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1.
Surg Neurol Int ; 3: 74, 2012.
Article in English | MEDLINE | ID: mdl-22937475

ABSTRACT

BACKGROUND: Ischemia/reperfusion (I/R) causes the production of toxic free radicals and leads to pathological changes in nerve tissue. We investigated the effect of alpha-melanocyte stimulating hormone (α-MSH) in a rat model for sciatic nerve I/R and discuss the possible cytoprotective and antioxidant mechanism of α-MSH against ischemic fiber degeneration. METHODS: Experiments were performed using 42 adult male Wistar rats. Rats were divided into six experimental groups: control group, ischemia group, I/R groups, and α-MSH treated groups. Ischemia was produced by clamping of the femoral vessels. Immediately after ischemia that lasted 3 h, 75 µg/kg of α-MSH was administered subcutaneously before reperfusion and the tissue malondialdehyde (MDA) level was evaluated as an indicator of lipid peroxidation in groups with different reperfusion periods. RESULTS: The reperfusion injury did not begin in the first hour of reperfusion after 3 h of ischemia, and MDA levels increased on the first day of reperfusion. During the first day, blood MDA levels were decreased in the α-MSH group compared to the control group. The tissue from animals pre-treated with α-MSH showed fewer morphological alterations. Myelin breakdown was significantly diminished after treatment with α-MSH, and the ultrastructural features of axons showed remarkable improvement. Two-way analysis of variance was used for comparing three or more groups. When a significant difference existed, the post-hoc multiple-comparison test was applied to demonstrate the differences. CONCLUSIONS: The results confirm that pre-treatment with α-MSH after ischemia protected the peripheral nerves against I/R injury.

2.
Ophthalmic Res ; 44(2): 119-24, 2010.
Article in English | MEDLINE | ID: mdl-20523103

ABSTRACT

PURPOSE: To develop a new experimental ocular allergy animal model induced by beta-lactoglobulin (BLG), a major cow's milk allergen, and to discuss the clinical, histopathological and immunohistochemical findings. METHODS: Forty Balb/c mice were randomized and separated into groups of 10. Groups were determined according to the different concentrations of BLG drops used. Study groups were immunized with 2.5, 5 or 10 mg/ml topical BLG (groups 2, 3 and 4, respectively) following intraperitoneal injection for the systemic immunization. The control group (group 1) was immunized with aluminium hydroxide (alum) alone within the same intervals. After ocular challenge, all the animals were evaluated clinically, histopathologically (mast cell and eosinophil infiltration) and immunhistochemically in terms of both T helper type 1- (IFNgamma, TNFalpha) and T helper type 2- (IL-3, IL-4, IL-5, IL-10) specific cytokines. RESULTS: Both clinical and immunohistochemical findings showed that an allergic conjunctivitis was induced in all study groups, with an optimized dosage of topical 5 mg/ml BLG. The conjunctivitis was associated with both Th1 and Th2 response, with a slight predominance of Th1 reaction. CONCLUSION: We describe a new murine model of acute allergic conjunctivitis induced by BLG. We believe that this new preliminary model has the immune parameters of the late phase of acute allergic conjunctivitis and it provides an alternative means for studying the pathogenesis and future treatments of ocular allergy. Our results should be enhanced with more detailed cellular and humoral parameters.


Subject(s)
Conjunctivitis, Allergic/etiology , Disease Models, Animal , Lactoglobulins/adverse effects , Milk Hypersensitivity/etiology , Acute Disease , Animals , Conjunctivitis, Allergic/immunology , Conjunctivitis, Allergic/pathology , Eosinophils/immunology , Female , Immunohistochemistry , Interferon-gamma/metabolism , Interleukins/metabolism , Mast Cells/immunology , Mice , Mice, Inbred BALB C , Milk Hypersensitivity/immunology , Milk Hypersensitivity/pathology , Th1 Cells/immunology , Th2 Cells/immunology , Tumor Necrosis Factor-alpha/metabolism
3.
Maturitas ; 60(3-4): 248-52, 2008.
Article in English | MEDLINE | ID: mdl-18774243

ABSTRACT

OBJECTIVES: The aim of the study was to investigate the effect of testosterone alone and testosterone+estradiol therapy on bladder functions and smooth muscle/collagen content in surgically menopause induced rat model. METHODS: The study included 34 female Sprague-Dawley rats, and the rats were divided into four groups. After bilateral oophorectomy, during a 60 days period, six rats received IM saline injection for one time, as a control group, and nine rats received testosterone undecanoate 100mg/kg IM for one time, and nine rats received testosterone undecanoate 100mg/kg IM for one time + daily 0.50mg nasal spray of 17beta estradiol. Ten rats were taken as sham group. Urodynamic studies were performed in all groups before and after the study. The rats were sacrificed after 60 days, and cystometric findings and smooth muscle/collagen ratio of the bladders were compared between the groups. RESULTS: Increase in maximal bladder capacity and compliance were significantly higher in the testosterone treatment group and testosterone + estradiol treatment group than in the control group (p = 0.01 and p = 0.002, respectively for bladder capacity; p = 0.04 and p = 0.005, respectively for bladder compliance). Smooth muscle/collagen ratio of the bladders was significantly higher in the testosterone and testosterone + estradiol treatment groups than in the control group (p = 0.04 and p = 0.008, respectively). CONCLUSIONS: This study shows that bladder functions may deteriorate in postmenopausal period. In addition to estrogen replacement therapy, testosterone has a significant role to increase bladder smooth muscle, leading to improvement in bladder functions in postmenopausal women with urogenital system dysfunction.


Subject(s)
Estradiol/pharmacology , Estrogen Replacement Therapy , Testosterone/analogs & derivatives , Urinary Bladder/drug effects , Animals , Collagen/drug effects , Disease Models, Animal , Female , Muscle, Smooth/drug effects , Ovariectomy , Rats , Rats, Sprague-Dawley , Testosterone/pharmacology , Urinary Bladder/pathology , Urinary Bladder/physiopathology , Urinary Bladder, Overactive/prevention & control , Urodynamics/drug effects
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