Histology and histopathology最新文献

Objective: Polycystic ovary syndrome (PCOS) is a common reproductive endocrine disorder that adversely affects women's health and quality of life. Pachymic acid (PA), a bioactive ingredient from Poria cocos (Schw.) Wolf, has demonstrated protective effects against PCOS in a murine model. This study aims to investigate the underlying mechanism by which PA exerts protective effects against PCOS.

Methods: Female Sprague-Dawley rats were treated with letrozole to induce PCOS. The ovarian granulosa cell line (KGN) was exposed to lipopolysaccharide (LPS) to mimic PCOS in vitro. Hematoxylin-eosin staining and TUNEL assay were used for ovarian histological analysis. The cell counting kit-8 assay was used to assess the viability of KGN cells. Flow cytometry was used for in vitro cell apoptosis analysis. Western blotting revealed molecular protein expression levels in rat ovaries and KGN cells.

Results: PA attenuated LPS-induced lactate dehydrogenase release (p<0.01), reduced the cell apoptosis rate (p<0.001), Bax, and cleaved-caspase3 protein expression (p<0.001), and increased Bcl-2 protein expression (p<0.01) in KGN cells. PA attenuated letrozole-induced increases in testosterone (p<0.01), luteinizing hormone (p<0.01), and estradiol levels (p<0.05) and decreases in progesterone levels (p<0.05) in PCOS rats. PA promoted corpus luteum formation (p<0.001) and reduced the number of cystic follicles and cell apoptosis (p<0.001) in PCOS rats. PA blocked Akt and ERK signaling transduction in PCOS rats and KGN cells (p<0.001).

Conclusion: PA protects against PCOS and attenuates cell apoptosis by inactivating Akt and ERK signaling.

Trophoblast cells are crucial structural units of the placenta, responsible for maintaining its integrity and function. These cells synthesize and secrete specific proteins that play essential roles in placental vascularization, maternal and fetal immune tolerance, and other critical processes. An abnormal level of trophoblast-derived secreted proteins has been closely linked to pregnancy-related diseases. Preeclampsia, a severe complication of pregnancy characterized by de-novo development of hypertension and proteinuria after 20 weeks of gestation, poses significant health risks to both the mother and fetus. This article reviews several key trophoblast-derived proteins that are widely recognized for their roles in preeclampsia. The specific mechanisms of action and interconnections among these proteins in preeclampsia are discussed, along with novel insights into the underlying pathological mechanisms of this disease.

Cerebral ischemia-reperfusion (IR) injury is a critical pathological event that leads to extensive neuronal loss, neuroinflammation, and blood-brain barrier (BBB) dysfunction. Porphyran, a sulfated polysaccharide derived from Porphyra spp., has demonstrated anti-inflammatory and neuroprotective effects in various neurological conditions. This study aimed to evaluate the post-ischemic therapeutic potential of porphyran in a gerbil model of transient forebrain ischemia. Our findings reveal that porphyran administration (50 mg/kg orally once daily for five days) following IR significantly mitigated IR-induced cognitive decline, as evidenced by the Y-maze test, but porphyran treatment did not significantly prevent neuronal death in the CA1 subregion of the hippocampus, as revealed by Cresyl Violet (CV) and Fluoro-Jade B (FJB) staining. However, porphyran treatment after IR injury effectively attenuated the IR-induced decrease in acetylcholine (ACh) levels, suggesting potential preservation of cognitive function in surviving neurons. Furthermore, porphyran significantly mitigated microglial activation and reduced the levels of proinflammatory cytokines (IL-1β, IL-6, and TNF-α), indicating its anti-inflammatory properties. Additionally, porphyran administration reduced BBB disruption, as evidenced by decreased extravasation of immunoglobulin G (IgG), suggesting a role in maintaining vascular integrity. In summary, although porphyrin administration after IR does not protect pyramidal neurons directly, it may improve cognitive function by mitigating ACh depletion, suppressing microglial activation, and reducing inflammatory cytokine levels.

Chemotherapy-induced diarrhea (CID) is a common adverse event in cancer patients treated with 5-fluorouracil (5-FU). This study aimed to investigate the potential protective effects of Tuoli Xiaodu (TLXD) powder on CID and to explore its possible mechanisms. Mice with CID induced by 5-FU were randomly divided into seven groups: Blank group, CID group, positive drug (loperamide) group, and TLXD powder low, medium, and high groups. The degree of diarrhea, tumor growth, intestinal barrier damage, intestinal inflammation, oxidative stress, and gut microbiota diversity were assessed. The study showed that TLXD powder significantly inhibited diarrhea and tumor growth in 5-FU-induced CID mice. H&E staining and western blot showed that TLXD powder improved the intestinal mucosa and intestinal permeability of 5-FU-induced CID mice. Furthermore, TLXD powder elicited a reduction in the expres-sion of inflammatory factors within the intestinal tract of mice with CID while simultaneously augment-ing the expression of anti-inflammatory factors and maintaining a balanced Th17/Treg ratio. TLXD pow-der decreased intestinal oxidative stress and intestinal epithelial cell ferroptosis and activated the Nrf2/HO-1 signaling axis in CID mice. The results of the gut flora analysis showed that TLXD powder improved the intestinal flora structure of CID mice. TLXD powder significantly reduced the proportion of Proteobacteria, Actinobacteria, Deferribacteres, and TM7 at the phylum level and Desulfovibrio, Mucis-pirillum, Adlercreutzia, and Odoribacter at the genus level. These findings provide a new therapeutic approach for the management of CID in cancer patients treated with 5-FU.

Background: Although not widely known, several types of cancers express histamine. Squamous cell carcinoma (SCC) of the tongue is one such cancer, and histamine expression is associated with the tumor microenvironment. Our aim was to examine whether histamine expression is a useful prognostic factor for tongue SCC.

Methods: Histamine cannot be accurately measured directly because it is rapidly degraded after secretion. Therefore, L-histidine decarboxylase (HDC), an enzyme that synthesizes histamine in a single step, was used to estimate histamine secretion. In a retrospective study, tongue SCC samples from patients were immunohistochemically stained for HDC; the staining intensity was semi-quantified and evaluated relative to indices used in histopathological diagnosis.

Results: High expression of HDC was associated with the worst tumor invasion and tumor budding. Overall survival curves revealed that patients with tongue SCC showing high HDC expression had a poor prognosis.

Conclusion: The expression of histamine may be a prognostic indicator for tongue SCC.

The paper examines what the mast cell, a cell that arose in urochordates and reached humans with the same morphological profile, is used for. Activated mast cells contribute to the regulation of the local immune response and major inflammation and healing processes with the help of a broad range of mediators. Located primarily at the interface between the host and the external environment, mast cells are widely distributed. The local microenvironment directly affects mast cell development, phenotype, and function, which in turn affects the cells' capacity to identify and react to different stimuli by releasing a variety of physiologically active mediators. By interacting with a range of other cells involved in physiological and immunological responses, mast cells can react to changes in their surroundings and serve as first responders in dangerous situations. Consequently, the mast cell's crucial function in innate and adaptive immunity, including immunological tolerance, has come to light more frequently. On the other hand, mast cell malfunction has identified these cells as the primary culprits in a number of autoimmune illnesses, cancer, and chronic allergic/inflammatory conditions.

The poor prognosis of hepatocellular carcinoma (HCC), especially in advanced stages, underscores the need for new therapeutic strategies. In this study, we show that hyaluronan-mediated motility receptor (HMMR) is highly expressed in HCC tumors compared with normal liver tissues. Knockdown of HMMR using siRNA significantly reduced cell proliferation and migration in both parental and doxorubicin-resistant HCC cell lines without inducing apoptosis. Similarly, treatment with 4-Methylumbelliferone (4-MU), a pharmacological HMMR inhibitor, led to dose-dependent decreases in proliferation and migration in vitro. In vivo, 4-MU treatment significantly inhibited tumor growth in a HepG2 xenograft model, resulting in a 44% reduction in tumor volume by day 20 and an 80% decrease in HMMR expression in tumor tissues. These results demonstrate that HMMR promotes growth and migration in HCC, and targeting HMMR effectively inhibits both parental and drug-resistant HCC cells. Additionally, our findings suggest that 4-MU, an approved drug for biliary tract disorders, holds promise as a repurposed therapeutic candidate for HCC treatment.

Background and aims: Gallbladder adenocarcinoma (GBAC) is associated with high mortality because of the difficulty in its early detection and treatment. Therefore, identifying prognostic factors is crucial for managing patients with GBAC. We aimed to elucidate the relationship between immunohistochemical profiles of mucin expression, clinicopathological behavior, and prognosis for curatively resected gallbladder adenocarcinoma (GBAC) and to prove that mucin expression is a prognostic factor for GBAC.

Methods: We examined the expression of mucins (MUC1, MUC2, and MUC4) using immunohistochemical analyses and compared the prevalence of each mucin with clinicopathological features in patients with early-stage (stage 0 to IIB) GBAC.

Results: MUC1 expression was significantly expressed in patients with GBAC with lymphatic invasion, vascular invasion, perineural invasion, and recurrence. MUC2 was significantly expressed in patients with GBAC with perineural invasion and recurrence but not with prognosis. Patients with MUC1-high expression exhibited worse prognoses than those with MUC1-low expression. In contrast, patients with positive MUC4 expression had significantly better prognoses than those without MUC4 expression.

Conclusion: The expression of MUC1 and MUC4 in GBAC is an independent prognostic factor for survival and a useful marker for predicting the outcomes of patients with GBAC.

Osteofibrous dysplasia (OFD) and adamantinoma constitute rare bone tumors. Currently, the World Health Organization (WHO) classification of soft tissue and bone tumors stratifies adamantinoma into three main subtypes, namely OFD-like adamantinoma, classic adamantinoma, including its various growth patterns, and an extremely uncommon subtype, dedifferentiated adamantinoma. Given the wide clinicopathological spectrum of adamantinoma, several tumors constitute the differential diagnoses. An exact diagnosis in these scenarios has significant treatment-related implications, such as synovial sarcoma vs. spindle cell-type adamantinoma, and metastatic sarcomatoid carcinoma vs. adamantinoma, to name but a few. There have been studies attempting to explore the proximity/relationship between OFD, OFD-like adamantinoma, and classic adamantinoma. This review focuses on the clinical, radiological, and pathological features of OFD, as well as the histopathological spectrum of adamantinoma, including its updates and various subtypes and tumors that constitute its differential diagnosis.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent metabolic disorder characterized by excessive lipid accumulation in the liver. The glycolytic enzyme enolase 3 (ENO3) is reported to be most significantly elevated in the analysis of MASLD-related sequencing results based on the GEO database. However, the specific mechanism by which ENO3 regulates MASLD is not fully understood.

Objective: To investigate the role and possible molecular mechanism of ENO3 in MASLD.

Methods: The expression of ENO3 and PKM2 in the liver tissues of control and MASLD rats was detected by immunohistochemistry and western blot. In vitro studies involved treating THLE-2 cells with free fatty acids (FFA) and Ferrostatin-1 (Fer-1), as well as manipulating ENO3 expression via small interfering RNA (siRNA) and overexpression plasmids, and manipulating PKM2 expression via siRNA. Fat accumulation was assessed using Oil Red O staining and measurements of intracellular total cholesterol (TC) and triglycerides (TG). Ferroptosis markers, including SLC7A11, GPX4, Fe²⁺, and malondialdehyde (MDA), were evaluated. Protein-protein interactions between ENO3 and PKM2 were examined using co-immunoprecipitation (Co-IP) and immunofluorescence.

Results: MASLD liver tissues exhibited significantly higher levels of ENO3 and PKM2. Silencing ENO3 in FFA-treated THLE-2 cells reduced fat accumulation, downregulated PKM2 expression, and decreased ferroptosis markers. Conversely, ENO3 overexpression promoted fat accumulation and ferroptosis, which were mitigated by Fer-1 or si-PKM2. Co-IP and immunofluorescence confirmed the physical interaction and co-localization of ENO3 and PKM2 in THLE-2 cells.

Conclusions: ENO3 interacted with PKM2 to regulate ferroptosis and further promoted the progression of MASLD.