Tympanometric changes in an experimental myringosclerosis model after myringotomy

Hypothesis: The goal of this experimental study was to investigate the specific effect of myringosclerosis on tympanograms in the tympanic membranes of myringotomized rats by using otomicroscopy, tympanometry, and histopathology

Esterified hyaluronic acid improves cartilage viability in experimental tracheal reconstruction with an auricular graft

PubMed: 21109076Objective The aim of this study was to determine the efficacy of esterified hyaluronic acid (HYAFF) on the vitality of auricular cartilage grafts used for tracheoplasty, with respect to macroscopic and microscopic parameters. Study Design Prospective, controlled. Setting Academic research laboratory. Subjects and Methods The study included 14 New Zealand rabbits acquired specifically for the study. The rabbits were divided into two groups: the control group, in which free cartilage grafts were not exposed to any materials or additional procedures (n = 7), and the hyaluronic acid (HA) treatment group, in which auricular grafts and anastomosis lines were covered with HYAFF (n = 7). Free auricular cartilage grafts used for the reconstruction of experimentally created tracheal defects were anastomosed extraluminally. All the rabbits were sacrificed two months post surgery. Samples were collected and examined histopathologically. The sections were stained with hematoxylin-eosin, Masson's trichrome, and inducible nitric oxide synthase (iNOS) and examined under a light microscope. Results Fibrosis and cartilage mass significantly differed between the control and HYAFF group (P < 0.05). Immunohistochemical examination showed that more chondrocytes stained with iNOS in the control group than in the HYAFF group, according to histologists' observations. Conclusion HYAFF catalyzed wound healing with less fibrous tissue formation, had chondroprotective and stimulatory effects on chondrocyte metabolism, and decreased nitric oxide production and apoptosis via improving the nourishment of free auricular cartilage grafts, subsequently preventing hypoxia and oxidative stress, particularly in the early postimplantation period. © 2010 American Academy of OtolaryngologyHead and Neck Surgery Foundation. All rights reserved

Protective effect of melatonin against maternal deprivation-induced acute hippocampal damage in infant rats

It is known that maternal deprivation induces hippocampal damage in the developing brains. In the present study, we examined the effects of melatonin on maternal deprivation-induced hippocampal damage both during and after stress-hyporesponsive period (SHRP). Hippocampal damage was examined by cresyl violet staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. The results showed that a single episode of maternal deprivation for 24 It at post-SHRP induced neuronal loss in hippocampus regions of the brain in the infant rats, while it did not influence hippocampal neurons in SHRP. Melatonin prevented maternal deprivation-induced hippocampal damage in the infant rats at post-SHRP. These results suggest that melatonin is a potentially beneficial agent to improve the neurobehavioral outcomes of maternal deprivation in later developmental period. (C) 2006 Elsevier Ireland Ltd. All rights reserved

Effect of melatonin on testicular damage in streptozotocin-induced diabetes rats

Background: It is well known that diabetes mellitus is associated with impairment of testicular function. In the present study, we aimed to demonstrate the effect of melatonin on testicular damage in male rats with streptozotocin (STZ)-induced diabetes. Methods: Male Wistar rats were divided into 4 groups: (1) control group, (2) melatonin-treated nondiabetic group, (3) diabetic group and (4) melatonin-treated diabetic group. Diabetes was induced by STZ injection. Melatonin was administered intraperitoneally at the dose of 10 mg/kg for 5 days. Testicular damage was examined by using hematoxylin and eosin staining and periodic acid-Schiff staining, and apoptosis was determined by terminal-deoxynucleotidyl-transferase-mediated dUTP nick end labeling (TUNEL). Potential disorders associated with seminiferous tubular sperm formation were evaluated using the Johnsen score. Results: Diabetic rats showed a reduction in seminiferous tubule diameter, increased thickening of the basement membrane in seminiferous tubules and degenerated germ cells. TUNEL-positive cells were significantly more numerous in diabetic rats than in control rats. Melatonin significantly attenuated the diabetes-induced morphological changes and germ cell apoptosis in the diabetic rat testis. The number of polymorphonuclear leukocytes was signifi cantly decreased in group 4 when compared to group 3. Conclusions: These results suggest that intraperitoneal administration of melatonin for 5 days is a potentially beneficial agent to reduce testicular damage in adult diabetic rats, probably by decreasing oxidative stress. Copyright (C) 2008 S. Karger AG, Basel

Methamphetamine induces oligodendroglial cell death in vitro

We investigated whether the psychostimulant methamphetamine (METH) has a cytotoxic effect on oligodendrocytes and which cell-death pathways are involved in the cytotoxic process. METH caused concentration- and time-dependent cytotoxicity in rat oligodendrocyte cultures. METH induced apoptotic cell death and mRNA expression of pro-apoptotic proteins (bax and DP5), but not anti-apoptotic proteins (bcl-2 and bcl-XL). These results suggest that METH induces cytotoxicity in rat oligodendrocytes via the differential regulation of the expression of genes involved in the apoptotic process. (C) 2003 Elsevier B.V. All rights reserved

Age-related changes in apoptosis in rat hippocampus induced by oxidative stress

Also known as programmed cell death, apoptosis is a sequence of events that leads to elimination of cells without releasing harmful substances into the surrounding area. Apoptosis may be induced by intracellular or extracellular signals. Certain apoptotic signals activate mitochondrial proapoptotic events and increase reactive oxygen species (ROS). Increased ROS production may lead to oxidative stress. The goal of our study was to characterize age-related changes in apoptosis induced by oxidative stress in the hippocampus. Rats 2, 7, 21 and 38 days old, and adult rats were used for our study. Hippocampal CA1, CA2, CA3 and dentate gyrus apoptosis, and hippocampal superoxide dismutase (SOD), glutathione peroxidase (GPx) enzyme activities and thiobarbituric acid reactive substances (TBARS) levels were measured. We found that numbers of hippocampal neurons were low in rats 2, 7 and 21 days old (CA1, p < 0.001; CA3, p < 0.05; gyrus dentatus, p < 0.001). The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) positive cell count was highest in the CA1 and dentate gyrus of 21-day-old rats. Among 21-day-old rats, the hippocampal TBARS levels and SOD enzyme activity were high, whereas GPx activity was low. These results demonstrate that the hippocampal CA1 and dentate gyrus of 21-day-old rats are more prone to damage by oxidative stress