ABSTRACT
OBJECTIVE@#To evaluate the effects of Zhumeria majdae essential oil (ZMEO) on morphine dependence and tolerance in mice.@*METHODS@#ZMEO (10, 20, and 40 mg/kg) and clonidine (0.1 mg/kg) as the positive control were injected intraperitoneally (i.p.). The effect of ZMEO and clonidine on the dependence were evaluated by counting the number of jumps induced by naloxone (5 mg/kg) while the tolerance was evaluated by the tail-flick test.@*RESULTS@#ZMEO at the dose of 10 mg/kg during the development period led to a significant inhibition of morphine tolerance (P0.01), and significantly reduced the withdrawal signs (number of jumps) of mice (P>0.01).@*CONCLUSIONS@#ZMEO had significant effects on morphine tolerance and dependence. The linalool rich essential oil of Z. majdae plays a major role in the reduction of tolerance and dependence induced by morphine.
ABSTRACT
OBJECTIVE@#To evaluate the effects of Zhumeria majdae essential oil (ZMEO) on morphine dependence and tolerance in mice.@*METHODS@#ZMEO (10, 20, and 40 mg/kg) and clonidine (0.1 mg/kg) as the positive control were injected intraperitoneally (i.p.). The effect of ZMEO and clonidine on the dependence were evaluated by counting the number of jumps induced by naloxone (5 mg/kg) while the tolerance was evaluated by the tail-flick test.@*RESULTS@#ZMEO at the dose of 10 mg/kg during the development period led to a significant inhibition of morphine tolerance (P0.01), and significantly reduced the withdrawal signs (number of jumps) of mice (P>0.01).@*CONCLUSIONS@#ZMEO had significant effects on morphine tolerance and dependence. The linalool rich essential oil of Z. majdae plays a major role in the reduction of tolerance and dependence induced by morphine.
ABSTRACT
Cerebral ischemia is known as a main cause of morbidity and mortality in the world and there was no effective treatment yet. Global cerebral ischemia causes loss of pyramidal cells of brain cortex following global ischemic/reperfusion. Recently, using immunophilin ligands has been considered as a potential and appropriate strategy for neuroprotection. Since it was observed that tacrolimus [FK506], a useful immunosuppressant used in organ transplantation, provides neuroprotection and prevents neuronal damage,the importance of immunophilins in the development of neuroprotectors has emerged. In this study, we investigated the neurotrophic effect of the immunosuppressant agent FK506 in rat after global cerebral ischemia. In this experimental study, 25 Wistar rats were assigned to control [intact], ischemia and 3 FK506 treated [1, 3, 6 mg/kg] groups. Both common carotid arteries were occluded for 20 minutes followed by reperfusion. In 3 experimental groups, tacrolimus or FK506 was given as a single dose exactly at the time of reperfusion respectively as 1, 3, 6 mg/kg by intravenous administration [IV]. The same doses repeated by intraperitoneally administration [IP] 48 hours after reperfusion. After 4 days, the rats were sacrificed and brain sections were stained by H and E and Nissl. Our findings showed that 20 min ischemia decreased the number of the cortex pyramidal cells. But there were significant differences between number of cortex pyramidal cells in ischemia and FK506 [6mg/kg] groups. Our study suggests that tacrolimus has a neurotrophic effect on pyramidal cells of brain cortex and may candidate for treatment of ischemia brain damage
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The short break in cerebral blood flow causes permanent brain injury and behavioral dysfunction. The hippocampus, specifically the CA1 pyramidal cells, is highly vulnerable to ischemic injuries. There is no effective pharmacological strategy for improving brain tissue damage induced by cerebral ischemia. Previous studies reported that pentoxifylline has a neuroprotective effect on brain trauma and it is well known that endogenous estrogen improves stroke outcome during vascular occlusion. In this study, the possible positive effects of pentoxifylline and estrogen on behavioral deficit and neuronal damage were studied in female Wistar rats in estrous phase subjected to an experimental model of transient global brain ischemia. In this experimental study, female Wistar rats [n= 56] were assigned to control, ischemia, vehicle, and pentoxifylline - treated [200 mg/kg IP] groups and all of them were in their estrous phase. Pentoxifylline was administered at 1 h before and 1 h after ischemia. Global cerebral ischemia was induced by bilateral common carotid artery occlusion, followed by reperfusion.Morris water maze and nissl staining was used for all groups. According to Morris water maze test results, cerebral ischemia could not exert any negative effect on cognitive spatial abilities after reperfusion and there were no significant differences between groups. In Nissl study, there were significant differences between number of pyramidal cells in both control and pentoxifylline - treated groups [P
ABSTRACT
Ecstasy is a psychoactive, hallucinogen drug and a member of amphetamines family and is used commonly worldwide. Ecstasy overdose leads to restlessness, anxiety, hallucination, cardiovascular disorders and liver toxicity. Recently, the use of vasodilators, such as pentoxifylline [PTX], is one of the new strategies for protection against liver lesions caused by some substances such as alcohol consumption. There are few studies about the protective effect of pentoxifylline on liver damages due to MDMA long administration. Therefore, a comprehensive study on the protective effect of pentoxifylline on liver lesions caused by prolonged use of ecstasy seems to be necessary. This experimental study was performed on five groups: control, Ecstasy [7.5 mg/kg], Experimental 1 [100 mg/kg PTX simultaneously with the last dose of Ecstasy], experimental 2 [100 mg/kg PTX a week before Ecstasy injection], and vehicle [normal saline] groups [n=25]. After two weeks, animals were killed and their livers were prepared for histological studies [H and E method] and TUNEL technique for investigating of apoptotic bodies. The apoptotic bodies and hepatocytes lesions in experimental group 1 were lower than the other groupsm except control. It seems that the use of pentoxifylline after consumption of pure ecstasy can decrease tissue damage and prevent the induction of apoptosis in rat liver
Subject(s)
Animals, Laboratory , Rats, Wistar , Pentoxifylline , Pentoxifylline/pharmacology , Apoptosis , Liver , Hepatocytes/drug effectsABSTRACT
Indomethacin increases generation of mitochondrial reactive oxygen species [ROS] which have a crucial role in the indomethacin-induced gastric ulcer. Coenzyme Q10 has an antioxidant activity on mitochondria and cell membranes and protects lipids from oxidation and is essential for stabilizing biological membranes. Superoxide dismutase [SOD] acts as one of the defense mechanisms against free radicals. When the generation of ROS overwhelms, the antioxidant defense, lipid peroxidation of cell membrane occurs and cause cell damage. Male adult Wistar rats were divided into A and B groups. The rats in group A were then further divided into three subgroups of 6 animals each and received one of the following treatments: Animals in the first subgroup received saline. Animals in the second subgroup received saline and indomethacin. Animals in the third subgroup received vitamin C and indomethacin. The rats in group B were also further divided into 3 subgroups of 6 rats each and treated with one of the following treatments: Animals in first subgroup received 1% Tween 80 as vehicle. Animals In second subgroup received 1% Tween 80 and indomethacin. Animals in third subgroup received CoQ10 and indomethacin. Four hours after the last treatment, animals were killed by an overdose of ether and 2 ml blood was drawn from left ventricle into syringe containing EDTA [1mg/ml] and the stomachs removed were cut and gastric mucosal lesions were examined. Ulcer indexes were determined and SOD activity measured in plasma. Pre-treatment with both vitamin C and coenzyme Q10 was associated with attenuation of ulcer index and increased SOD activity comared with animals treated with indomethacine alone [p<0.001]. This effect of CoQ10 may be due to its electron donating property that inhibits the decrease in SOD activity in gastric tissue [replenishment of endogenous SOD] and inhibiting lipid peroxidation
Subject(s)
Male , Animals, Laboratory , Ubiquinone/analogs & derivatives , Ascorbic Acid , Indomethacin , Stomach Ulcer , Rats, Wistar , Superoxide DismutaseABSTRACT
Although there is evidence that diabetes affects seizure susceptibility, the underlying mechanism has not been completely understood. On the other hand, several studies have suggested a pivotal role for K[ATP] channels in the seizure modulation. So, the present study was designed to evaluate the seizure threshold induced by pentylenetetrazole [PTZ] in diabetic mice at different times and to examine the possible role of ATP-sensitive potassium [K[ATP]] channels. In this experimental study, NMRI were diabetic with streptozocine. Then clonic seizure thresholds were determined at different times after induction of diabetes compared with corresponding non-diabetic groups. Each experimental group consisted of ten mice. There was a time-dependent alteration in the threshold in diabetic mice, reaching a peak on week 2 after STZ injection and declining significantly afterwards. The seizure threshold in 8-week diabetic mice was even lower than control levels, though the difference was not significant. The non-effective dose of K[ATP] channel blocker glibenclamide [1 mg/kg, i.p.], but not the voltage-dependent K+ channel blocker 4-aminopyridine [1 mg/kg, i.p.], decreased the seizure threshold in 2-week diabetic mice to the control levels which was blocked by pre-treatment with the K[ATP] channel opener cromakalim [10 micro g/kg, i.p.]. Moreover, the non-effective dose of cromakalim [10 micro g/kg, i.p.] increased significantly the seizure threshold in 8-week diabetic mice which was inhibited by pre-treatment with glibenclamide [1 mg/kg, i.p.] but not with 4-aminopyridine [1 mg/kg, i.p.]. This study indicated that the PTZ-induced seizure threshold is altered in diabetic mice in a time-dependent manner which could be due to the probable alteration in the K[ATP] channel functioning during diabetes