PHARMACEUTICAL SCIENCES
Year:2010 | Volume:16 | Issue:3|Papers Count:10

Objectives: The term of aggression with different meaning applied to wide range of integrative behaviors. Two main classes of aggressive behavior include defensive and offensive. The defensive behavior is tactics for protection of vulnerable parts of body but offensive behaviors is defense against intruders. In the natural state defensive animals can flee from the territory but in restrained condition such as laboratory animals, they show flight, crouching, up right defensive posture. The VTA (Ventral Tegmental Area) with dominant dopaminergic neurons is widely implicated in psychotic disorders. Bupropion as an antidepressant agent is used for smoke cessation widely under FDA approval. The clinical data have showed that it can induce aggressive behavior as side effect. Despite clinical evidence, the mechanism of Bupropion on aggression is not known well.Methods: Rats defensive aggression were registered online and offline in control, sham and 3 doses of bupropion. Intra VTA injection was carried out by standard stereotaxic surgery.Results: Aggressive behaviors were only affected by 0.25 mg of bupropion and there were no significant difference between other groups.Conclusion: These data showed that bupropion have complex effect on aggression behavior. Bupropion can inhibit reuptake of dopamine and have effect on VTA neuronal activity for modulation of aggression.

Objectives: Curcuma longa possesses anti-inflammatory effects and inhibits growth of cancer cells. Principle compound of Curcuma longa is curcumin which could interferes with biological pathways. Telomerase is a ribonucleoprotein complex which prevents telomeres from shortening during cell division. In the most cancers, including breast cancer, expression and activity of this enzyme increases to compensate for chromosomes shortening and could be an attractive target of cancer therapy. Therefore, we aimed to study inhibitory effect of curcuma longa total extract on MCF-7 breast cancer cell line for evaluation of its possible anti-telomerase effect in these cells.Methods: MCF-7 cells were cultured, IC50 of extract was determined by MTT assay test and then, cells were treated with serial dilutions of extract. Finally, we used TRAP assay to determine inhibition level of telomerase in treated and control cells.Results: IC50 was determined as 0.057mg/ml. Percentage of relative telomerase activity (expression) (%RTA) was decreased with increasing of Curcuma longa n-hexane extract.Conclusion: Considering inhibitory effect of Curcuma longa total extract on telomerase in the breast cancer cells, it is possible to use it for developing novel breast cancer therapeutics in the future.

Objective: Previous studies have indicated that memory retrieval is impaired under high levels of glucocorticoids as seem in severe stress. In this study, we investigated the effect of peripheral injection of Metyrapone (an inhibitor of glucocorticoid synthesis) on memory retrieval and reconsolidation in rats.Methods: I this experimental study 80 Wistar rats (200-220 gr) were trained (1 mA, 3s) in a passive avoidance task. Retention test was done 48hr after training. Metyrapone (25, 50 and 100 mg/kg) or vehicle was injection IP 90 min before of retention test. Memory retention of each animal was measured as latency takes to enter the dark chamber of the task. Also immediately after reactivation, rats were injected with Metyrapone (100 mg/kg) Cycloheximide (2.8 mg/kg as a protein synthesis inhibitor and sham group) and reconsolidation assessed 2, 9, 11 days after memory reactivation, that rats were returned to the context for 10 min, and step-through latency was recorded.Results: The results showed that administration of Metyrapone at doses of 25 and 100mg significantly impaired memory retrieval as compared with control group. No significant effect was found with intermediate dose of Metyrapone (50 mg/kg). Also Metyrapone 100 mg/kg impaired memory reconsolidation.Conclusion: These findings provide evidence that inhibition of glucocorticoid synthesis by Metyrapone impair memory retrieval in a U shape manner and impair reconsolidation in high doses.

Objectives: Ornithogalum cuspidatum is one of the medicinal plants that has been used in Iranian traditional medicine as treatment for respiratory and inflammatory diseaes. Previous studies on other Ornithogalum species showed that thay have anti-cancer and cytotoxic activities. However, the exact mechanism has not yet been determind. In present study, the growth inhibitory and apoptotic effects of methanolic extract of Ornithogalum cuspidatum (MEOC) on WEHI-164 fibrosarcoma cell line, a type of soft tissue cancer, were evaluated.Methods: MTT assay was used for measuring the cytotoxicity and cell viability at 6, 12 and 24 hours and in different concentrations of MEOC. Also, ELISA was used to measure apoptosis after 12 hours in different concentrations of MEOC.Results: The results showed that MECO had growth inhibitory and cytotoxic activities on WEHI-164 cell line, in three mentioned times. The MECO changed morphology of WEHI-164 cell lines in to apoptotic cells.Conclusion: Increasing extract concentration and time caused decreased in cell viability. MEOC caused induction of apoptosis in WEHI-164 cell line. In general, these effects depends on the concentration of MEOC (P<0.01).

Objectives: Ascorbate which is presented in high concentration in nervous system, inhibit nitric oxide synthase enzyme (NOS). We investigated the involvement of NO pathway in the analgesic effects of ascorbic acid (AA) in CCI model of neuropathic rats.Methods: In this experimental study, neuropathic pain is induced by 4 loose ligature around sciatic nerve on left paw of male rats using 4.0 chromic gut (CCI model). Ascorbic acid (1, 5 or 10 mg/kg) or saline was injected intraperituneally two weeks after CCI. Heat and mechanical hyperalgesia and mechanical allodynia were investigated 15 and 30 min after injection. To investigate the involvement of NO on antinociceptive effect of AA on the second week after CCI, 30 min after injection of saline or AA, animals received intraperitunealy injection of L-arginin (500 mg/kg), or L-NAME (20mg/kg) and were tested 20 min after on.Results: Acute injection of 5 and 10 mg/kg but not 1 mg/kg of AA increased pain threshold in the second week after CCI. Injection of 5 mg/kg AA inhibited the nociceptive effect of L-arginin and potentiates the antinociceptive effect of L-NAME and pain threshold was significantly different in these two groups comparing the animals which received normal saline instead of AA.Conclusion: Injection of AA increase pain threshold after nerve injury. Antinociceptive effect of ascorbic acid is dose dependant and that seems to be mediated at least partially via NO pathway.

Objectives: Lindane is organochlorine compound which is widely used in agriculture and medicine for treatment of pediculosis (as shampoo) and scabies (as lotion). Sometimes Lindane is absorbed through inhalation and leads to intoxication. The purpose of this investigation is studying of the protective effects of N-Acetyl Cysteine (NAC) on cellular damage that caused by lindane in Tracheal and pulmonary cells of Rats.Methods: The first 250mg/kg NAC (or its solvent) and then 40mg/kg Lindane (or its solvent) were intraperitoneally given. After 24 hours the animal were killed by Ether and The Lung and Tracheal tissues were fixed in 10% formalin. After preparation of microscopic segments, H&E (Hematoxylin & Eosin) staining for histopathologic studies and AB (Alcian Blue) and PAS (Periodic Acid Schiff) staining for cytochemistry cells were used.Results: The results indicated that the tissue of lung and pneumocyte cells was intact in control group. Different cellular damages including swell of cells, formation of Vacuole, reduction of staining ability in the type II pneumocytes, thickening of Alveolar walls and injury in ciliated and nonciliated cells. Lindane caused changes of epithelium from pseudostratified to simple. Cytochemically, in control group, the epithelial tissue of trachea, neutral (PAS+) and acidic (AB+) glycoprotein secreting cells were observed. In all cases intensity of damages was dose dependent.Conclusion: The results indicated that Lindane cause cellular damage in the Respiratory system cells. The mechanism of this toxic effects is unknown, but reported that Lindane is converted into intermediate substance by the action of hepatic microsomal enzymes, and this new substance can deplete the glutathione of hepatic cells and as a resulst cause cellular damage. NAC with increasing the amount of glutathione will reduced Lindane-induced damage.

Objective: Nicotine is one the chemical substance by high level of toxically which can rapidly absorbed from the lungs of smokers. It crosses the placenta and accumulates in the developing fetus. Our previous investigation indicated that collagen type IV appearance has a key role in basement membrane of various embryonic organs. We evaluated the effect of maternal nicotine exposure pre and postnatal period on collagen IV expression during bronchogenesis and alveolarization in the lung of mouse newborns.Methods: Pregnant Balb/C mice, were divided into 2 experimental and 2 control groups. Experimental group 1, received 3 mg/kg nicotine intrapritoneally from day 5 of gestation to last day of pregnancy. Experimental group 2 were received the same amount of nicotine during the same gestational days as well as 2 first week after birth (lactation). The control groups received the same volume of normal saline during the same periods. At the end of exposure times, all of newborns were anesthetized and their lungs were removed and immunohistochemical study for tracing collagen were carried out.Results: Our finding indicated that collagen reaction in the bronchial basement membrane (BBM) and extra cellular matrix (ECM) of lung parenchyma in experimental groups increased significantly in compared to control groups. Our finding showed that an alveolar remodeling and abnormal bronchogenesis in experimental group especially group 2 were observed.Conclusion: These data indicate that maternal nicotine exposure may induces an abnormal collagen IV expression and cause a defect in bronchopulmonary development.