Objectives: The present work was designed to studythe role of endocannabinoid system in the obesity associated atherogenesis and trying to clarify its possible mechanism/s of action. Methods: Thirty adult male wistar albino rats were utilized in the present experiment. They were divided into three equal groups (10 rats each); Group 1: Lean control group, which were fed normal laboratory chow diet and gavaged once daily by dimethyl sulfoxide in a dose of 0.6ml/kg /day for 10 weeks. Group 2: Atherogenic diet group which were fed high fat diet and gavaged once daily by dimethyl sulfoxide as group 1. Group 3: Atherogenic diet treated group which were fed high fat diet and gavaged once daily by NIDA-41020 (a selective cannabinoid receptor 1 blocker) in a dose of 10mg/ kg /day for 10 weeks. Then body mass index (BMI), bleeding time, and total clotting time were assessed. After that, the animals were sacrificed and lipid profile, atherogenic index, bleeding time, platelet aggregation percentage, clot retractions, clotting time, prothrombin time (PT), activated partial thromboplastin time (aPTT), total & differential leukocytic counts and serum adiponectin levels were assessed in all groups. The aorta was obtained from each animal dissected and stained by haematoxylin/eosin and oil Red O staining for histological examination and detection of aortic thickness and foam cells deposition. Results: The laboratory investigations and histological examination revealed, significant increases in BMI, lipid profile, atherogenic index, platelet aggregation%, peripheral monocytic count, and aortic thickness in the high fat diet received group versus lean controls which were otherwise associated with significant decreases in total clotting time, PT, aPTT, serum HDL & adiponectin levels. These changes were significantly and profoundly inhibited by the administration of the cannabinoid receptor antagonist. Conclusion: The endocannabinoid system is involved in the atherogenic changes associated with obesity. These effects were attributed to interference with serum adiponectin level, dyslipidemia, hypercoagulability, increased platelet activation & peripheral as well as endothelial recruitment of monocytes. These effects were found to be via activation of cannabinoid 1 receptor.
The motor function of GIT can be modulated by prokinetics or myorelaxant drugs depending on the nature of the disorder. There is a frequent need for facilitation of gastric emptying in treatment of functional dyspepsia. Among prokinetic drugs used there are compounds belonging to cholinergic and adrenolytic classes. In addition, drugs having affinity for serotonin, motilin and opioid receptors, also participate in alleviating delayed gastric emptying. Itopride is a prokinetic that acts via blocking D 2 receptors in addition to inhibition of choline esterase. Metoclopramide prokinetic effect on the other hand is mediated through D 2 receptor blockade. This study was designed to investigate the effect of the two prokinetic drugs (itopride and metoclopramide) on the motility of different parts of GIT. The results of the present work demonstrated that both itopride and metoclopramide produced significant increments in the amplitude of contraction of fundus stomach of rats, pylorus, jejunum and colon of rabbit in a concentrationdependent manner, It was also proved that itopride is more potent as a prokinetic on these parts of GIT which is evident by the low ED50 of itopride compared to that of metoclopramide. In conclusion, itopride is preferred as a prokinetic than metoclopramide because it has higher potency in addition to acceleration of upper and lower GIT motility.
Background: Ivabradine, Hyperpolarization activated cyclic nucleotide gated (HCN) channel blocker, is the most specific blocker of central nervous system Ih current. Valporate is one of the most commonly used antiepileptic drugs. Objectives: investigate the possible anticonvulsant effect of Ivabradine and its interaction with valporate in pentylenetetrazole (PTZ) induced-kindling in mice. Materials& Methods: mice were divided into four groups, "Group 1", "vehicletreated group" "Group 2", "PTZ kindling Control group "Group 3: Ivabradine ", group 4 Valproate (VPA) group 5" Ivabradine and VPA. Kindling was produced by repeated intraperitoneally (i.p). administration of PTZ (40mg/kg), every other day for 9 doses. Both drugs were administered i.p., 30 minutes before each PTZ injection. Seizure score, latency were recorded. Their brains were removed for assessment of oxidant/antioxidant status and anti-inflammatory cascades. Results: Ivabradine and VPA individually significantly decreased seizure score and co administration of both drugs significantly decreased seizure score less than either vaporate or Ivabradine. Both drugs significantly increased latency to seizures. Ivabradine, VPA and their combined administration significantly elevated brain level of GSH, catalase and significantly decreased levels of nitrite, MDA, IL1β, and TNFα as compared to PTZ control group. Co-administration of both drugs resulted in a significant elevation in the brain level of GSH, catalase concomitant with a significant reduction in the brain levels of MDA, IL1β and TNFα as compared to either VPA or ivabradine groups. Conclusion: Ivabradine has anticonvulsant effect and potentiates the effect of VPA which may be attributes to HCN channel blockade, antioxidant and anti-inflammatory effects.
Background: Pain is an unpleasant sensation experienced when tissues are damaged. Therapeutic management of pain requires consideration of many factors due multiplicity of etiopathogenesis. Objectives: The present study was designed to assess and compare the analgesic effects of gabapentin, diclofenac and tizanidine as well as their combinations in acute and chronic pain. Methods: 128 rats were randomly allocated into two main equal categories; one for acute inflammatory and other for chronic neuropathic pain study. The acute category was divided into 8 equal groups; control, carrageenan, diclofenac, gabapentin, tizanidine, gabapentin-diclofenac, gabapentintizanidine and tizanidine-diclofenac groups. Acute inflammatory pain was induced by carrageenan injection in the animals paw. In the chronic category neuropathic pain was induced by right sciatic nerve ligation except for control and sham groups. This category was divided into; control, sham, gabapentin, tizanidine, gabapentin-diclofenac, gabapentin-tizanidine and tizanidinediclofenac groups. The mean reaction time was assessed in all groups. Results: In acute pain the three drugs and their combinations had significant analgesic effects. Tizanidine potentiated the analgesic effects of diclofenac and gabapentin. In chronic neuropathic pain diclofenac and gabapentin had significant analgesic action while, tizanidine had no analgesic effect. Conclusion: Tizanidine didn't show analgesic effect on chronic pain but potentiated the analgesic effect of gabapentin and diclofenac in acute pain model.
Despite extensive vaccinations attempts, genotype VII Newcastle disease viruses (NDV) continue to circulate at the Middle East and Asia causing significant economic losses. In this investigation, we assessed the effectiveness of three inactivated NDV vaccines; genotype II NDV, recombinant genotype VII NDV-matched and laboratory prepared autogenous velogenic NDV genotype VII against challenge by genotype VII velogenic NDV. The following vaccinations were given: group 1(G1) received an inactivated genotype II vaccine, group 2 (G2) received an inactivated recombinant genotype VII NDV-matched vaccine, and group3 (G3) received a velogenic inactivated autogenous NDV genotype VII vaccine. While the live genotype II (Lasota) vaccine was administered to all groups. At the age of 28 days, birds in all vaccination groups were challenged with NDV genotype VII, and protection against infection was assessed based on the mortality number, clinical symptoms, Post mortem lesions, virus shedding, and histological changes. The results of clinical protection were78%, 87% and 96% in vaccinated groups G1, G2 and G3 respectively, against 7 % in the control non-vaccinated challenged group. Virus shedding in all vaccinated groups significantly reduced when compared to the nonvaccinated group (G4). The mean lesion score on 4 and 7 days post challenge were significantly reduced in G3 and G2 compared to G1.In conclusion, more protection against challenge was offered by a velogenic inactivated autogenous NDV genotype VII vaccine that was closely related to genotype VII.1.1 strain than by other vaccines. So we recommended the use of genotype matched vaccine to control NDV in endemic countries.
Genotype VII Newcastle disease viruses (NDV) are still circulating in Egypt despite extensive vaccination programs. In our study, we evaluate the protective efficacy of commercial (HVT-ND) vector vaccine against velogenicNDV GenotypeVII.1.1challengein broiler chickens. Five vaccination strategies were established; G1 vaccinated by HVT-ND vaccine, G2 vaccinated by HVT-ND and 2 live ND vaccines, G3 vaccinated by HVT-ND, inactivated ND and 2 live ND vaccines, G4 vaccinated by 2 live ND vaccines, G5 vaccinated by inactivated ND and 2 live ND vaccines and G6 Non-vaccinated challenged. All birds were challenged atthe age of 28 days-old. The protection evaluation based on mortality, clinical symptoms, gross pathological lesions, immune response and the mean lesion scores (MLS) of histopathological lesions in brain and trachea at 14 days post challenge.Our findings showed that mortality rates were 26.6 %, 16.6%, 30% and 3.3%, respectively, in G1, G2, G4 and G5,while the best protection was in G3 that did not show any mortality versus 93.3 % in G6. Moreover the MLS on 7dpc were 1.75, 1.6, 1.18 , 1.65 and 1.23, in G1, G2, G3, G4 and G5,respectively,while it reached to 2.5 in G6. Results of virus shedding in all vaccinated groups significantly reduced while (G3) also show the more reduction of virus shedding. It could be concluded that full clinical protection against challenge with genotype VII.1.1. NDV can be achieved by co-administrating ofHVT-ND, inactivated ND and live ND vaccines as a vaccination program in endemic regions.
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