Effects of thymol on serum biochemical and antioxidant indices in kindled rats

Background and Aims: Kindling is regarded as an experimental model of temporal lobe epilepsy that reflects a process of progressive and persistent intensification of seizure. Experimental and clinical evidence suggest that there is an interrelationship among epileptogenesis, local inflammation and antioxidant activity. In this study, the possible antioxidant and anti-inflammatory effects of thymol was investigated in epileptic rats

Materials and Methods: Kindling was induced by repeated injections of intraperitoneal pentylenetetrazole [PTZ] every other day. Then, the rat hippocampi were isolated, weighed and prepared as a 5% tissue homogenate in ice-cold 0.9% saline solution. Serum malondialdehyde [MDA] and superoxide dismutase [SOD] levels were assessed by thiobarbituric acid reacting substance and nitroblue tetrazolium methods respectively. Hyppocampal tumor necrosis factor alpha [TNF-alpha;] and interleukin-1 beta [IL-1beta;] were evaluated using enzyme-linked immunosorbent assay method

Results: As the study findings revealed, epileptic seizures increase the serum level of MDA, hyppocampal levels of TNF-alpha; as well as IL-1beta; and decrease the SOD activity

Conclusions: thymol exerts anticonvulsant activity through the antioxidant and anti-inflammatory mechanisms

Effects of hydrogen peroxide oxidative stress on the pattern of pro-apoptotic and anti-apoptotic genes expression during PC12 cells differentiation

Background and Aims: in neurodegenerative disorders,oxidative stress mediated by reactive oxygen species is strongly associated with increased neuronal damages which can lead to apoptosis. Pro-apoptotic and anti-apoptotic gene expressions are changed during the cell differentiation that affect cell viability and differentiation. Therefore, this study was conducted to determine the effects of hydrogen peroxideinduced oxidative stress on the apoptotic cell death in the differentiated rat pheochromocytoma [PC12] cells

Materials and Methods: semi-differentiated PC12 cells were treated with 400 microM hydrogen peroxide [H2O2]. Characteristic morphological changes as apoptotic index were evaluated by DAPI staining. MTT assay were applied in order to evaluate the cells survival as well as cell activity.Pro-apoptotic and anti-apoptotic gene expressions were estimated by real time-PCR

Results: the obtained data indicated that PC12 cell survival rate decreased H2O2 treated condition during the differentiation. Moreover, H2O2 was proved to increase apoptotic genes expressions including caspase 6 as well as PIN1 and to decrease antiapoptotic genes including SIRT1 as well as SIRT7

Conclusion: the findings of the present study revealed that H2O2-induced oxidative nstress can retard the differentiation of PC12 cell in the form of neural-like cells through the apoptotic gene expression. On the other hand, although the PIN1 acts as an apoptotic gene, this study illustrated that this gene expression can get increased during the differentiation under oxidative stress conditions

Morphine reduces expression of TRPV1 receptors in the amygdala but not in the hippocampus of male rats

Background: Chronic use of opioids usually results in physical dependence. The underlying mechanisms for this dependence are still being evaluated. Transient receptor potential vanilloid type 1 [TRPV1] are important receptors of pain perception. Their role during opioid dependence has not been studied well. The aim of this study was to evaluate the effect of morphine-dependence on the expression of TRPV1 receptors in the amygdala and CA1 region of the hippocampus

Methods: This study used four groups of rats. Two groups of rats [morphine and morphine+naloxone] received morphine based on the following protocol: 10 mg/kg [twice daily, 3 days] followed by 20, 30, 40 and 50 mg/kg [twice daily], respectively, for 4 consecutive days. Another group received vehicle [1 ml/ kg] instead of morphine given using the same schedule. The morphine+naloxone group of rats additionally received naloxone [5 mg/kg] at the end of the protocol. The control group rats received no injections or intervention. The amygdala and CA1 regions of the morphine, saline-treated and intact animals were isolated and prepared for real-time PCR analysis

Results: Administration of naloxone induced withdrawal signs in morphine-treated animals. The results showed a significant decrease in TRPV1 gene expression in the amygdala [P<0.05] but not the CA1 region of morphine dependent rats

Conclusion: TRPV1 receptors may be involved in morphineinduced dependence

Prolonged oral administration of oleuropein might protect heart against aconitine-induced arrhythmia

In this study, it was surveyed to know whether an oral single dose of oleuropein could mimic the cardiac preconditioning in rats' hearts or whether its prolonged oral administration could protect the heart against the aconitine-induced arrhythmia in rats. Eighty male Wistar rats were divided into two series [n = 8 in each group]. In the first series, all groups [except the control [Con] group] were given a single oral dose of oleuropein [20 mg/Kg] 1, 3, 24 and 48 h before the infusion of aconitine. In the second series, except the Con group, the other four groups were given oral oleuropein [20 mg/Kg/day] for 3, 7, 14 and 28 days, before the infusion of aconitine. Electrocardiogram was recorded to monitor arrhythmia. Data of the first series showed that the initiation time of arrhythmia, the initiation of ventricular tachycardia [VT], the numbers of reversible ventricular fibrillation [VF] and the death time had no significant difference compared with Con group. In the second series, a significant protection was occurred only in the 28 days group that was evident with increased initiation time of arrhythmia, increased initiation time of VT, and increased the number of reversible VF and death time in compared to the Con group. The findings of this study show that the oral administration of a single dose of oleuropein could not mimic the preconditioning effects in rat hearts, but the prolonged administration of oleuropein for about four weeks could protect the heart against aconitine-induced arrhythmia

Effect of morphine withdrawal syndrome on cerebral ischemia outcome in rats

Opioid abuse is still remained a major mental health problem, a criminal legal issue and may cause ischemic brain changes including stroke and brain edema. In the present study, we investigated whether spontaneously withdrawal syndrome might affect stroke outcomes. Addiction was induced by progressive incremental doses of morphine over 7 days. Behavioral signs of withdrawal were observed 24, 48 and 72 hr after morphine deprivation and total withdrawal score was determined. Cerebral ischemia was induced 18-22 hr after the last morphine injection by placing a natural clot into the middle cerebral artery [MCA]. Neurological deficits were evaluated at 2, 24 and 48 hr after ischemia induction, and infarct size and brain edema were determined at 48 hr after stroke. Morphine withdrawal animals showed a significant increase in total withdrawal score and decrease of weight gain during the 72 hr after the last morphine injection. Compared to the addicted and control animals, infarct volume and brain edema were significantly increased in the morphine deprived animals [P< 0.05] at 48 hr after cerebral ischemia. Also, neurological deficits were higher in the morphine-withdrawn rats at 48 hr after stroke [P< 0.05]. Our data indicates that spontaneous withdrawal syndrome may worsen stroke outcomes. Further investigations are necessary to elucidate mechanisms of opiate withdrawal syndrome on stroke

Expression of regulated oncogen-alpha by primary hepatocytes following isolation and heat shock stimulation

High levels of regulated oncogen-alpha [GRO-a] expression have been observed in the liver. GRO-a stimulates proliferation of epithelial cells and induction of rolling and extravascular migration of neutrophils and mononuclear cells. Given the above observations, this chemokine was chosen to be analyzed in freshly isolated and cultured hepatocytes. In this study, hepatocytes [2_106 cell/ml] were isolated from male Sprague Dawley rat liver and cultured on plates that were pre-coated with collagen type-I matrix. The western and northern blot analyses were employed to detect GRO-a at the protein and mRNA levels in freshly isolated and cultured hepatocytes in response to isolation and heat shock stresses. GRO-a was shown to be expressed by isolated rat hepatocytes immediately after isolation and early culture and decreased with time. mRNA was also expressed in freshly isolated cells [0 h] and did not decrease after 48h of culture and further time points [P<0.01]. These results also demonstrated that expression of GRO-a by hepatocytes increased in response to heat shock at different time points in comparison with the control [P<0.01]. These results demonstrated that the isolation and heat shock stresses induced the expression of GRO-a in hepatocytes in a time-dependent manner. Thus, it seems that hepatocytes mimic the experiences that the liver encounters after injury in vivo. In such a situation, liver produces stress related agents like chemokines to overcome injurious conditions