Caffeine has dose-dependent effects on mood, attention, and physiology. Behavioral effects of caffeine in humans have also been well documented. This article aimed to study the effect of different caffeine concentrations on behavior and motor activity of mice. The experiments was carried out using 24 male mice (25-30gm). Plus maze was used for screening of antianxiety effect of caffeine. While swimming maze was used to test antidepressant effect. Statistical analysis were performed using computer program SPSS (version 22). At dose of 100 mg/kg, caffeine acted as anxiolytic compound. Caffeine increased motor activity at dose of 25mg/kg and decreased motor activity at dose of 200mg/kg. At dose of 100mg/kg, caffeine acted as antidepressant. In conclusion, caffeine can act as stimulant, while in over dose it acts as depressant. Caffeine showed to have anxiolytic effect in certain doses. arabic 14 English 91
Sakina Salem Mohammed Saadawi, ٍSuhera Mehemed Abdulsalam Aburawi, SUMAYA ESEDEEG ABDALLAH BAAIO(4-2018)

Abstract Benzodiazepines are frequently prescribed as anxiolytics, sedatives hypnotics, and muscle relaxants as well as anticonvulsants. Non-steroidal anti-inflammatory drugs (NSAIDs) are also the most widely used for their anti-inflammatory, analgesic and antipyretic activities. Because of the chronic nature of epilepsy, NSAIDs may be used with benzodiazepines in patients with epilepsy. Therefore, there’s a probability of an interaction of NSAIDs and benzodiazepines in clinical practice. In order to study such interactions experimentally, an animal model was used. Thus, this thesis was aimed to explore pharmacological interactions between selective and non selective NSAIDs and diazepam anticonvulsant effect. Convulsion was induced in male albino mice by picrotoxin in two different doses (6 and 8 mg/kg), NSAIDs were used according to selectivity to cyclooxygenase enzyme (COX): Aspirin at 10 mg/kg (COX-1 selective inhibitor) and Aspirin at 100 and 200 mg/kg, diclofenac 10 and 20 mg/kg (non selective COX inhibitors) and celecoxib 20 mg/kg (COX-2 selective inhibitor). Diazepam at 1 and 2 mg/kg were chosen as low doses and parameters of convulsive behavior of picrotoxin deviation. psy, NSAIDs may be used with benzodiazepines in patients with epilepsy. Therefore, there’s a probability of an interaction of NSAIDs and benzodiazepines in clinical practice. In order to study such interactions experimentally, an animal model was used. Thus, this thesis was aimed to explore pharmacological interactions between selective and non selective NSAIDs and diazepam anticonvulsant effect. Convulsion was induced in male albino mice by picrotoxin in two different doses (6 and 8 mg/kg), NSAIDs were used according to selectivity to cyclooxygenase enzyme (COX): Aspirin at 10 mg/kg (COX-1 selective inhibitor) and Aspirin at 100 and 200 mg/kg, diclofenac 10 and 20 mg/kg (non selective COX inhibitors) and celecoxib 20 mg/kg (COX-2 selective inhibitor). Diazepam at 1 and 2 mg/kg were chosen as low doses and parameters of convulsive behavior of picrotoxin were observed in this thesis: onset time, episode frequency and death occurrence within post-injection of picrotoxin for 24 hrs. Aspirin in low dose (10 mg/kg) showed protection against death to about 50%. This protection which seems to be partially effective as anticonvulsant agent, however, higher dose of Aspirin (100 mg/kg) did not produce any significant change against convulsing in mice, Aspirin 200 mg/kg showed highly significant reduction of episode frequency (P < 0.001) and decreased percent of death. Furthermore, Aspirin 200 mg/kg in combination with diazepam has potentiated the effect of diazepam to complete protection against convulsion induced by picrotoxin. With respect to diclofenac, diclofenac pretreated-mice did not show any significant effect at 10 and 20 mg/kg with picrotoxin but in combination with diazepam showed significant potentiated effect of diazepam. Moreover, COX-2 inhibitor (celecoxib) alone delayed onset of convulsion without significant influence against the control but significantly decreased episodes and percent of death. Also in combination of celecoxib and diazepam, a highly potentiation of the effect and almost complete protection against convulsion behavior were noted (P < 0.001). Thus, it can be concluded that the studied NSAIDs have anticonvulsant behavior-like activity alone and in combination with diazepam. The most profound effect of anticonvulsant activity was showed in low episodes and mortality rate. In combination with diazepam, NSAIDs have more positive potential role in diazepam anticonvulsant effect. The present findings may also suggest that NSAIDs most likely COX-2 selective inhibitor is more potentiated diazepam’s anticonvulsant activity than COX-1 selective and non-selective inhibitors and such interaction could be more likely to be pharmacodynmic type.
نجمية محمد الزواوي (2014)

Paracetamol is one of the most widely used drug as antipyretic and analgesic for mild to moderate pain. Currently, paracetamol is the first-line choice for pain management and antipyresis. Ion channels are pore-forming proteins that allow the flow of ions across membranes and involved in many cellular processes; drugs acting on ion channels have long been used for the treatment of many diseases. Objective: To estimate the effect of voltage gated ion channel blockers on analgesic activity of Paracetamol and explore the interaction between ion channel blockers and paracetamol on pain behaviour. Materials and Methods: Male albino mice were used. The central antinociceptive activity was determined by hot plate test and formalin test (Phase I; neuropathic pain). Antiinflammatory activity was determined by formalin test (Phase II). Intraperitoneal injection was adopted. Five groups of mice were used. Group 1; control group (1% T80), group 2; treated with (200mg/kg) paracetamol, group 3; treated with different drugs of ion channel blockers, group 4; received standard drugs, Aspirin (200mg/kg) for formalin test (phase II) or tramadol (5mg/kg) for hot plate test and formalin test (phase I), group 5; received combined treatment of ion channel blockers and paracetamol. Results: Pain produced by noxious stimuli (heat and formalin) was significantly reduced by acute administration of paracetamol. Inflammation pain produced by formalin injection was significantly decreased by acute administration of paracetamol. Acute administration of nifedipine showed significant decrease in nociception and inflammation pain. Combined treatment of nifedipine and paracetamol produced antinociceptive and anti-inflammatory activity but less than the additive effect. Verapamil has no analgesic effect in the two models, and did not change the affect of paracetamol analgesic activity when administered together. Phenytoin produces significant decrease in nociceptive pain using hot plate but not in formalin test (Phase I), and produce significant decrease in inflammatory pain (Phase II). The combined treatment of phenytoin and paracetamol showed analgesic activity less than the additive effect. 4-Aminopyridine produces significant antinociceptive and anti-inflammatory activity. The combined administration of 4-aminopyridine and paracetamol showed analgesic activity, which is less than the additive effect using formalin test, while paracetamol analgesic activity is potentiated by 4-aminopyridine using hot plate test. Conclusion: Paracetamol has antinociception and anti-inflammatory activity on pain model used (Hot plate test and Formalin test). Ion channel blockers produce antinociception and anti-inflammatory activity. Verapamil has no effect on nociception or inflammation pain and no effect on paracetamol analgesic activity. Nifedipine, phenytoin and 4-aminopyridine interact with paracetamol producing less additive analgesic effect, except 4-aminopyridine in thermal stimuli (Hot plate) is more sensitive compared to chemical stimuli (formalin test – phase I), where potentiates paracetamol action.
هناء مدحت الزقلعي (2014)