Biotechnic & Histochemistry最新文献

Klebsiella pneumoniae frequently causes pneumonia; it is the eighth leading cause of death and one of the most common infectious causes of mortality. Artemisia judaica is well known for its various therapeutic effects. The goal of this study is to evaluate the efficacy of ciprofloxacin and A. judaica in treating pneumonia in K. pneumoniae infected rats. Transmission electron microscopy (TEM) demonstrated that ciprofloxacin and A. judaica extract had substantial antibacterial properties against K. pneumoniae. Five groups, each with ten rats, were studied: Group 1 (negative control), Group 2 (infected with 1 × 10⁵ CFU/mL of K. pneumoniae solution), Group 3 (infected and treated with 250 mg/kg of A. judaica extract), Group 4 (infected and treated with 500 mg/kg of A. judaica extract), and Group 5 (infected and treated with 500 mg/kg of ciprofloxacin). Animals were sacrificed after 24, 48, and 72 hours of treatment. We found that the A. judaica extract or ciprofloxacin treatment improved the rate of survival of infected rats and reduced bacterial spread in the lungs, liver, and spleen. Groups 3, 4, and 5 had substantial histological improvement in lung pathology, with lower TNF-α levels and elevated IL-4, SOD, and CAT levels relative to the positive controls. We conclude that A. judaica has antioxidant, anti-inflammatory, and antibacterial effects that can help combat pneumonia caused by K. pneumoniae in rats.

Glial precursor cells are among the major types of glia in the dorsal root ganglias (DRGs) of the peripheral nervous system. Previous studies have shown that the transdifferentiation of DRGs-derived glial precursor cells contributes to peripheral neurogenesis. In the present study, we investigated the mRNA expression profiles and examined the effects of differential expression mRNAs (DEMs) during the differentiation of glial precursor cells derived from the rat DRGs. We characterized glial precursor cells derived from rat DRGs explants using immunofluorescence. Sequencing was subsequently conducted, followed by enrichment analysis utilizing gene ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. The identified genes were subsequently subjected to protein-protein interaction (PPI) network analysis during the differentiation process of glial precursor cells derived from the rat DRGs. The establishment of a sciatic nerve injury (SNI) model was followed by the detection of the expression of key genes in the Wnt and Neurotrophin pathways in the DRGs of SNI rats via qRT-PCR. Additionally, the terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay was employed to assess apoptosis in the DRGs. We detected the mRNA expression profiles during the neuronal differentiation of rat DRGs-derived glial precursor cells. More DEMs and GO terms were detected on the third day of DRGs-derived glial precursor cells transdifferentiation, accompanied by morphological alterations in the cells; that is, some cells presented neuronal-like phenotypic characteristics (the early neuronal marker Tuj1 was positive). KEGG enrichment and PPI network analyses revealed that Wnt and Neurotrophin pathways play crucial roles in the process of glial precursor cell differentiation into neuronal-like cells. After knocking down cadherin-associated protein beta 1 (Ctnnβ1) in the SNI model, the number of apoptotic cells was significantly reduced, and the expression of Wnt4 and Ntrk3 was significantly increased. The Ctnnβ1 gene may be a crosstalk factor between the Wnt and Neurotrophin pathways that negatively regulates the differentiation of glial precursor cells.

Palmitic acid (PMA) is abundantly present in substantial quantities within palm oil and manifests neurodegenerative propensities. Conversely, the ingestion of Hesperidin (HSD) is correlated with a reduction in inflammatory markers and mediators. This investigation was meticulously devised to scrutinize the protective potential of HSD against the deleterious repercussions of PMA administration on the cerebral cortex. A cohort comprising forty albino Wistar rats was stratified into four groups, each receiving supplements of HSD and PMA. Remarkably, HSD was observed to fortify the histological framework of the cerebral cortex subsequent to PMA exposure, concurrently diminishing the percentage of apoptotic cells. Furthermore, HSD upregulated the levels of antioxidant markers, preserved the levels of neurotransmitter-associated enzymes, and downregulated the expression of inflammation-regulating genes. In conclusion, PMA exerts toxic effects on the cerebral cortex of albino Wistar rats, leading to increased apoptosis and neuroinflammation, thereby reducing brain cholinergic activity. HSD was found to attenuate the cerebral cortex content of MPO, 5-NTD, ROS, MDA, and NF-κB. Additionally, it elevated the cerebral cortex content of antioxidants and anti-inflammatory markers, thereby shielding it from the deleterious effects of PMA.

Leiomyomas (fibroids) are the most common benign tumors of the uterus and are present in greater than half the female population over 50 years old in the United States. Leiomyosarcomas are the malignant variation of leiomyomas and, while far less common, have a high mortality rate. Differential protein expression between both benign and malignant tumors and normal tissue samples forms the basis of many treatment strategies. This study evaluated protein expression of several markers using immunohistochemistry (IHC) methods on 74 leiomyomas, 14 uterine leiomyosarcomas, and 26 normal uterine myometrial samples which had been formalin-fixed and paraffin-embedded. Markers included the Ki-67 proliferation marker, estrogen receptor (ER), progesterone receptor (PR), aldehyde dehydrogenase (ALDH), B-cell lymphoma 2 (BCL-2), and cytokeratin 8/18 (CK 8/18). The Ki-67 positivity was significantly higher in leiomyosarcomas when compared with benign uterine tissues and was also higher in leiomyomas than in normal uterine smooth muscle. ER and PR were highly expressed in benign tissues but exhibited reduced expression in malignant lesions. Both CK 8/18 and ALDH were expressed in a significantly higher proportion of normal myometrial tissues as compared with leiomyomas and leiomyosarcomas. Conversely, BCL-2 expression in normal tissues was lower than in both leiomyomas and leiomyosarcomas with leiomyosarcomas producing the highest expression. The Ki-67 value can reliably differentiate between benign and malignant smooth muscle uterine tissues. Because CK 8/18 and ALDH were more frequently or strongly expressed in normal myometrium vs. leiomyoma or leiomyosarcoma, pathological changes to the cells may be the cause for a reduction in protein production. Future investigations may determine that upregulation of either of these two markers in leiomyomas or leiomyosarcomas could lead to slower tumor growth.

We investigated the effects of ecstasy on the expression of heat shock protein 70 (HSP70) and apoptosis in rat kidney. We used 20 adult male Wister rats divided into four groups of five: control, sham, Ecs 5 and Ecs 10; the latter two groups were administered by intraperitoneal (i.p.) injection 5 and 10 mg/kg ecstasy, respectively. At the end of the experiment, the kidneys were removed, fixed, and prepared for immunohistochemistry and TUNEL staining to evaluate the expression of HSP70 and apoptosis, respectively. HSP70 expression and apoptosis cells were significantly increased in most parts of the kidneys, and kidney weight and volume were decreased in rats administrated 10 mg/kg ecstasy compared to the control group. Administration of 5 mg/kg ecstasy significantly increased HSP70 expression in the distal and collecting tubules and the number of TUNEL-positive cells in the proximal, distal convoluted tubules and renal corpuscles compared to the control group. We found that ecstasy increases HSP70 expression and apoptosis in renal tissue.

We aimed to investigate TLR-4 receptor activity in the development of endometriosis and the effect of trastuzumab in experimentally induced endometriotic tissue via TLR-4 in this study. Twenty-eight female Wistar-Albino rats were divided into four groups: Group 1 (Control Group), Group 2 (Endometriosis Group), Group 3 (Endometriosis + Trastuzumab Group), and Group 4 (Trastuzumab Group). All animal tissue samples were collected. Histopathological, immunohistochemical, and biochemical analyses were performed. In histopathological analysis, there was a significant difference between Group 2 and other groups in terms of connective tissue edema, inflammation, hemorrhage, epithelial damage, and mast cell density. In immunohistochemical analysis with TLR-4, Group 2 exhibited strong staining. In biochemical analysis, it was found that there was a highly significant difference between Group 2 and Group 1 considering the Malondialdehyde (MDA) levels in plasma samples. There was no significant difference in terms of the MDA levels among other groups. Considering the glutathione levels in the plasma samples, it was found that there was a highly significant difference between Group 2 and Groups 3 and 4. Trastuzumab may play a role in the treatment of histopathological damage and fibrosis in experimentally induced endometriotic implants by showing anti-inflammatory and antiproliferative activity.

Paracetamol (PAR) is a drug that is widely used throughout the world and has limited treatment options in case of use-related hepatotoxicity. Apilarnil (AP), a bee product has high levels of antioxidant properties, which result from the rich polyphenols found in its structure. Despite it being shown that AP treatment might have a protective effect on liver damage induced by carbon tetrachloride and lipopolysaccharide, there is no study investigating the possible role of this agent in PAR-induced hepatotoxicity using an experimental in vivo model. Therefore, we aimed to investigate the therapeutic effects of AP on paracetamol-induced hepatotoxicity and its relationship with apoptosis and oxidative stress. Our results indicated that PAR administration caused irregularities in hepatocyte cords, bleeding and dilatation of sinusoids, and inflammatory cell infiltration in the portal area and liver parenchyma. PAR caused an increase in p53 and caspase3 expressions and malondialdehyde (MDA) levels, while it caused a decrease in catalase (CAT) and glutathione peroxidase (GSHpx) levels. AP treatment significantly improved histopathological changes in liver tissues and decreased p53 and caspase3 expressions. Our data suggest that AP alleviates paracetamolinduced hepatotoxicity by regulating p53 and caspase-3 expressions and modulating oxidative stress mechanisms.

Tendon injuries remains a challenge to treat owing to its poor intrinsic reparative ability. It is hypothesised that hypoxic conditioning of mesenchymal stem cells (MSC) through the activation of hypoxia-inducible factor-1 alpha (HIF-1α), may enhance tendon repair process by promoting cellular proliferation and tenogenic differentiation. To demonstrate this, a study using roxadustat, a specific hypoxia mimetic mediator and HIF-1α inducer was conducted on adipose-derived mesenchymal stromal cells (AD-MSCs). Cellular morphology, proliferation rates, tenogenic protein and gene expression levels in untreated AD-MSCs (Group 1), roxadustat pre-conditioned AD-MSCs (Group 2), AD-MSCs subjected to CAY10585 (Group 3), roxadustat pre-conditioned AD-MSCs with CAY10585 (Group 4) and untreated primary tenocytes (Group 5) were evaluated. MSCs pre-conditioned with 12.5µM roxadustat for 24 hours showed the highest expression of HIF-1α without affecting the proliferation rates of AD-MSCs. However, significant reduction of HIF-1α levels was observed when the cells were treated with 3.5µM CAY10585. Roxadustat significantly up-regulated collagen I and III expressions by 6.6 and 6.3-fold respectively. HIF-1α promoted Scleraxis, Tenascin-C and Collagen III expressions, resulting in an increase of 6, 7, and 3 folds respectively. Conversely, using CAY10585 reduced these expressions to 3, 2 and 1 folds respectively. These trends were observed in the gene expression levels across Groups 1 to 4. However, the expression of these genes in Group 2 was significantly lower as compared to Group 5. Conclusion: HIF-1α accumulation promotes superior cell proliferation and tenogenic differentiation of AD-MSCs, indicating that roxadustat may be a potential therapeutic mediator in tendon repair strategies.

The anti-inflammatory effect of the ethanol extract of Momordica charantia in two different chemically induced inflammatory bowel disease models, which are frequently used in experimental studies, was investigated. For this purpose, IBD models were created with acetic acid (AA) and 2,4,6 trinitrobenzene sulphonic acid (TNBS) in rats and 300 mg/kg M.charantia extract was given by oral gavage for 10 days. In the animal experiment phase, a total of 42 animals in six groups were arranged so that two different experimental models could be studied simultaneously. Colon tissues were examined at light and electron microscopy levels. In the microscopic examination, areas of inflammation extending to the muscularis externa were observed in the macroscopically severely damaged areas in both IBD model groups, and epithelial damage, mucosal inflammation, and crypt abscess were observed in the macroscopically less damaged areas. Microscopic large intestine damage was significantly reduced in M.charantia administered groups compared to disease models. TNF-α and IL-1β expression, which was determined to be increased in the AA and TNBS groups immunohistochemically, was observed to decrease in the treatment groups. The surface epithelium was evaluated by electron microscopic observations. This study demonstrates the positive effect of M.charantia ethanol extract on colon histopathology in two different IBD models and highlights the importance of considering inflammation-related cell populations in the treatment of this disease.

Corneal injuries are common in human and veterinary ophthalmology. There are many studies which have investigated the treatment of corneal epithelial defects. This study aimed to investigate the effects of Neutral Protamine Hagedorn (NPH) insulin as an ointment for wound healing in experimental corneal defects. First, a superficial keratectomy was performed on 12 rabbits using a corneal trephine. The animals were divided into two groups, Group I (treated, n = 6) and Group II (vehicle control, n = 6). Insulin ointment was applied topically once daily in the treated group, and saline ointment was applied in the same manner in the vehicle control group. Corneal defects were observed and photographed, and changes in wound surface were recorded on days 7, 14, 21, 30, and 60. In both groups, a significant reduction in the wound surface area was noticeable on the 30th day after defect creation. Between the 30th and 60th days, while the changes in the wound surface area in Group II remained limited, the decrease continued rapidly in Group I. At the end of the study, the corneal opacity score observed was lower in Group I than in Group II. In conclusion, we determined that topical NPH insulin may accelerate corneal wound healing after superficial lamellar keratectomy. A new alternative treatment may be developed for treating corneal wounds through continuing studies on this subject.