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| 1 | Neuroprotection by misoprostol against rotenone-induced neurotoxicity in rat brain显示文摘Objective: To investigate the effect of the prostaglandin E1 analogue misoprostol on oxidative stress and neurodegeration caused by subcutaneous rotenone administration in rats. Methods:Rotenone was administered in a dose of 1.5 mg/kg every other day for 2 weeks. Starting from the 1 st day of rotenone injection, rats were subcutaneously treated with misoprostol at doses of10, 100 or 1 000 μg/kg. Rats were evaluated for brain lipid peroxidation(malondialdehyde:MDA), reduced glutathione(GSH), nitric oxide(NO) levels, and paraoxonase-1(PON-1) activity.The concentrations of the anti-apoptotic protein B cell/lymphoma-2(Bcl-2) were determined in the striatum. Histopathologic examination and the expression of inducible nitric oxide synthase(iNOS) in the cerebral cortex and striatum were also performed. Results: Compared with the vehicle-treated group, rotenone caused a significant increase in brain lipid proxidation(MDA)by 61%(P<0.05) accompanied by an increase in NO by 73.1%(P<0.05) and a decrease in GSH concentration by 29.4%(P<0.05). In addition, brain PON-1 activity significantly decreased by63.0%(P<0.05) and striatal Bcl-2 significantly decreased by 27.9%(P<0.05) with respect to the corresponding control value. Brain sections from rotenone treated rats showed extensive dark pyknotic and apoptotic nuclei in neurons, shrunken cytoplasm and perineuronal vacuolation.Rotenone also caused pronounced expression of iNOS in the cerebral cortex and striatum.Treatment with misoprostol at doses of 100 and 1 000 μg/kg resulted in decreased brain MDA(by 16.5%-23.0%)(P<0.05) and NO levels(by 37.1%-40.7%)(P<0.05) and increased GSH concentrations(by 18.8%-30.1%)(P<0.05). PON-1 activity was significantly increased by80.0%-114.8%(P<0.05) by misoprostol at 100 and 1 000 μg/kg, respectively. In addition,misoprostol treatment restored striatal Bcl-2 concentrations to its normal value. Misoprostol treatment resulted in markedly reduced brain injury and decreased iNOS expression in the cerebral cortex and striatum of rotenone intoxicated rats. Conclusions: These data suggest that misoprostol prevents the rotenone-induced neurodegeneration in rat brain by reducing brain oxidative stress. | Omar M.E.Abdel-Salam Amany A Sleem Eman R Youness Nadia A Mohammed Enayat A Omara | 2018 | Asian Pacific Journal of Tropical Medicine2018，11，1： | 1 |
| 2 | Perforated aPPendicitis:is early Laparoscopic appendectomy显示文摘 | Sleem R Fisher S Gestring M | 2009 | Pro Priate Surg2009，146，4： | 1 |
| 3 | Modu- lation of lipopolysaccharide -induced oxidative stress by cap-saicin显示文摘 | AbdeI-Salam O M AbdeI-Rahman R F Sleem A A et aI | 2012 | Inflammopharmacology2012，20，4： | 1 |
| 4 | Perforated aPPendicitis:is earlylaparoscopic appendectomy显示文摘 | Sleem R Fisher S Gestring M | 2009 | Pro Priate Surg2009，146，4： | 1 |
| 5 | Perforated appendicitis : is early laparoscopic appendectomy appropriate ? 显示文摘 | Sleem R Fisher S Gestring M | 2009 | Surgery2009，146，4： | 1 |
| 6 | Preventive effects of cannabis on neurotoxic and hepatotoxic activities of malathion in rat显示文摘Objective: To investigate the effect of Cannabis sativa extract on the development of neuroand hepato-toxicity caused by malathion injection in rats. Methods: The extract of Cannabis sativa was obtained from the plant resin by chloroform treatment. Δ~9-Tetrahydrocannabinol content of the extract(20%) was quantified using gas chromatography–mass spectrometry. The doses of cannabis extract were expressed as Δ~9-tetrahydrocannabinol content of 10 or 20 mg/kg. Malathion(150 mg/kg) was intraperitoneally administered followed after 30 min by the cannabis extract(10 or 20 mg/kg, subcutaneously). Rats were euthanized 4 h later. Malondialdehyde(MDA), reduced glutathione(GSH), nitric oxide and paraoxonase-1(PON-1) activity were determined in brain and liver. Brain 5-lipoxygenase and butyrylcholinesterase(BChE) activity were measured as well. Histopathological examination of brain and liver tissue was also performed. Results: Compared to controls, malathion resulted in increased oxidative stress in brain and liver. MDA and nitric oxide concentrations were significantly increased(P<0.05) and GSH significantly decreased with respect to control levels(P<0.05). Malathion also significantly inhibited PON-1 and BChE activities but had no effect on brain 5-lipoxygenase. Brain MDA concentrations were not altered by cannabis treatment. Cannabis at 20 mg/kg, however, caused significant increase in nitric oxide and restored the GSH and PON-1 activity. Brain BChE activity significantly decreased by 26.1%(P<0.05) after treatment with 10 mg/kg cannabis. Cannabis showed no effect on brain 5-lipoxygenase. On the other hand, rats treated with cannabis exhibited significantly higher levels of liver MDA, nitric oxide and PON-1 activity compared with the malathion control group. Rats treated with only malathion exhibited spongiform changes, neuronal damage in the cerebral cortex and degeneration of some Purkinje cells in the cerebellum. There were also hepatic vacuolar degeneration and dilated and congested portal vein. These histopthological changes induced by malathion in brain and liver were reduced to great extent by cannabis administration at 20 mg/kg. Conclusions: Our data suggest that acute treatment with cannabis alleviates the malathion-induced brain and hepatic injury in rats possibly by maintaining the levels of GSH and PON-1 activity. | Omar M.E.Abdel-Salam Amany A Sleem Eman R Youness Fatma A.Morsy | 2018 | Asian Pacific Journal of Tropical Medicine2018，11，4： | 0 |
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