Studies have indicated that spleen and white pulp atrophy develops within 5 weeks following hyperglycemia onset in streptozotocin-induced diabetic rats. This study aimed to delineate the histopathological alterations in the spleen across two stages of diabetes progression using design-based stereology. Twenty-six rats were categorized into four groups based on condition (normal control [NC] or diabetic model [DM]) and observation period post-induction (5 or 10 weeks): NC5, DM5, NC10, and DM10. Diabetes was induced using streptozotocin-nicotinamide combination. Histological evaluations were performed using standard staining techniques, whereas spleen compartment volumes were quantitatively assessed through point-counting methods on histological sections. Additionally, immunohistochemistry (IHC) and flow cytometry analyses were utilized to determine the distribution and percentages of T and B lymphocytes. Compared to its NC5 control, the DM5 group exhibited inflammatory responses, including polymorphonuclear leukocyte infiltration, but no significant atrophy. DM5 showed a significantly elevated IHC score for T lymphocytes ( < 0.01) and a higher percentage of CXCR5 + B lymphocytes ( < 0.05) compared to NC5, suggesting an active adaptive immune response. In contrast to the NC10 group, the DM10 group displayed significant spleen atrophy ( = 0.005), with marked reductions in total white pulp volume ( = 0.015) and marginal zone volume ( = 0.008). Furthermore, compared to NC10, DM10 exhibited an increased connective tissue volume fraction ( < 0.001). Across all groups, spleen atrophy was directly correlated with reductions in body weight. These findings underscore an initial inflammatory phase characterized by immune cell recruitment in the spleen during early diabetes, subsequently evolving into significant atrophy, reduced white pulp and marginal zone volumes, and an increased connective tissue volume fraction in advanced stages of the disease, all proportional to body weight loss.

The ability to escape immune surveillance is a hallmark of malignancy. Programmed death ligand 1 (PD-L1) facilitates tumor progression by binding to the immune inhibitory receptor known as programmed cell death protein 1 (PD1) on immune cells, resulting in suppression of the cytotoxic T lymphocyte function. The degree of PD-L1 expression may have a prognostic value in some cancer types, and it may vary according to the genetic makeup and the ethnicity of patients. The expression level of PD-L1 in 63 cases of primary head and neck squamous cell carcinoma (HNSCC) tumor tissues was evaluated using immunohistochemistry (IHC). Also, PD-L1 association with various clinicopathologic characteristics and overall survival was studied. The positive expression rate of PD-L1 in HNSCC was 85.7%, 60.3%, and 52.3% of the total number of cases using combined positive score (CPS)1, CPS5, and CPS 20 cutoff values, respectively. Statistical analysis revealed no significant relationship between the expression of PD-L1 protein and clinicopathological features except for tobacco use using a cutoff CPS ≥ 20. The log-rank chi-square results showed that PD-L1 was not a significant factor affecting the 4-year overall survival of HNSCC patients. Also, the overall survival rate was not significantly affected by the patient's age, tumor differentiation, tumor size, and lymphovascular invasion. However, survival curves demonstrated lower overall survival in HNSCC female patients, disease recurrence, and positive perineural invasion. Our findings showed relatively high PDL-1 expression in most HNSCC patients. No significant association was found between PD-L1 protein expression and overall survival.

Beta-glucans (βTGs) are a class of dietary fibers and biologically active polysaccharides derived from natural sources, known for their diverse bioactive properties. Their documented effects include anti-tumor, anti-inflammatory, prebiotic, anti-obesity, anti-allergic, anti-microbial, antiviral, anti-osteoporotic, and immunomodulating activities. Despite these well-established benefits, the role of βTG in dehydroepiandrosterone (DHEA)-induced polycystic ovary syndrome (PCOS) remains largely unexplored. This study investigated the protective effects of βTG treatment on PCOS and its potential to reverse PCOS-induced changes. Female Sprague-Dawley (SD) rats were randomly divided into four groups (n = 8 each): control, PCOS, PCOS+βTG, and βTG. We assessed biochemical markers related to oxidative stress, antioxidant status, inflammation, cytokines, and hormone levels. Additional analyses included immunohistochemistry and histopathology. Membrane array analysis was used to profile growth factors, cytokines, and chemokines. However, βTG normalized deviations in the estrous cycle caused by PCOS and positively affected the reproductive system ( < 0.05). It also reduced the inflammatory response in PCOS rats by decreasing inflammatory cytokines ( < 0.05). Furthermore, oxidative stress was significantly reduced, and antioxidant enzyme activities were markedly elevated in the βTG group ( < 0.05). Histopathological alterations were prevented by βTG, which also induced the expression of essential proteins such as beta-nerve growth factor (bNGF), tissue inhibitor of metalloproteinase-1 (TIMP-1), Agrin, cytokine-induced neutrophil chemoattractant-1 (CINC-1), brain-derived neurotrophic factor (BDNF), and basic fibroblast growth factor (FGF-2/bFGF) ( < 0.05). In conclusion, βTG treatment effectively protects against oxidative stress, inflammation, hormone imbalance, and histopathological damage in ovarian tissue caused by PCOS.

Acute kidney injury (AKI) is a clinical syndrome that can be caused by a variety of factors, leading to rapid decline of kidney function and increased morbidity and mortality, whilst also exerting significant economic burden on the affected patient. is a highly valued plant in traditional Chinese medicine (TCM). Tanshinone IIA (Tan IIA) is an important active compound that can be extracted from salvia miltiorrhiza, which has reported anti-inflammatory effects. The objective of the present investigation was to explore the potential effects of Tan IIA on folic acid-induced AKI and elucidate its underlying mechanism. A comprehensive analysis was conducted utilizing the TCM Systematic Pharmacology Database and Analytical Platform database to screen for chemical components and their corresponding targets. Subsequently, by using network pharmacology techniques and Cytoscapes 3.7.2 software, a protein-protein interaction (PPI) network was constructed and analyzed. Through Venn diagram analysis of the DeGeNET, OMIM, PharmGKB, and GeneCards databases using the key word "acute kidney injury," a total of 76 overlapping targets were obtained. Building upon this, a compound-target gene network was constructed and analyzed by Cytoscapes 3.7.2 software, revealing TP53, STAT3, CASP3, VEGFA, and JUN to be pivotal therapeutic targets. Subsequently, an AKI mouse model was established to investigate the renal effects of Tan IIA. By immunohistochemistry, Western blot results showed the Tan IIA ameliorated kidney function by alleviating inflammation, mitigating necrosis of renal tubular cells, promoting their proliferation and attenuating kidney injury. These beneficial effects were found to be achieved by inhibiting the PI3K/AKT signaling pathway and inhibiting the expression of TP53 by Western blot. In conclusion, TP53may be a potential target for folic acid-induced AKI, whilst Tan IIA exerts its renoprotective effects and improves renal function by PI3K/AKT signaling pathways.

Clinical and experimental studies have shown that sitagliptin regulates blood glucose levels. This study was designed because it is thought that sitagliptin may reduce diabetes-induced apoptosis in testes by affecting blood glucose levels and may have a beneficial effect on spermatogenesis by regulating hormonal activity. Thirty-four male Sprague-Dawley rats were divided into three groups: Control group (n = 10), given citrate buffer only; Diabetes group (n = 12), after 2 weeks of the high-fat diet, given a single dose of 35 mg/kg streptozotocin (STZ, dissolved in citrate buffer, intraperitoneally); Diabetes + Sitagliptin group (n = 12), after 2 weeks of the high-fat diet, diabetes was induced with STZ and 10 mg/kg sitagliptin (intragastric) was administered daily for 6 weeks. At the end of the experiment, blood glucose levels measured in the sitagliptin-treated group were found to be significantly lower than in the diabetes group. Serum testosterone, follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels, seminiferous tubule diameter, Johnsen score, and proliferation indices were significantly lower in the diabetic groups compared to the control group, while no significant difference was found between the diabetes and sitagliptin groups. Basement membrane thickness, apoptotic cell and apoptotic tubul indexes, Fas, FasL, and caspase8 immunoreactivities were higher in diabetic groups compared to the control group, while no difference was found between the diabetic and sitagliptin groups. In conclusion, although 10 mg/kg sitagliptin reduced blood glucose levels in diabetes-induced hyperglycemia, it did not alter serum testosterone, FSH and LH levels, and did not appear to have a beneficial effect on diabetes-induced apoptosis and proliferation in the testes.

Cultivating cells in 3D is considered a significant advancement in cell culture models, as it better reflects natural cellular environments compared to 2D cultures. However, analytical methods like standard light microscopy are less effective for 3D cultures. In this study, 3D cell cultures were generated using the liquid overlay technique with 10,000, 50,000, 100,000 and 200,000 Normal Human Dermal Fibroblasts, analyzed on days 1, 2, and 3 post-seeding. We quantified the influence of fixation with paraformaldehyde or glutardialdehyde/dehydration on their morphology compared to living 3D cell cultures. They were analyzed by light microscopy, scanning electron microscopy as well as by digital light microscopy (height profile measurement). Over time, the cultures decreased in size, likely due to cell shrinkage and structural reorganization. The size reduction could be mathematically described by an exponential decay function. The proportion of round spheroids versus indented aggregates depended on cell number, culture age, and fixation method. On day 1, cultures seeded with 10,000 cells formed nearly 100% round spheroids, regardless of fixation. Higher cell numbers led to fewer round spheroids, and fixation further reduced their number. This suggests that large cell quantities sediment in layers due to steric hindrance, forming indentations. Since aldehydes are responsible for cross-linking proteins, we hypothesize that this chemical reaction, combined with low stability of the 3D cell cultures, leads to the increased formation of the indented 3D cell aggregates. This is consistent with an overall increase in the number of round spheroids and a decrease of the negative influence of fixation over time. In summary, it is important to consider the number of seeded cells, the incubation time, as well as the possible fixation effects when generating stable spheroids using the liquid overlay technique for down-stream experiments.

Groundwater pollution with lead, fluoride, and nitrate presents a growing environmental and health challenge. This study aimed to evaluate the nephrotoxic effects of these pollutants in male albino rats and assess the potential ameliorative effects of curcumin and ascorbic acid in counteracting their toxicity for 135 days. A total of ten treatment groups were established viz. control, lead + fluoride + nitrate (BIS), lead + nitrate, lead + nitrate + curcumin + ascorbic acid, lead + fluoride, lead + fluoride + curcumin + ascorbic acid, fluoride + nitrate, fluoride + nitrate + curcumin + ascorbic acid, lead + fluoride + nitrate, lead + fluoride + nitrate + curcumin + ascorbic acid. Exposure to lead, fluoride, and nitrate resulted in a significant decrease in the activity of oxidative stress enzymes viz. superoxide dismutase, catalase, glutathione reductase, and glutathione peroxidase, and a notable increase in the lipid peroxidation levels. Further, significantly increased urea and creatinine levels in plasma and renal damage including glomerular shrinkage, widened Bowman's space, and tubular degeneration were also observed. The greatest damage was recorded in the lead + fluoride + nitrate group followed by lead + fluoride, lead + nitrate, and fluoride + nitrate. Co-treatment with curcumin and ascorbic acid demonstrated remarkable protective effects, with improvements in oxidative stress markers, plasma urea, and creatinine levels along with a significant restoration of glomerular structure and normalization of Bowman's space reflecting improved renal function. This research highlights the kidneys' susceptibility to environmental toxicants and the combined efficacy of curcumin and ascorbic acid in mitigating nephrotoxicity.

In this study, we aimed to investigate the specific role of the acetyl-CoA carboxylase (ACACA) gene in oral squamous cell carcinoma (OSCC). We constructed the human tongue carcinoma cell line SAS with low ACACA expression and evaluated changes in cell proliferation, apoptosis, and ferroptosis. Then, the effect of combined treatment with cisplatin and ferroptosis inducer erastin was measured. To assess the impact of ACACA expression on tumor growth in vivo, we established xenograft models with varying ACACA levels in twelve male BALB/c nude mice. ACACA knockdown significantly reduced the proliferation ability of SAS cells, and increased the number of apoptotic cells. ACACA knockdown also induces ferroptosis, and this effect was enhanced by combined treatment with cisplatin and erastin. In vivo experiments demonstrated lower tumor volume and weight in the ACACA knockdown group than those in the control group. Exploring the combined effect of ACACA knockdown and cisplatin treatment revealed a promising synergistic effect against ferroptosis signaling and downstream signaling pathways in SAS cells and in vivo. These findings suggest that targeting the ACACA gene has the potential to be a novel therapeutic strategy for oral cancer treatment.

Ulcerative colitis is a chronic inflammatory condition of the gastrointestinal tract that can predispose patients to colonic neoplasms. Various natural compounds have been explored for their therapeutic potential. Indole-3-carbinol (I3C), a natural compound derived from cruciferous vegetables, is recognized for its tissue-protective and regenerative properties. This study aimed to investigate the effects of I3C on experimental ulcerative colitis in rats. Thirty-two Wistar rats were randomly assigned to four groups: a control group receiving isotonic saline, a TNBS group administered trinitrobenzene sulfonic acid (TNBS) intrarectally, an I3C group receiving I3C via gastric gavage, and a TNBS+I3C group treated with I3C following TNBS induction. After 7 days, all animals were euthanized under anesthesia, and pathological, histochemical, and immunohistochemical evaluations were conducted. The results revealed that I3C mitigated the severity of TNBS-induced colonic lesions and facilitated tissue repair. The I3C-treated group exhibited reduced tissue damage and enhanced mucosal regeneration. Additionally, vessel count, collagen, and myofibroblastic activity were markedly increased following I3C treatment. In conclusion, I3C exhibits both protective and reparative effects in experimental ulcerative colitis, potentially through anti-inflammatory mechanisms and the activation of tissue repair pathways.

Dogs represent the most common domesticated animal outside of the research arena for whom tissue for pathological diagnosis is requested. Currently, there is a paucity of literature describing the cross-reactivity of anti-human antibodies on canine tissue for oncological diagnosis. This study aimed to evaluate the cross-reactivity of commonly used anti-human diagnostic antibodies in veterinary histopathology. One hundred seventy-one various samples from 153 canine tissues were processed to paraffin and tested with 76 fully validated anti-human antibody clones frequently employed in hospital pathology laboratories using immunohistochemistry methods to determine which ones exhibited comparable cross-reactivity and therefore potential use in veterinary pathology laboratories. Some of the anti-human antibodies were excluded from the study due to a lack of comparable canine tissues on which to test. However, almost half of the antibodies demonstrated results similar to those in human tissues and about one quarter showed weaker or less consistent labeling. The antibodies that demonstrated weaker or inconsistent labeling suggest areas where further development and modification could improve their employment on canine specimens. Fully one-third of antibodies tested failed to show labeling congruent with human tissues. The outcomes from this study could facilitate the adoption of established anti-human antibody markers in veterinary histopathology practices.

Testicular torsion, a medical condition contributing to male infertility, results in severe scrotal pain and ischemia. Oxidative stress factors contribute to germ cell death following surgical reperfusion, suggesting postoperative pharmacotherapy could mitigate testicular ischemia/reperfusion (I/R) injury. Ivermectin, a GABA receptor modulator for treating parasitic infections such as onchocerciasis, has demonstrated anti-oxidative stress and anti-apoptotic properties. Therefore, this study aimed to evaluate the efficacy of ivermectin administration after detorsion using a rat model of testicular torsion/detorsion (T/D). This study utilized 40 male Wistar rats weighing 200-250 grams. The studied groups were the sham (no T/D induction), control (T/D and no treatment), and T/D following administration of ivermectin administration and the doses of 1, 2, and 5 mg/kg intraperitoneally. For I/R surgery, both testes were twisted 720 degrees clockwise for 4 h to cause torsion. Subsequently, the levels of malondialdehyde (MDA) and superoxide dismutase (SOD) activity were assessed using ELISA, while the expression of GABA receptors and apoptosis were examined using the immunohistochemical method. Histopathological alterations were evaluated with hematoxylin and eosin (H&E) staining to evaluate cell counts and seminiferous tubule diameters. Administration of ivermectin effectively reduced oxidative stress levels, as evidenced by decreased MDA levels and increased SOD activity, compared to the control group (P < 0.01 and P < 0.05, respectively). Ivermectin also modulated the expression of elevated GABA receptors and caspase 3 (P < 0.05 and P < 0.001, respectively). Furthermore, histopathological analysis revealed that ivermectin prevented germ cell degeneration, edema, and hemorrhage in the testis (P < 0.05). Ivermectin may be a potential treatment option for protecting against testicular torsion and may have beneficial effects on mitigating germ cell death, oxidative stress, and GABA receptor modulation. Further research is needed to explore dosages, long-term impacts, and clinical trials to determine the potential for patients with testicular torsion.

Tartrazine, a coal tar-derived azo color, is utilized in food, drinks, cosmetics, and pharmaceuticals. Its azo group catabolizes in the gut, poisoning the liver. This study investigated the efficacy of melatonin, an endogenous antioxidant from the pineal gland against hepatotoxicity in tartrazine-intoxicated rats. Thirty-two adult male wistar albino rats were allocated into four groups: control group, melatonin group (10 mg/kg), tartrazine-treated group (7.5 mg/kg), and tartrazine + melatonin-treated group (7.5 mg/kg tartrazine + 10 mg/kg melatonin). Doses were taken daily for 4 weeks. Melatonin's influence on hepatotoxicity was assessed by monitoring liver enzyme activity, antioxidant state, apoptotic and inflammatory markers, DNA fragmentation, histological and ultrastructural changes. Rats exposed to tartrazine exhibited elevated liver enzymes, oxidant-antioxidant imbalance, and elevated hepatic inflammatory markers (TNF-α, IL-6). Tartrazine also damaged DNA and induced histological and ultrastructural alterations in liver tissue, as shown by the comet assay. Alpha-fetoprotein (AFP) and proliferating cell nuclear antigen (PCNA) were strongly expressed in immunohistochemistry. In rats, melatonin significantly reduced all tartrazine effects. Conversely, melatonin treatment significantly alleviated all aforementioned effects induced by tartrazine in rats by decreasing liver enzymes, elevating antioxidant enzymes, and reducing hepatic inflammatory markers. Enhanced histological assessment and the ultrastructure of the liver was detected following melatonin use. The use of melatonin may safeguard against tartrazine-induced hepatic DNA damage. In conclusion, the current findings indicate that tartrazine administration has detrimental health effects and deleterious impacts on liver function and structure. Melatonin mitigated tartrazine-induced liver damage via antioxidant, anti-inflammatory, and anti-apoptotic pathways.

Safeguarding the integrity and functionality of the gastrointestinal system is paramount, given its vulnerability to several detrimental effects. One of the factors that can cause functional disorders is oxidative stress, which can disrupt the homeostasis of intestinal tissue and cause various diseases. In this study, we aimed to evaluate the expression patterns of nuclear factor erythroid 2-like 1 (Nrf1) and nuclear factor erythroid 2-like 2 (Nrf2) transcription factors, which are part of an important cleaning system that protects cells against oxidative stress, in the adult rat small intestine by immunohistochemical means. Six Wistar albino adult rats were used in this study. After taking 5 μm thick sections of the small intestine, immunohistochemistry labeling was performed to investigate the expression of Nrf1 and Nrf2. Both transcription factors were found to exhibit immunopositivity in the duodenum, jejunum, and ileum segments of the small intestine. In the crypt epithelium, Nrf1 and Nrf2 showed similar intensity and distribution of staining, whereas, in the villus epithelium, Nrf2 immunoreactivity was most prominent in the ileum and weakest in the jejunum. Nrf1 exhibited lower staining intensity in the ileum. In the smooth muscle layers and the myenteric plexus, Nrf2 immunopositivity was highest in the duodenum, while it was weaker in the jejunum and ileum. These findings indicate that Nrf1 and Nrf2 display region-specific expression patterns in the small intestine and suggest that these transcription factors may play distinct roles in the regional oxidative stress response of intestinal tissues.

Periodic acid-Schiff (PAS) staining is useful for visualizing glycogen and mucus. 7-amino-4-methylcoumarin (AMC), an organic reagent, exhibits blue fluorescent signals upon UV excitation. We recently showed that AMC can be used as a fluorescent substitute for Schiff's reagent in PAS staining. In-resin correlative light-electron microscopy (CLEM) is an excellent technique employing fluorescent and electron microscopy (EM) images obtained from the same resin-embedded ultra-thin sections, and provides a high level of morphological concordance between the fluorescent and EM images. Here we studied whether AMC was useful in detecting PAS-positive cells in in-resin CLEM using human pathological samples. Formalin-fixed, paraffin-embedded sections of human colonic and renal tissues and colonic amoebiasis were used. After staining with AMC, these samples were subjected to EM preparation and embedded in epoxy resin. Semi-thin and ultra-thin sections were prepared, and fluorescent and EM images were obtained. AMC signals were well preserved in colonic goblet cells, renal basement membrane, and amoebic bodies in epoxy resin-embedded sections. Using the CLEM technique, a small number of amoebic bodies were easily detected in an inflammatory background of colonic amoebiasis. In conclusion, we successfully detected PAS-positive cells in in-resin CLEM with AMC. Our method may enhance EM analysis in human pathology.

Amyloidosis is caused by the extracellular deposition of amyloid fibrils with a β-pleated sheet structure. Diagnosis typically relies on Congo red or Thioflavine T staining. Recently, DAPI (4',6-Diamidino-2-Phenylindole), which is a common nuclear fluorochrome, has been reported to stain amyloid. DAPI staining is simpler than Congo Red and Thioflavine T staining, but its staining mechanism remains unclear. Thus, this study aimed to investigate the mechanism and specificity of DAPI staining for amyloid and its utility. The staining properties of DAPI and Thioflavine T for amyloid were compared on the basis of their stereochemical similarity. In addition, formic acid-treated amyloid specimens were used to investigate the mechanism by which structural changes affect DAPI binding to amyloid fibrils. DAPI staining was also evaluated in four specimens with different types of amyloid. DAPI and Thioflavine T had similar stereochemistry and staining behavior. The amyloid present in formic acid-treated specimens was negative for DAPI staining, indicating that DAPI may recognize the conformation of amyloid fibrils. DAPI stained positively in specimens deposited with AA, Aβ, AL, and AIAPP. DAPI staining recognizes the β-pleated sheet structure of the amyloid fibril structure, and is a simple and sensitive method for detecting amyloid deposition.

Endothelial progenitor cells (EPCs) play a crucial role in neovascularization and tissue repair, with significant therapeutic potential in ischemic diseases, tumor therapy, and as gene carriers. However, the current methods for isolating and culturing EPCs are not standardized, leading to inconsistencies in cell numbers and functionality. This study aimed to optimize the in vitro culture conditions for EPCs using an orthogonal design, focusing on four main factors: cell density, culture medium, fetal bovine serum (FBS) concentration, and vascular endothelial growth factor (VEGF) concentration. The most effective conditions among those tested were a cell density of 1 × 10/cm, EGM-2 medium, 10% FBS, and 20 ng/mL VEGF. Under these conditions, EPCs exhibited significantly enhanced proliferation, migration, and pro-angiogenic (paracrine) capacity. Immunohistochemistry and fluorescent staining confirmed high expression of EPC-specific markers, such as CD133 and KDR, and the ability to uptake DiI-ac-LDL and bind FITC-UEA-1. Angiogenesis assays showed that most effective conditions among those tested significantly increased the number of vessel-like structures. Additionally, the migration rate and proliferative activity of EPCs were significantly higher under the most effective conditions among those tested compared to conventional conditions. These findings provide a robust foundation for further refining in vitro EPC culture and pave the way for more effective clinical applications. Future studies should validate these optimized conditions in in vivo models to fully realize the therapeutic potential of EPCs.

Breakthrough progress has been made in the molecular mechanism research and clinical application of PD-1/PD-L1 in the regulation of immunosuppression and tolerance mainly in human and mouse fields, but is relatively slow in other species. The eukaryotic expression vectors pECFP-Fc-1 and pEYFP-Fc-L1 for high expression of canine PD-1 and PD-L1 proteins were constructed and transfected into human embryonic kidney 293 T cells. Fluorescence microscopy, laser scanning confocal microscopy, and immunofluorescence technology were used to identify the expression and membrane localization of the target proteins in human embryonic kidney 293 T cells. The binding activity of the target proteins expressed on the model cell was identified by eukaryotic expression vector co-transfection and immunocoprecipitation. The results showed that canine PD-1 and PD-L1 proteins were expressed on the membrane surfaces of their respective positively transfected cells. The cell membrane complex was further analyzed by co-immunoprecipitation technology, PD-L1 protein components were successfully detected in the pull-down complex of canine PD-1 antibody, and the two target proteins expressed in the model cells showed good mutual binding activity. Further research is needed to evaluate high throughput and a reliable method for screening drugs that block the PD-1 and PD-L1 pathway.

Liver ischemia and ischemia/reperfusion (I/R) injury are common in hepatic resection, trauma surgery, and transplantation and contribute to postoperative morbidity and mortality. This study aimed to investigate the relationship between early histopathological changes due to liver I/R injury and serum levels of perilipin-2 (Plin2) and other oxidative stress biomarkers. Fifty female Wistar albino rats were divided into five groups: Group 1 (control), Group 2 (ischemia for 30 minutes), and Groups 3-5 (ischemia followed by 1, 2, or 3 hours of reperfusion). Intracardiac and arterial blood samples were collected for biochemical analysis, while liver tissue samples were used for histopathological examination. Serum levels of Plin2, ischemia-modified albumin (IMA), total antioxidant status (TAS), and total oxidant status (TOS) were measured. Plin2 levels were significantly lower in the ischemia group compared to others ( < 0.01). The control group had significantly lower IMA, TOS, aspartate aminotransferase (AST), and alanine aminotransferase (ALT) levels ( < 0.01) and lower TAS levels ( < 0.05). Rats with Grade 1 liver injury showed significantly lower Plin2 ( < 0.01) and higher IMA levels ( < 0.05). Reduced serum Plin2 following ischemia suggests its potential as a biomarker for acute liver injury. Further studies are needed to clarify its role across different reperfusion durations.

Our study aimed to investigate the antidiabetic, antioxidative, and antiapoptotic effects of liraglutide on the testes of rats with diabetes and ischemia/reperfusion injury. Subjects were divided into three groups: control, diabetes, and torsion groups. Rats with diabetes were further divided into two subgroups such as diabetes and diabetes+Liraglutide groups. The torsion group was divided into three subgroups such as torsion, torsion/detorsion, and torsion/detorsion+Liraglutide groups. Malondialdehyde (MDA), superoxide dismutase (SOD), and testosterone levels were measured from blood samples. Also, testicular tissue samples were examined by light and electron microscopy. Apoptosis was assessed using immunohistochemistry for caspase-3. Degeneration of seminiferous tubules and interstitium was observed in the diabetes, torsion, and torsion/detorsion groups, while Liraglutide treated groups showed normal seminiferous tubules morphology. Elevated levels of apoptosis, i.e. caspase-3, were observed in diabetes, torsion, and torsion/detorsion groups (P < 0.05), whereas Liraglutide treated groups had similar levels of apoptosis as the control group. MDA levels of diabetes, torsion, and torsion/detorsion groups were increased (P < 0.05), while SOD and testosterone levels were decreased (P < 0.05). However, Liraglutide treated groups, SOD, MDA, and testosterone levels were found similar to the control group. In conclusion, Liraglutide positively affects structural changes and hormone levels in diabetes and torsion/detorsion groups.

The present study investigated the protective effect of extract against the toxic effects of doxorubicin (DOX) on mice ovaries cultured in vitro. Female mice with regular estrous cycle were used. The animals (n = 48) had their ovaries collected and cultured individually in a 24-well plate at 37.5°C in 5% CO for 6 days. The ovaries were culture DMEM alone or supplemented with DOX (0.3 μg/ml), as well as both DOX and (5%, 10%, 25%, or 50%). After culture, ovaries were fixed for histological analysis (follicle morphology, growth and activation, extracellular matrix (ECM) configuration and stromal cell density), immunohistochemistry ( expression) or stored at - 80°C to evaluate the levels of mRNA for superoxide dismutase (), catalase (), nuclear factor-erythroid 2-related factor 2 () and tumoral necrosis factor-α () by real-time PCR. The results showed that ovaries cultured with DOX had a lower percentage of normal follicles and reduced stromal cell density, but when extract was added to the culture medium, there was a protective effect on the ovarian structure against the deleterious effects of DOX. In addition, ovaries cultured with both DOX and (10 and 25%) had reduced immunostaining and increased expression of mRNA for antioxidant enzymes (, , and ). In conclusion, is associated with a protective effect on ovarian follicles and stromal cells against DOX-induced toxicity. Therefore, has great potential to preserve fertility in patients undergoing chemotherapy treatment, which often cause irreversible damage to oocytes.