Cengiz Baycu

Protective Effects of Zinc on Testes of Cadmium-Treated Rats

In this microscopic study, the toxic effects of cadmium (Cd) and the protective role of a zinc (Zn) co-treatment were investigated in the testes of the rats treated with Cd. At the dose and duration used, Cd severely damaged the seminiferous tubules and caused the degeneration and disintegration of spermatogenic cells. Leydig cells were also lost after Cd treatment. The present study showed that zinc co-treatment protected testes against toxic effects of cadmium.

Protective effects of silymarin against acetaminophen-induced hepatotoxicity and nephrotoxicity in mice

This study was designed to estimate protective effects of silymarin on acetaminophen (N-acetyl-p-aminophenol, paracetamol; APAP)-induced hepatotoxicity and nephrotoxicity in mice. Treatment of mice with overdose of APAP resulted in the elevation of aspartate aminotransferase (AST), alanine transaminase (ALT), blood urea nitrogen (BUN), and serum creatinine (SCr) levels in serum, liver, and kidney nitric oxide (NO) levels and significant histological changes including decreased body weight, swelling of hepatocytes, cell infiltration, dilatation and congestion, necrosis and apoptosis in liver, and dilatation of Bowman’s capsular space and glomerular capillaries, pale-stained tubules epithelium, cell infiltration, and apoptosis in kidney. Posttreatment with silymarin 1 h after APAP injectionfor 7 days, however, significantly normalized the body weight, histological damage, serum ALT, AST, BUN, SCr, and tissue NO levels. Our observation suggested that silymarin ameliorated the toxic effects of APAP-induced hepatotoxicity and nephrotoxicity in mice. The protective role of silymarin against APAP-induced damages might result from its antioxidative and anti-inflammatory effects.

Interleukin-10 Gene Transfer: Prevention of Multiple Organ Injury in a Murine Cecal Ligation and Puncture Model of Sepsis

IntroductionThe aim of this study was to determine the effect of immunoregulatory cytokine interleukin-10 (IL-10) gene therapy on multiple organ injury (MOI) induced by a cecal ligation and puncture (CLP) model of sepsis in mice.MethodsMale Balb/c mice subjected to CLP were treated with either an hIL-10-carrying vector or an empty control vector. We assessed the degree of lung, liver, and kidney tissue destruction biochemically by measuring myeloperoxidase (MPO) and malondialdehyde (MDA) activity. Histologic assessments were based on neutrophil infiltration in lung and liver tissue. IL-10 protein expression was examined immunohistochemically, and ultrastructural changes in the liver were studied by transmission electron microscopy. We analyzed the expression of tumor necrosis factor-α (TNFα) mRNA by reverse transcription polymerase chain reaction 3, 8, and 24 hours after CLP in all organs.ResultsOrgan damage was significantly reduced by hIL-10 gene transfer, which was associated at the tissue level with reduced MPO activity in the liver, lung, and kidney and decreased leukocyte sequestration and MDA formation in the lung. The liver MDA was not significantly higher in the hIL-10 gene therapy group than in the controls and seemed not to be affected by hIL-10 gene transfer. The reduced portal tract neutrophilic infiltration and preserved ultrastructure of the hepatocytes also showed that tissue function was not impaired. The lung and kidney TNFα mRNA expression was suppressed markedly in the hIL-10 gene therapy group, but liver TNFα mRNA expression varied over time.ConclusionsThese findings showed that IL-10 gene therapy significantly attenuated sepsis-induced MOI.

Effects of rolling inhibition on smoke inhalation injury

Inhalation of chemical and particulate products of smoke is one of the principal determinant of mortality following burn injury. Inflammatory responses have been implicated in the pathogenesis of lung injury after smoke inhalation. In the current study, we tested the inhibitory effect of Fucoidin on the neutrophil rolling stage of inflammatory response and determined the degree of pulmonary injury. Fifteen rats were divided into three groups: sham group (N: 5) of rats inhaled room air; control group (N: 5) inhaled smoke, and experimental group inhaled smoke and received Fucoidin. All the rats were sacrificed 24h after smoke inhalation. The trachea and lungs were removed totally; samples for histopathological and biochemical (myeloperoxidase (MPO)) analysis were taken from each lung and trachea. Morphologic studies using light and electron microscopes showed a decrease in lung parenchymal and tracheoepithelial injury in the experiment group of rats. Also, biochemical analysis of tissue MPO was significantly lower in test group than in control group. These results suggest that the inhibition of neutrophil rolling leads to a reduction of neutrophil invasion to pulmonary parenchyma and trachea, which may be beneficial for attenuating neutrophil mediated inhalation injury.

Resveratrol reduces IL-6 and VEGF secretion from co-cultured A549 lung cancer cells and adipose-derived mesenchymal stem cells

Stem cell therapies are important treatment methodologies used in many areas of experimental or clinical medicine. In recent studies of cancer models, Mesenchymal stem cells (MSCs) suppressed the growth of cancer cells. However, also in some studies, stem cell treatments have been shown to induce cancer formation, increase tumor volume, induce the formation of new vessels, and lead to cancer invasion. The presence of MSC-secreted cytokines and their effects on cancer cells limits the reliability of MSC-based treatments. Resveratrol (trans-3,5,4′-trihydroxystilbene), an antioxidant found in red wine, has been shown to have therapeutic effects against several cancers. The aim of this study was to co-culture MSCs with A549 cancer cells to suppress the release of cancer-promoting cytokines from MSCs and to increase the applicability and reliability of stem cell therapies with resveratrol. MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) and neutral red cell viability assays were used to find safety dose of resveratrol. The MSCs secreted the cytokines IL-6 and VEGF, and the effect of resveratrol on these cytokines was analyzed by ELISA and western blot analysis of conditioned medium. One μM of resveratrol was found to be the safety dose for the A549 cancer cells and MSCs. We observed the highest release of IL-6 and VEGF from the co-cultured A549 cells and MSCs, and resveratrol was found to significantly decrease the release of these cytokines. Our study suggests that resveratrol exerts a positive effect on the release of cytokines. The safety dose of resveratrol can be administered together with stem cells during stem cell treatment.

Effects of nonsteroidal anti-inflammatory meloxicam on stomach, kidney, and liver of rats

Nonsteroidal anti-inflammatory (NSAI) drugs are the most commonly used group of drugs today. Increase in the use of standard NSAI for treating pain and inflammation was restricted by the fact that these drugs were proven to possibly cause gastrointestinal and renal toxicity. Meloxicam is a NSAI that has anti-inflammatory, analgesic, and antipyretic effects. This study aims to investigate the effects of meloxicam on stomach, kidney, and liver of rats under light microscopy level. Based on the light microscopic observations, mononuclear cell infiltration and pseudolobular formation was established in liver samples of animals in the experimental group. Metaplasia in surface and glandular epithelia and atrophy were observed in stomach samples. Glomerular stasis-related hypertrophy and focal interstitial nephritis were found in kidneys. It was concluded in this study that meloxicam might cause hepatotoxicity, nephrotoxicity, and gastric metaplasia in rats at a used dose and duration.

Neuroprotective Effect of Genistein In Peripheral Nerve Injury.

AIM To investigate the effects of genistein in a rat model of sciatic nerve crush injury and complete sciatic nerve transection. The effects of genistein were compared with those of gabapentin, which is widely used in clinical practice for peripheral nerve injury. MATERIAL AND METHODS Forty-eight rats were randomly divided into six groups (8 rats in each group): group 1 (sham); group 2, sciatic nerve crush injury (control); group 3, sciatic nerve crush injury+genistein 20 mg/kg; group 4, sciatic nerve crush injury+gabapentin 90 mg/kg; group 5, sciatic nerve transection+genistein 20 mg/kg; group 6, sciatic nerve transection+gabapentin 90 mg/kg. The effects of genistein and gabapentin were assessed with immunohistochemical staining for growth associated protein-43 (GAP-43) and myelin basic protein (MBP). Interleukin-1β and tumor necrosis factor α levels in the injured nerve specimens were assessed as a measure of inflammatory response; walking track analysis and sciatic function index for neurological recovery and the paw mechanical withdrawal threshold were examined for neuropathic pain. RESULTS On histopathological examination, genistein use was associated with a greater immunoreactivity for GAP-43 and MBP compared with that associated with gabapentin. Genistein and gabapentin had similar effects on anti-inflammatory activity, functional recovery, and neuropathic pain. CONCLUSION Genistein and gabapentin exhibit positive effects on histopathology, inflammation, and clinical findings of peripheral nerve injury. When the systemic side effects of gabapentin are considered, genistein (a basic soy isoflavone that has no side effects) can be used as an alternative to medical treatment in peripheral nerve injury.

Comparison of the effects and mechanism of the Curcumin with different acting drugs in Experimental Vasospasm after Subarachnoid Hemorrhage.

AIM Cerebral vasospasm following subarachnoid hemorrhage (SAH) is the most important complication that effects the mortality and morbidity of patients with intracranial aneurysm. Today, the mechanisms of vasospasm are not understood in spite of experimental and clinical researches. The aim of our study was to investigate the effects of curcumin on vasospasm following SAH. MATERIAL AND METHODS In this study, 64 rats (200-250 g weight) were divided into 7 groups. Group 1: having no treatment after SAH; Group 2: treatment with nimodipine after SAH; Group 3: treatment with nicorandil after SAH; Group 4: treatment with sildenafil citrate after SAH; Group 5: treatment with 150 mg/kg curcumin after SAH; Group 6: treatment with 300 mg/kg curcumin after SAH, Group 7: treatment with 600 mg/kg curcumin after SAH. The experimental SAH was induced by injection of autologous blood into the cisterna magna. After medical treatment, in the first hour, blood was taken for quantified the levels of TNF-α, IL-1β and IL-6. Then, cerebrum and cerebellum were removed for analysis. Basilar artery luminal diameter was measured and apoptotic cell count was performed with tissue samples. RESULTS Histopathological findings showed that, in sufficient dose, curcumin dilated the basilar artery beside anti-oxidant effect. CONCLUSION Curcumin can be used for the treatment of vasospasm as a new medical drug.

A missense mutation in the M1S1 gene found in a turkish patient with gelatinous droplike corneal dystrophy.

Purpose: To report a missense mutation in the M1S1 gene found in a Turkish patient with gelatinous droplike corneal dystrophy (GDLD). Methods: A Turkish patient with GDLD was examined. Keratoplasty was performed and a diagnosis of GDLD was made by histopathologic and electron microscopic studies. Genomic DNA was extracted from peripheral blood and the paraffin-embedded tissue of the corneal button. A 248-bp DNA fragment of the M1S1 gene was amplified, and sequencing reactions were analyzed. The results were compared with those of 30 healthy, nonrelated individuals. Results: On light microscopic examination, sheets of amorphous amyloid deposits were observed in subepithelial regions and in the anterior and midcorneal stroma. Electron microscopy revealed dense collagen fibrils and entrapped filamentous amyloid fibrils in the corneal stroma. A substitution of T→C at nucleotide 557 was found in the peripheral blood DNA sequence analysis, which resulted in an amino acid substitution of L→P (L186P). Results were confirmed by direct DNA sequencing analysis of the paraffin-embedded corneal button. The patient with GDLD was homozygous for the mutation, resulting in amino acid substitution L186P. Conclusions: This is the first report, to our knowledge, of a homozygous mutation (L186P) in the M1S1 gene found in a Turkish patient. The clinical examination may be insufficient in sporadic cases, and histopathologic examination and molecular genetic analysis can accelerate and improve the accuracy of diagnosis in patients with GDLD.