Use of caffeic acid phenethyl ester and cortisone may prevent proliferative vitreoretinopathy.

PURPOSE: To investigate whether caffeic acid phenethyl ester (CAPE) and cortisone prevent proliferative vitreoretinopathy (PVR). METHODS: Twenty pigmented rabbits were used in this study. All rabbits except controls received an intravitreal injection of 0.15 ml (75,000 U) of platelet-rich plasma into their left eye. The animals were divided into four groups: group I was treated with intraperitoneal injection of 0.5 ml (15 micromol/kg) of CAPE for 3 days, group II received 0.15 ml (4 mg/kg) of intravitreal cortisone, group III received nothing (blank group), and group IV (control group) received only 1 ml of 1% ethanol intraperitoneally daily for 3 days. Proliferative changes were graded in a masked fashion by indirect ophthalmoscopy for a 15-day follow-up period. The malondialdehyde (MDA), reduced glutathione (GSH) and total nitrite (NO) levels were measured in the vitreous humor. RESULTS: The grades of PVR were B-C in group I, and C-D in group II. The PVR grade in the control group was C-D. The mean MDA level in group I (4.0+/-0.8 micromol/l) was significantly lower than in the blank group (6.0 micromol/l) (p < 0.05). The mean GSH level in group I (71.0+/-11.2 micromol/l) was significantly different than in the blank group (p < 0.05). The MDA and GSH levels in group II were 4.7+/-0.6 micromol/l and 53.8+/-7.8 micromol/l, respectively. Both these levels were not significantly different from the blank group (p > 0.05). The NO levels in both treatment groups were significantly lower than in the blank group (p < 0.001). CONCLUSION: These findings suggest an inhibitory effect of CAPE on PVR. The inhibitory effect was supported by lower MDA and NO with higher GSH levels in treatment groups than in the blank group. There was no detected significant effect of cortisone for preventing PVR experimentally

ASSOCIATION OF BDNF / TRKB AND NGF / TRKA LEVELS IN POSTMORTEM BRAIN WITH MAJOR DEPRESSION AND SUICIDE

Background: Suicide Attempts are the main complications of Major Depressive Episodes and are difficult to predict. There is still a lack of knowledge about its neurochemical aspects. There is increasing evidence that Brain-derived neurotrophic factor (BDNF) and Nerve growth factor (NGF) play a role in the pathophysiology and treatment of depression by binding and activating cognate receptors Tyrosine Kinase B (TrkB) and Tyrosie Kinase A (TrkA), respectively. This study was conducted to examine whether BDNF and / or TrkB as well as NGF and / or TrkA expression profiles were changed in the hippocampus of postmortem brain of individuals with depression who committed suicide. Subjects and methods: This study was conducted with the brain tissue of 61 victims who died as a result of suicide due to depression and 25 people who died due to traffic accidents. The psychiatric history of the cases was determined by the psychological autopsy method. Samples were taken from the hippocampus region of the brain at the forensic medicine institution. After storage under appropriate conditions, protein and mRNA levels of BDNF, TrkB, NGF and TrkA were determined in the genetics laboratory. Results: Average age of the suicide group was 30 and the average age of the control group was 24.5. The suicide group consisted of 70.5% male and 29.5% female cases. There was no significant difference between the groups in terms of age (p=0.062) and gender (p=0.718). BDNF, NGF, TrkA and TrkB values were found to be lower in the suicide group compared to the control group and there was a significant difference between the groups (p=<0.001; p=0.001; p=0.001; p=0.011). Conclusion: Given the importance of BDNF and NGF and their cognate receptors in mediating physiological functions, including cell survival and synaptic plasticity, our findings regarding decreased expression of BDNF, TrkB, NGF and TrkA in both protein and mRNA levels of postmortem brains of suicide victims suggests that it may play an important role in the pathophysiological aspects of its behavior. Further studies in this context may be useful both in understanding the molecular basis of suicide and in designing therapeutic models targeting these molecular pathways

The Effect of Apocynin on Motor and Cognitive Functions in Experimental Alzheimer’s disease.

Scope: We investigated the potential beneficial effect of Apocynin (APO) on motor and cognitive functions in experimental Alzheimer’s disease (AD). Materials and Methods: Experimental AD was induced in rats by intraventricular streptozotocin (STZ) injection. Sham group received artificial cerebrospinal fluid (CSF). Both groups were randomly divided into two subgroups. One of the subgroups received intraperitoneal APO for while the other had normal saline (NS). The animals were evaluated with rotarod, accelerod and Water-Maze tests before and after the treatment. Additionally, biochemical markers of oxidative stress such as malondialdehyde (MDA) and reduced glutathione (GSH) were analyzed from brain specimens. Standard histological evaluation and transmission electron microscopy (TEM) were used to evaluate the neural damage. Results: The difference between STZ+NS in comparison with CSF+NS, CSF+APO and STZ+APO were statistically significant on 30 and 40 rpm on rotarod test. GSH levels, accelerod and Water-Maze test results were not statistically significant between subgroups. However, MDA differences between STZ+NS in comparison with CSF+NS, CSF+APO and STZ+APO were statistically significant. Hemotoxilene eozine staining and TEM results showed apocynins protective effect. Conclusion: These results indicate that APO can provide neuro-protective effect for motor but not for cognitive performance in experimental AD.   Keywords: Alzheimer’s disease, Streptozotocin, Apocynin, Rotarod test, Accelerod test, Water-Maze test</p

Caveolin-1 gene expression in rats model of chronic renal failure

In this study, gene expression profile of caveoline and the kidney MDA levels and serum BUN and creatinine levels were investigated in experimentally induced renal failure case of rats. In the experimental group, rats were injected with 30 mg/kg of cyclosporin A via subcutaneous route for 28 days. In the control group, rats were injected with cremophor EL, vehicle for cyclosporin A, for 28 days. Caveolin gene analysis and MDA analysis in the kidney tissue as well as serum BUN and creatinine analysis were performed at the end of the experiment. Caveolin gene expression of experimental group was significantly reduced (P &lt; 0.05), while the MDA level was significantly increased compared to those of control (P &lt; 0.05). Serum BUN and creatinine levels were significantly increased in the experimental group compared to the control group (P &lt; 0.05). In the Cyclosporin A induced chronic renal failure model, we suggest that the induction of the Cav-1 gene expression may prevent the renal tissue damage. [Med-Science 2017; 6(3.000): 401-5

Effect of caffeic acid phenethyl ester (CAPE) on vascular endothelial growth factor a (VEGF-A) gene expression in gentamicin-induced acute renal nephrotoxicity

Vascular endothelial growth factor-A (VEGF-A) gene expression in an experimental gentamicin-induced nephrotoxicity and ameliorative effect of caffeic acid phenethyl ester (CAPE) was investigated in rats. Animals were divided into four groups (n=8); control (C) group animals were given 10% dimethylsulfoxide (DMSO); gentamicin (G) group animals were given 100 mg/kg/day gentamicin; CAPE group animals were given 30 mg/kg/day CAPE and CAPE+G group animals were given 100 mg/kg/day gentamicin plus 30 mg/kg/day CAPE. Serum creatinine and BUN levels significantly increased in gentamicin group as compared to the control group (p0.05). Gene expression level of VEGF-A in gentamicin group significantly decreased as compared to the control group, however, CAPE treatment did not have any increasing effect on the gene expression level. According to histopathological investigation, gentamicin treatment caused prominent degeneration in kidney tissue and CAPE treatment had only slight beneficial effect on lowering the tissue degeneration. The results showed that gentamicin decreases VEGF-A gene expression and this might be related to the tissue degeneration at cellular level. However, CAPE treatment did not have significant ameliorative effect in lowering the gentamicin induced nephrotoxicity. [Med-Science 2018; 7(4.000): 805-9

The Gene Expression of Antioxidant Enzymes in Streptozotocin-Induced Experimental Diabetes in Rat Liver Tissue

In this study, Wistar rats were experimentally induced diabetes and the gene expression profile of CuZn-SOD and CAT enzymes were investigated in the liver tissue of these rats. The rats were divided into two groups as control and the experimental diabetes group (DM). In group DM, as a single dose of 50 mg/kg streptozotocin (STZ) dissolved in 0.01 M citrate buffer (pH: 4.5) was given intraperitoneally to the rats. 0.01 M citrate buffer which is the vehicle for STZ was applied to the rats in control group. 72 hours after STZ treatment, blood samples were collected from the tail vein, and the blood sugar levels were measured. Rats with fasting blood sugar levels above 350 mg/dl were considered to be diabetic. The rats were decapitated 21 days after STZ treatment. The liver tissues were collected, and the gene expression profile of CuZn-SOD and CAT in the liver was measured using real-time PCR technique. In conclusion, it was found that a significant decrease was observed in the expression of CuZn-SOD and CAT genes in DM group when they were compared to that of control group. [Med-Science 2015; 4(4.000): 2834-48

Three-dimensional Spinal Deformity: Scoliosis [Uc Boyutlu Omurga Deformitesi: Skolyoz]

In human body, average of 33 separate vertebrae of the spinal column is sorted and connected to each other in a row. The primary task of this column is to support the head, chest and abdominal organs and form a stable and strong sheath to the spinal canal where the medulla spinal passes through. Spinal column of a new born baby is straight, but after the baby starts to hold his head, cervical lordosis is formed. After the baby starts to sit and stands up, thoracic kyphosis, lumbar lordosis and sacral kyphosis develops. Although, normal physiological curves of spine is normal, deviations from the front or rear view is considered pathological. Scoliosis is characterized as lateral deviation, the reduction in sagittal slope and axial rotation. Scoliosis can also be defined as the deviation of the normal vertical line, deviating more than 10 degrees, as seen in X-ray. All treatment methods used in the treatment of scoliosis aims to perform physically normal, balanced, painless and a stable backbone. Although, the treatment of Scolyosis is performed in several different ways, further studies are still being conducted. [Med-Science 2015; 4(1.000): 1796-808

The effects of lack of melatonin in experimental rat model of Alzheimers Disease: relationship with FEZ1 gene expression

Alzheimers Disease (AD), which is the most common reason for dementia, is an irreversible neurodegenerative brain disease. FEZ1 is a protein expressed in the brain. High expressions of FEZ1 mRNA have been interpreted as an indicator of high neural plasticity for memory and learning. This study was planned to determine the effect of melatonin deficiency (pinealectomy; PnX) on AD and to reveal its association with FEZ1. 30 male rats were used in the study. The rats were divided into three as SHAM, PnX+streptozotocin (STZ) and PnX+STZ+melatonin (MLT) groups. The pineal glands of rats were surgically removed (except SHAM group) and STZ was intracerebroventricularly (icv) administrated at the first and third days. MLT (10 mg/kg/day) was intraperitoneally (ip) injected 1 hour before the first STZ application and it was continued for 14 days. STZ and MLT solvents were applied to the rats in the SHAM group. At the end of the applications, Morris water maze (MWM) test was carried out the rats. At the end of MWM tests, the rats were sacrificed and their blood and hippocampus tissues were taken. FEZ1 gene expression and protein levels were determined from hippocampus tissue, while serum nonadrenaline, dopamine and serotonin levels were detected from blood samples. FEZ1 protein levels of PnX+STZ+MLT group were found to be statistically significantly lower than those of SHAM and PnX+STZ groups (p [Med-Science 2017; 6(2.000): 217-23

Resveratrol ameliorates cisplatin-induced oxidative injury in New Zealand rabbits

This study investigated the preventive role of resveratrol in cisplatin-induced nephrotoxicity. The study used groups of New Zealand rabbits that were treated as follows: group C (cisplatin treated), group R (resveratrol treated), group R+C (resveratrol + cisplatin treatment), and group E (control group). Kidney levels of glutathione were significantly lower in group C than in groups E and R, whereas glutathione levels in group R+C were found to be similar to the control values. Malondialdehyde levels in group C were significantly higher than in groups E and R. However, malondialdehyde levels in group R+C were similar to group E. Kidney levels of nitric oxide were significantly higher in the cisplatin group than in the control, whereas nitric oxide levels were at basal values in group R+C. Cisplatin treatment significantly reduced kidney levels of glutathione peroxidase, superoxide dismutase, and catalase activity compared with those of group E, whereas resveratrol treatment significantly increased levels of glutathione peroxidase, superoxide dismutase, and catalase activity in group R+C. However, cisplatin injection did not affect mRNA levels of glutathione peroxidase, superoxide dismutase, or catalase enzymes. Histopathological and immunohistochemical analyses indicated that cisplatin caused kidney damage, which was mostly prevented by resveratrol treatment. In conclusion, resveratrol ameliorates cisplatin-induced oxidative injury in the kidney of rabbit