Biotechnic & Histochemistry最新文献

We investigated the effects of β-glucan (βg) on kidney and liver damage caused by cisplatin (CP), an antineoplastic agent widely used to treat many types of cancer, in a rat model. The side effects of CP in many tissues and organs limit its usage. βg is a natural polysaccharide that is an effective free radical scavenger. A total of 28 rats were randomly divided into four groups. Group 1 was a non-intervention control, only feed and water were given. Group 2 was administered 7 mg/kg CP in a single dose. Group 3 was administered 50 mg/kg βg orally for 14 days. Group 4 was administered βg for 14 days, following a single dose of CP. At the end of the experiment, kidney and liver tissues were evaluated biochemically and histopathologically. Increased thiobarbituric acid-reactive substances (TBARS) levels, as well as decreased catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) activities, and reduced glutathione (GSH) levels, as well as histological damage, were noted in both the kidney and liver tissues of the CP group. However, βg treatment prevented the oxidative and histopathological effects of CP. The study demonstrates the protective efficacy of βg against CP-induced kidney and liver damage through the effect of its antioxidant properties.

Three genes are associated with cerebral cavernous malformations (CCMs): CCM1, CCM2 and CCM3. These genes participate in microvascular angiogenesis, cell-to-cell junctions, migration and apoptosis. We evaluated the expression in vivo of CCM genes in primary tumors and metastastases in a murine model of metastatic breast carcinoma. We used cell lines obtained from metastasis of 4T1, 4TLM and 4THM breast cancer to liver and heart. These cells were injected into the mammary ridge of Balb/C female mice. After 27 days, the primary tumors, liver and lung were removed and CCM proteins were assessed using immunohistochemistry and western blot analysis. CCM proteins were expressed in primary tumor tissues of all tumor-injected animals; however, no CCM protein was expressed in metastatic tumor cells that migrated into other tissues. CCM proteins still were observed in the lung and liver tissue cells. Our findings suggest that CCM proteins are present during primary tumor formation, but when these cells develop metastatic potential, they lose CCM protein expression. CCM protein expression was lost or reduced in metastatic tissues compared to the primary tumor, which indicates that CCM proteins might participate in tumorigenesis and metastasis.

Myonectin is a hormone that is produced mainly by skeletal muscle. We investigated the effects of exercise and energy drink (ED) administration on myonectin expression in skeletal muscle, liver and kidney tissue in rats; myonectin is produced by all three tissues. We used 28 male albino rats in four groups: untreated control (C), exercise (E), energy drink (ED) and exercise + energy drink (E + ED). The E and E + ED groups were exercised using a treadmill for 4 weeks. We also administered 3.5 ml/kg/day ED during week 1, 7 ml/kg/day during week 2 and 10 ml/kg/day during weeks 3 and 4 in the E and E + ED groups. We used ELISA to measure the levels of myonectin in skeletal muscle, liver and kidney tissues. We used immunohistochemical staining to investigate the localization and intensity of myonectin in these tissues. The amount of myonectin in skeletal muscle tissue was increased significantly in all experimental groups compared to group C. The amount of myonectin in the ED group was significantly greater than group E. No significant difference was observed in liver tissue; however, the amount of myonectin in the liver of group C was the greatest among all groups. The amount of myonectin in kidney tissue exhibited no significant difference among groups. Consumption of ED during exercise increased the amount of myonectin in kidney and skeletal muscle tissues and decreased it in liver tissue. We suggest that consumption of ED might adapt metabolism to incresed exercise by controling synthesis of myonectin in liver, kidney and skeletal muscle.

Squamous cell carcinoma (SCC) often develops from an underlying premalignant lesion. Factors that affect the progression of actinic keratosis (AK) to invasive SCC are not fully known. Asprosin (ASP) and meteorin-like peptide (METRNL) are adipokines that are involved primarily in glucose metabolism. We investigated the expression of ASP and METRNL in AK and SCC to evaluate the role of these adipokines in the development of SCC. We used 15 SCC specimens, 12 AK specimens and 12 healthy control skin specimens. ASP and METRNL protein expression in tumor and surrounding tissue was evaluated using immunohistochemistry. ASP expression in tumor tissue was significantly greater in the SCC group than in the control and AK groups, but it did not differ significantly between the AK and control groups. A positive correlation was observed for both ASP and METRNL expressions between tumor tissue and adjacent epidermis, hair follicles, sebaceous gland, eccrine gland, inflammatory cells and vascular structures. ASP and METRNL may exert pro-tumor effects toward development of invasive SCC. The expression intensity of ASP and METRNL can be used as a biomarker of risk of progression to SCC.

Oral cancer decreases quality of life despite timely medical management. The carcinogens in tobacco products and their role in tumorigenesis are well documented. Langerhans cells (LCs) are a subset of antigen-presenting cells (APCs) that monitor the tumor microenvironment and engulf carcinogens and foreign bodies. We investigated the distribution and size of LCs and their relation to the mode of tobacco consumption and clinical outcome in patients with buccal carcinoma. We recruited patients with oral cancer who were scheduled for tumor excision and men with urethral stricture undergoing substitution urethroplasty using buccal mucosa. Normal and tumor-adjacent tissues were stained with CD1a antibody. The distribution and mean diameter of 100 LCs/patient were determined. We found significantly smaller LCs in patients who chewed only tobacco compared to those who consumed tobacco by other means. The size of LCs decreased significantly with progressive stages of malignant disease. We found that patients with larger LCs survived longer than those with smaller LCs during an average follow-up of 24 months. We suggest a relation between the size of LCs and clinical outcomes in patients with buccal carcinoma.

Augmentation rhinoplasty sometimes is required for patients with saddle nose deformity caused by failed rhinoplasty or facial trauma; finding appropriate grafting material remains a significant problem for this procedure. We investigated hyaluronic acid matrix as an allograft for dorsal augmentation rhinoplasty in a rabbit model. We performed an osteotomy on the nasal bones of eight rabbits. Four animals were sham operated as the control group and four were administered a mixture of saline-gelled hyaluronic acid matrix and sliced cartilage. Ultrasonography and three-dimensional reconstruction tomography were performed at the end of the experimental period. After sacrifice of the animals, nasal tissues were examined for histopathology, and both collagen scores and number of capillaries were compared between the two groups. Increased collagen and capillaries were apparent in the hyaluronic acid matrix group compared to controls. The median collagen score was significantly greater for the hyaluronic acid matrix group than for the control group. Although the number of capillaries for the hyaluronic acid matrix group was greater than for the control group, the difference was not statistically significant. Three weeks is sufficient for adhesion of ends of fractures in clinical practice; however, we found no ossification at this time in either group. A hyaluronic acid matrix may be a useful alternative supplement for dorsal augmentation rhinoplasty. Development of collagen was commensurate with membranous ossification; however, assessment of complete ossification requires a longer experimental period.

Current conventional therapy for colorectal cancer includes surgery, radiation and chemotherapy, all of which produce side effects. Herbal medicine can control the side effects of conventional treatments. We investigated the synergistic effect of a mixture of Zingiber officinale Roscoe (Ginger) and Ganoderma lucidum extracts on colorectal cancer cell apoptosis in vitro. We prepared ethanolic extracts of ginger (GEE) and G. lucidum (GLEE). Cytotoxicity was evaluated using MTT assay and the half-maximal inhibitory concentration (IC₅₀) of each extract was calculated. The effect of these extracts on apoptosis in cancer cells was assessed using flow cytometry; Bax, Bcl2 and caspase-3 gene expression was evaluated using real-time PCR. GEE and GLEE decreased CT-26 cell viability significantly in a dose-dependent manner; however, the combined application of GEE + GLEE was most effective. Bax:Bcl-2 gene expression ratio, caspase-3 gene expression and the number of apoptotic cells were increased significantly in CT-26 cells treated at the IC₅₀ level of each compound, especially in the GEE + GLEE treatment group. Combined ginger and Ganoderma lucidum extracts exhibited synergistic antiproliferative and apoptotic effects on colorectal cancer cells.

Type 2 diabetes (T2D) and chronic periodontitis (CP) are common diseases worldwide. Although T2D increases the severity of CP and alveolar bone loss, the mechanism of this is not well understood. We investigated using immunohistochemistry the expression of three osteoclast proteins, TRAF6, cFos and NFATc1, in gingival tissues. Gingival tissues were obtained from three groups: HC group, healthy controls; CP group, patients with CP; T2D + CP group, patients with both T2D and CP. Strong immunostaining for TRAF6, cFos and NFATc1 was observed in the gingival epithelium as well as in inflammatory cells in the CP and T2D + CP groups. Immunostaining was most intense in the T2D + CP group. We found strong up-regulation of TRAF6, cFos and NFATC1 in gingiva tissue of subjects with both T2D and CP, which corroborates our hypothesis that T2D potentiates osteoclastogenesis in CP.