply, resulting in a hypoxic microenvironment. Ameloblastoma is one of the most common benign odontogenic tumors of the maxillofacial region. It is a slow-growing but locally invasive tumor with a high recurrence rate. The literature has demonstrated the correlation between hypoxia and ameloblastoma, revealing a discernible link between the heightened expression of hypoxic markers in low oxygen conditions. This association is intricately tied to the tumoral potential for invasion, progression, and malignant transformation. Hypoxia profoundly influences the molecular and cellular landscape within ameloblastic lesions. The present review sheds light on the mechanisms, implications, and emerging perspectives in understanding this intriguing association to clarify the dynamic relationship between hypoxia and ameloblastoma.

Fish ovaries exhibit a remarkable diversity in shape, size, and organization, reflecting the myriad reproductive strategies employed by different species. This review delves into the intricate biology of fish ovaries, highlighting their structural diversity and the hormonal regulation that governs ovarian development and oocyte maturation. Key hormones include pituitary gonadotropins (GTHs) and maturation-inducing hormones (MIHs), which initiate oocyte growth and maturation. GTHs stimulate ovarian production of estradiol-17β and 17α,20β-DP, which induce oocyte maturation via MPF formation. Sex steroids like estrogens and progestogens, synthesized from cholesterol, play crucial roles. Other hormones, including growth hormone, prolactin, thyroid hormones, IGFs, ACTH, and melatonin, influence ovarian activity. The review also explores the varied reproductive strategies among fish, including oviparity and viviparity, and discusses how environmental factors like water temperature and photoperiod influence ovarian histology. Understanding the complex interplay between these factors is essential for advancing fisheries management, conservation, and aquaculture practices. Additionally, the evolutionary trajectory of fish ovaries underscores their adaptation to diverse ecological niches, contributing to the survival and reproductive success of fish species. The ovarian stroma provides structural support and houses various cell types, including dendritic cells (DCs), endocrine cells, and telocytes, contributing to follicle growth and hormone production, essential for reproductive success in fish. Fish ovaries are a crucial aspect of fish biology, with their structure and function intricately regulated by hormonal, environmental, and seasonal factors.

Background: Sialic acid-bound immunoglobulin 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.

Background: 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. Immunohistochemical 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.

Background: 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.

Transfection is an experimental technique typically used in biological experiments. In this study, we verified whether this technique may cause the release of inflammatory cytokines and affect cell viability. We used lipopolysaccharide (LPS)-induced human bronchial epithelial (16-HBE) cells as a model to evaluate whether cell transfection with Lipofectamine 3000 would affect LPS-induced inflammatory factors in HBE cells. MicroRNA (miRNA) negative control (NC)- and miR-584-mimics were transfected into 16-HBE cell lines. The 584-mimic was used to increase the expression of miR-584, and the NC-mimic was used to add a negative control sequence. After 24h of transfection, the cells were incubated with LPS for another 24h, and the effects on the release of inflammatory cytokines, such as IL-1, IL-6, IL-8, TNF-α, MIP-1, MCP-1α, and cell viability were investigated. The optimal conditions for transfection were evaluated, and cytokine and chemokine mRNA levels were determined. Regardless of the NC- or 584-mimic, the results indicate that the expression of transfected genes in these cells leads to an increase in inflammatory factors and decreased cell viability. Microscope analysis revealed that the number of HBE cells was lower after transfection, and many small vesicles could be observed in the transfected cells, indicating that the insertion of gene vectors may affect the biological activity of HBE cells and experimental results. Results suggest that Lipofectamine 3000 transfected miRNA into HBE cells, providing better transfection rates, however, at the cost of higher toxicity.

Objective: Cervical cancer has a very important place in female infertility and ranks fourth among cancers affecting women. Curcumin (CUR) is closely associated with the expression and activity of various regulatory proteins. It is also known that curcumin has preventive and therapeutic effects on various types of cancer. In this study, the anticancer activities of curcumin were demonstrated in the human cervical cancer cell line (HeLa).

Methods: qRT-PCR and western blot analyses were used to evaluate mRNA and protein expression of curcumin in HeLa and immortalized human skin keratinocyte cell lines (HaCaT) (proliferation and apoptosis regulatory markers of the RAS/RAF signaling pathway). MTT analysis was performed, showing HeLa and HaCaT cell proliferation depending on the dose and duration of curcumin and doxorubicin. A wound scratch healing assay was applied to examine cell migration and invasion of HeLa after curcumin application. To determine the role of curcumin and doxorubicin in the apoptosis of HeLa cells, the mRNA levels of caspase-3 were examined by qRT-PCR. The results were analyzed with a one-way ANOVA SPSS 20.0 program.

Results: CUR (IC50: 242.8 μM) and DOX (IC50: 92.1 μM) were determined to have the ability to inhibit the proliferation of HeLa cells and induce apoptosis over a 72-hour period and dose-dependently. Moreover, the results revealed that the mRNA and protein expression levels of RAF and RAS in HeLa cells were downregulated by CUR and DOX.

Conclusions: The findings show that an alternative treatment method for cervical cancer can be developed with the application of CUR and DOX. Alternative methods for cervical cancer treatment may be developed using different methods in future studies.

Tissue microarrays (TMAs) are a cost-effective tool to study biomarkers in clinical research. Cervical cancer (CC) is one of the most prevalent in women worldwide, with the highest prevalence in low-middle-income countries due to a lack of organized screening. CC is associated with persistent high-risk human papillomavirus infection. Several biomarkers have been studied for diagnostic, therapeutic, and prognostic purposes. We aimed to evaluate and validate the effectiveness of TMA in CC compared to whole slide images (WSs). We selected and anonymized twenty cases of CC. P16, cytokeratin 5 (CK5), cytokeratin 7 (CK7), programmed death-ligand 1 (PD-L1), and CD8 expression were immunohistochemically investigated. All WS were scanned and 10 representative virtual TMA cores with 0.6 mm diameter per sample were selected. Ten random combinations of 1-5 cylinders per case were assessed for each biomarker. The agreement of scoring between TMA and WS was evaluated by kappa statistics. We found that three cores of 0.6 mm on TMA can accurately represent WS in our setting. The Kappa value between TMA and WS varied from 1 for p16 to 0.61 for PD-L1. Our study presents an approach to address TMA sampling that could be generalized to TMA-based research, regardless of the tissue and biomarkers of interest.