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The present study was designed to evaluate the effect of Naringin on memory of unstressed and stressed Swiss young albino mice. Naringin (80?mg/kg, i.p.) and donepezil (10?mg/kg) were administered for 21 successive days to separate groups of unstressed and stressed mice. The nootropic activity was evaluated using elevated plus maze and Hebbs Williams Maze. Brain acetylcholinesterase (AChE), brain nitrite and plasma corticosterone levels were also estimated. unpredictable chronic mild stress was produced by using different stressors. Naringin (80?mg/kg) and donepezil significantly showed memory enhancing activity in both unstressed and stressed mice. Naringin significantly reduced brain AChE activity and brain nitrite levels in both unstressed and stressed mice. Naringin (80?mg/kg) significantly reversed scopolamine-induced amnesia in unstressed and stressed mice. 7-Nitroindazole [a neuronal nitric oxide synthase (NOS) inhibitor] and aminoguanidine (an inducible NOS inhibitor) significantly enhanced memory improving activity and brain nitrite decreasing effect of naringin in unstressed and stressed mice respectively. Plasma corticosterone levels were significantly decreased by naringin (80?mg/kg) in stressed mice as compared to its control. Thus, naringin showed memory enhancing activity in unstressed mice probably by decreasing brain AChE activity and by inhibition of neuronal NOS. The memory enhancing activity of naringin in stressed mice might be due to decrease in brain AChE activity, inhibition of inducible NOS and also by decreasing the elevated plasma corticosterone levels.  相似文献   

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The aim of present study was to evaluate antianxiety-like activity of gallic acid in Swiss young male albino mice; and to explore the possible underlying mechanisms for this activity. Gallic acid (5, 10, 20 mg/kg, i.p.) and alprazolam (0.25 mg/kg, i.p.) were administered for 10 successive days to separate groups of mice. On 10th day, 45 min after the drug administration, stress was produced by immobilization of mice for 150 min and these mice were called as stressed mice. Anxiolytic activity was evaluated using elevated plus maze and light–dark test. The plasma nitrite and corticosterone levels were also estimated in unstressed and stressed mice. Effects of 7-nitroindazole (neuronal NOS inhibitor) and aminoguanidine (inducible NOS inhibitor) on antianxiety-like activity of gallic acid were also evaluated. Gallic acid (10 and 20 mg/kg) and alprazolam per se significantly showed antianxiety-like activity in both unstressed and stressed mice. The drugs did not show any significant effect on locomotor activity of the mice. Gallic acid significantly decreased the plasma nitrite levels in both unstressed and stressed mice. 7-nitroindazole and aminoguanidine significantly enhanced antianxiety-like activity and plasma nitrite decreasing effect of gallic acid in unstressed and stressed mice respectively. Plasma corticosterone levels were significantly decreased by gallic acid in stressed mice as compared to its control. Thus, gallic acid showed antianxiety-like activity in unstressed mice probably by inhibition of nNOS. On the other hand, antianxiety-like activity in stressed mice might be through inhibition of iNOS and reduction of plasma corticosterone levels.  相似文献   

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Wang  Wenbing  Kirumba  George  Zhang  Yongming  Wu  Yanqing  Rittmann  Bruce E. 《Biodegradation》2021,32(5):611-611
Biodegradation - The Editor in Chief and the authors have retracted this article because of multiple errors in the data that undermine the conclusions of the study. Bruce E Rittman agreed to this...  相似文献   

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We sought to examine interactions of the prion protein (PrPC) with monoaminergic systems due to: the role of PrPC in both Prion and Alzheimer diseases, which include clinical depression among their symptoms, the implication of monoamines in depression, and the hypothesis that PrPC serves as a scaffold for signaling systems. To that effect we compared both behavior and monoaminergic markers in wild type (WT) and PrPC-null (PrP−/−) mice. PrP−/− mice performed poorly when compared with WT in forced swimming, tail suspension, and novelty suppressed feeding tests, typical of depressive-like behavior, but not in the control open field nor rotarod motor tests; cyclic AMP responses to stimulation of D1 receptors by dopamine was selectively impaired in PrP−/− mice, and responses to serotonin, but not to norepinephrine, also differed between genotypes. Contents of dopamine, tyrosine hydroxylase, and the 5-HT5A serotonin receptor were increased in the cerebral cortex of PrP−/−, as compared with WT mice. Microscopic colocalization, as well as binding in overlay assays were found of PrPC with both the 5HT5A and D1, but not D4 receptors. The data are consistent with the scaffolding of monoaminergic signaling modules by PrPC, and may help understand the pathogenesis of clinical depression and neurodegenerative disorders.  相似文献   

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Biophysics - Abstract—We have previously demonstrated that hypothermia significantly modulates the effect of ATP on the contractile activities of various types of rodent locomotor muscles....  相似文献   

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Up to now, the serine-arginine protein kinase 1 (SRPK1) has been suggested as an important signal mediator, which is implicated in the development of cancers. Unfortunately, some molecular pathways in SRPK1-mediated epithelial-mesenchymal transition (EMT) in human spinal glioblastoma have been not elucidated. In this work, we detected the expression of SRPK1 in human spinal glioblastoma tissues and GBM cell lines and analyzed the relevant molecular proteins using in vitro experiments, including RT-PCR, gene silencing, and Western blot. In this study, RT-PCR and Western blot revealed that the expression of SRPK1 mRNA and protein became higher in all six spinal glioblastoma specimens; however, its expression was low in matched normal specimens. We also demonstrated SRPK1 expression facilitated the proliferation of U87 and U251 cells and inhibited the apoptosis in U87 and U251 cells. Also, SRPK1 promoted the expression of EMT-regulating markers, involving N-cadherin, Snail, and MMP9 and decreased the expression of mesenchymal marker E-cadherin. Moreover, knockdown of SRPK1 significantly inhibited the expression levels of p-Akt rather than t-Akt. In conclusion, knockdown of SRPK1 inhibited glioblastoma cell proliferation, invasion, and EMT process via suppressing p-Akt signaling pathway. This study also lays a new foundation for the clinically biological treatment.  相似文献   

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