The Protective Effect of N-Acetylcysteine Amide Against Paraquat-Induced Neurotoxicity

N-acetylcysteine amide (NACA) is a new antioxidant molecule with powerful radical scavenging properties. The aim of this study was to investigate neuroprotective effects of NACA against paraquat (PQ) toxicity in the midbrains of rats by using motor coordination tests and biochemical and histological analysis. Thirty adult Wistar albino rats were divided into three groups: Group 1: control (n = 10), Group 2: PQ (10 mg/kg) (n = 10), and Group 3: PQ (10 mg/kg) + NACA (100 mg/kg) (n = 10). NACA was administrated intraperitoneally 30 min before PQ injection. Performance was measured for a period of 28 days. The rotarod and accelerod tests were performed prior to and after the experimental period. After the experimental period, rats were sacrificed and midbrain tissues were removed. According to biochemical data, malondialdehyde levels exhibited a significant increase (P \u3c 0.05) when the PQ group was compared to the control group, whereas the NACA-treated group showed a significant decline (P \u3c 0.05). The total glutathione levels (P \u3c 0.01) and the glutathione peroxidase and butyrylcholinesterase activities (P \u3c 0.05) in the NACA treatment group were significantly raised compared with the PQ group. The main finding in the rotarod and accelerod tests was that the PQ+NACA group had improved motor coordination functions, whereas the PQ group had lost motor coordination (P \u3c 0.05). Our histological data were also outstanding and were consistent with biochemical and motor coordination results in terms of the protective role of NACA against PQ-induced neurotoxicity

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

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

The Antioxidant Effect of Melatonin on Myocardial Ischemia Reperfusion Injury in Experimental Studies

A lot of mechanisms play major role in the myocardial ischemia reperfusion injury (MI/R), especially reactive oxygen species (ROS) which they formed rapidly when molecular oxygen enters into the cell. Melatonin, major hormone of the pineal gland, is very strong antioxidant and free radical scavenger effects. Besides, melatonin plays an important role in the regulation of various body functions including circadien sleep rhythms, blood pressure, oncogenesis, retinal function, and immunity. It can be possible to say that oxidative stress occurs during MI/R and melatonin administration exerts an infarct size limiting effect, antiapoptic, antiarryhtmic effects , enhances antioxidant activity of the heart. [Med-Science 2014; 3(4.000): 1766-80

Pathophysiology of Myocardial Ischemia Reperfusion Injury: A Review

Cardiovascular events are one of the leading causes of death in the world. Thrombolysis, percutaneous transluminal coronary angioplasty, and coronary bypass surgery are the general treatment strategies of cardiovascular events. All of these treatment strategies can cause a myocardial ischemia reperfusion (MI/R) injury, which is known to occur on the restoration of coronary blood flow after a period of myocardial infarction (MI). Although there is an only way to save the myocardium from necrotic and apoptotic damages, reperfusion achieved by the restoration of blood flow often aggravates cardiac dysfunction. It is believed that MI/R injury is related to the increased reactive oxygen species (ROS), calcium overloading, and the loss of membrane phospholipids especially during the reperfusion. The harmful effects of ROS on cardiac tissue during the MI/R can be prevented by endogenous antioxidant systems. Also, the complement system plays a crucial role in the inflammatory events of ischemic injury; thereupon it is important in the pathogenesis of the MI/R injury. Polymorphonuclear leukocytes in the reperfusion period are also associated with MI/R injury. Therefore these circumstances can increase the irreversible tissue damage. Although sometimes the reperfusion is provided, blood flow cannot be supplied to the myocardial tissue. This is called a no-reflow phenomenon. A lot of exogenous antioxidant agents can be used to prevent this process of injury. Due to these properties of antioxidants, a number of studies have been carried out and have been reported anywhere in the world. These studies demonstrated that these agents can be used in the MI/R-induced tissue damage and protect the heart against ROS-related myocardial injury. [Med-Science 2013; 2(4.000): 935-54

Myocardial necrosis markers in myocardial ischemia reperfusion (MI/R) injury: a review

Myocardial ischemia/reperfusion injury is one of the main causes of morbidity and mortality in the world. This injury is experienced by patients suffering from cardiovascular diseases such as coronary heart diseases and subsequently undergoing reperfusion treatments in order to manage the conditions. Ischemia can be especially detrimental to the heart due to its high energy demand. Several cellular alterations have been observed upon the onset of ischemia. The danger created by cardiac ischemia is somewhat paradoxical in that a return of blood to the tissue, termed reperfusion, can result in further damage. The serum markers of myocardial injury are used to help in establishing the diagnosis of myocardial infarction. Use of various biochemical markers, including lactate dehydrogenase (LDH), creatine kinase (CK) total enzyme activity, CK-MB activity, Myoglobin, CK-MB mass, cardiac troponin I (cTnI), and cardiac troponin T (cTnT) have been investigated for noninvasive assessment of reperfusion. It is hoped that further studies will help refine the clinical use of new biomarkers like hs-cTn immunoassays in myocardial injury. [Med-Science 2017; 6(1.000): 163-71

Investigation of the protective and treatment effects of vinpocetine in myocardial infarctional with isoprotenol in rats

As aim of this study, the knowledge of whether vinpocetine (VINPO) is cardioprotective or not following isoprotenol (ISO) induced cardiac ischemia in rats. In myocard infarction, the one of the responsible mechanisms of injury is oxidative damage and inflammmation. The effect of Vinpo which is the potent antioxidant and anti inflammatory agent aimed to reveal as the biochemical, electrophysiological, and histopathologic parameters. In this study, thirty- two Wistar-Albino male rats (in the estimated weight of 250-400gm.) were divided into four groups, each consisting of eight rats. The group 1 named as sham, no any drug used in this group. Group 2 named as iso group, only isoprotenol was adminestered, the group 3 named as vinpo and iso group, here initially vinpocetine then isopretenol were used, and the group 4 named as iso and vinpo, here initially isoprotenol then vinpocetine were used. For the rats in group 2, in first and second day isoprotenol adminestered at a dose of 120mg/kg using an intraperitoneal injection. At third and fourth day no any drug used. And at fifth day the experiment terminated. For the rats in group 3, at the first and second day Vinponcetine adminestered at adose of 20 mg/kg using an intraperitoneal injection, after 30 minute isoprotenol administered at adose of 120mg/kg using an intraperitoneal injection. At third and fourth day no any drug was used. And at fifth day experiment was terminated. Lastly for the rats in group4, first and second day isoprotenol administered at adose of 120mg/kg using an intraperitoneal injection, at third and fourth day vinpocetine adminestered at adose of 20 mg/kg using an intraperitoneal injection, and at fifth day experiment terminated. Prior to termination of experiment the pulse rate and ECG changes were recorded. After completion of experiment protocols blood samples and cardiac tissue samples were recieved. For the knowledge of effects of vinpocetine experimental miyocardial ischemia induced in rats, and the serum myoglobulin, total creatine kinase (CK), lactate dehydrogenase (LDH), aspartate aminotransferase (AST), alanin aminotransferase (ALT), measured. In myocardial tissue as an antioxidative system and an oxidative stres markers; malonylaldehate (MDA), Superoxidedismutase (SOD), Catalase (CAT), Glutathionperoxidase (GPx), GSH, Total oxidant status (TOS),Total antioxidant status(TAS),Oxidative stres index (OSI) studied. As a result, Vinpocetin showed positive impact on cardiac functions. With all of these for the best clear results, advanced studies are needed. [Med-Science 2017; 6(4.000): 629-634

Chronic melatonin treatment reverses disruption of prepulse inhibition in pinealectomized and pinealectomized-plus-ovariectomized rats.

Although melatonin has been implicated in several neurophysiological systems, data on the relationship of melatonin with psychosis such as schizophrenia are limited and contradictory. Chronic effects of melatonin on sensorimotor gating deficits have also not been investigated yet. We investigated the neurobehavioral effects of chronic administration of melatonin in pinealectomized (Px) and ovariectomized (Ovx) rats. Px or Ovx or both operations were carried out together to the rats. The control group of rats was sham operated. A sham ovariectomy was carried out to Px rats, and vice versa. Fifth month later, melatonin (5 mg/kg) or vehicle was injected to rats for 28 days. Then, prepulse inhibition (PPI) of acoustic startle reflex, startle amplitude and startle reflex latency was measured. Locomotor activity, accelerod performance measurements, novel object recognition and passive avoidance tests were also evaluated. Px and Px + Ovx rats had impaired PPI compared to control rats. Melatonin reversed the impairments of PPI induced by Px or Px + Ovx. While melatonin treatment had no effect on locomotor activity of control rats, it significantly increased the locomotor activity of Px and Px + Ovx rats. Melatonin treatment (5 mg/kg/day, 28 days) reversed the locomotor hyperactivity caused by Ovx. Accelerod performance, passive avoidance, and object recognition responses of Px, Ovx or Px + Ovx rats were not different from the control group. Our results indicate that chronic melatonin deficiency by reason of Px results in impairment of PPI reflex and replacement of melatonin exerts beneficial effects on the impaired PPI reflex in Px and Ovx rats. Thus, melatonin may be useful in the treatment of some disorders characterized by sensorimotor gating deficits such as schizophrenia

Atorvastatin exerts anti-nociceptive activity and decreases serum levels of high-sensitivity C-reactive protein and tumor necrosis factor-alpha in a rat endometriosis model

Parlakpinar, Hakan/0000-0001-9497-3468WOS: 000343651400028PubMed: 24913463Purpose The purpose of this study was to examine the effects of atorvastatin in the treatment of experimental endometriosis. Methods Endometriosis was induced in 24 female rats. 4 weeks after the procedure dimensions of the foci were recorded. Rats were divided into three groups: in Group 1 (n = 8), a daily dose of 10 mg/kg atorvastatin was given for 14 days. In the second group (n = 8), a single dose of 1 mg/kg leuprolide acetate was injected intraperitoneally. The rats in Group 3 (n = 8) were received 1 mg/kg i.p. 0.9 % NaCl. At the end of the treatment, laparotomy was performed, and the dimensions of the endometriotic foci were recorded. Biochemical, histopathological and immunohistochemical studies were performed and nociception was compared in groups. Results Atorvastatin treatment exhibited significant analgesic activity in hot plate model (P = 0.022). The serum hs-CRP and tumor necrosis TNF-alpha levels were similar between the Group 2 and Group 3 (P > 0.05); however atorvastatin caused significant decrease in both serum markers. The histological and immunohistochemical scores were also found to be markedly lower in Group 1 and Group 2 (P < 0.05). Conclusion Atorvastatin treatment may have a therapeutic potential in the treatment of endometriosis through its anti-inflammatory and anti-nociceptive properties