The process of neurite outgrowth and branching is a crucial aspect of neuronal development and regeneration.Axons and dendrites,sometimes referred to as neurites,are extensions of a neuron's cellular body that are...The process of neurite outgrowth and branching is a crucial aspect of neuronal development and regeneration.Axons and dendrites,sometimes referred to as neurites,are extensions of a neuron's cellular body that are used to start networks.Here we explored the effects of diethyl(3,4-dihydroxyphenethylamino)(quinolin-4-yl)methylphosphonate(DDQ)on neurite developmental features in HT22 neuronal cells.In this work,we examined the protective effects of DDQ on neuronal processes and synaptic outgrowth in differentiated HT22cells expressing mutant Tau(mTau)cDNA.To investigate DDQ chara cteristics,cell viability,biochemical,molecular,western blotting,and immunocytochemistry were used.Neurite outgrowth is evaluated through the segmentation and measurement of neural processes.These neural processes can be seen and measured with a fluorescence microscope by manually tracing and measuring the length of the neurite growth.These neuronal processes can be observed and quantified with a fluorescent microscope by manually tracing and measuring the length of the neuronal HT22.DDQ-treated mTau-HT22 cells(HT22 cells transfected with cDNA mutant Tau)were seen to display increased levels of synaptophysin,MAP-2,andβ-tubulin.Additionally,we confirmed and noted reduced levels of both total and p-Tau,as well as elevated levels of microtubule-associated protein 2,β-tubulin,synaptophysin,vesicular acetylcholine transporter,and the mitochondrial biogenesis protein-pe roxisome prolife rator-activated receptor-gamma coactivator-1α.In mTa u-expressed HT22 neurons,we observed DDQ enhanced the neurite characteristics and improved neurite development through increased synaptic outgrowth.Our findings conclude that mTa u-HT22(Alzheimer's disease)cells treated with DDQ have functional neurite developmental chara cteristics.The key finding is that,in mTa u-HT22 cells,DDQ preserves neuronal structure and may even enhance nerve development function with mTa u inhibition.展开更多
Context:Trigonella foenum-graecum(TriFG)exhibits increased scavenger enzymatic activities and reduces the production of reactive oxygen species in diabetic rats.Objective:The present study was aimed to investigate the...Context:Trigonella foenum-graecum(TriFG)exhibits increased scavenger enzymatic activities and reduces the production of reactive oxygen species in diabetic rats.Objective:The present study was aimed to investigate the effect of TriFG on lipid peroxidation levels and antioxidant status in brain tissue of rats exposed to alloxan.Materials and Methods:Healthy male rats(180±10 g)were allocated into five groups.Animals in group 1 maintained on normal tap water served as controls and rats in groups 2,3,4,and 5 were treated as experimental groups.Rats in group 2 were intraperitoneally injected with alloxan(120 mg/kg BW)and treated as diabetic rats,whereas rats in groups 3 and 4 were maintained on same experimental regimen as that of rats in groups 1 and 2,respectively,and in addition,they were orally gavaged with herbal extracts of TriFG(0.25 g/kg BW).Diabetic rats treated with glibenclamide in group 5 were used as positive controls.Results and Discussion:Significant(P<0.001)increase in the antioxidant enzymes with a significant(P<0.001)decrease in the lipid peroxidation levels were observed in the brain tissue of diabetic rats treated with TriFG extract as compared to diabetic and glibenclamide-treated rats.No significant changes were observed in pro-and antioxidant levels in brain tissue of rats treated with TriFG extract alone when compared to normal rats.In diabetic rats,brain mitochondrial and cytosolic enzymes like succinate dehydrogenase,glutamate dehydrogenase,and glucose-6-phosphate dehydrogenase activity levels were significantly(P<0.05)decreased with reversely increased was observed in lactate dehydrogenase activity(P<0.05).Conclusions:The findings of the present study suggested that TriFG,through its antioxidant properties,protects brain tissue by mitigating oxidative stress induced by alloxan-exposed rats.TriFG extract significantly increased the antioxidant and oxidative properties in diabetic rats when compared with the control group rats.展开更多
基金supported by NIH grants AG079264(to PHR)and AG071560(to APR)。
文摘The process of neurite outgrowth and branching is a crucial aspect of neuronal development and regeneration.Axons and dendrites,sometimes referred to as neurites,are extensions of a neuron's cellular body that are used to start networks.Here we explored the effects of diethyl(3,4-dihydroxyphenethylamino)(quinolin-4-yl)methylphosphonate(DDQ)on neurite developmental features in HT22 neuronal cells.In this work,we examined the protective effects of DDQ on neuronal processes and synaptic outgrowth in differentiated HT22cells expressing mutant Tau(mTau)cDNA.To investigate DDQ chara cteristics,cell viability,biochemical,molecular,western blotting,and immunocytochemistry were used.Neurite outgrowth is evaluated through the segmentation and measurement of neural processes.These neural processes can be seen and measured with a fluorescence microscope by manually tracing and measuring the length of the neurite growth.These neuronal processes can be observed and quantified with a fluorescent microscope by manually tracing and measuring the length of the neuronal HT22.DDQ-treated mTau-HT22 cells(HT22 cells transfected with cDNA mutant Tau)were seen to display increased levels of synaptophysin,MAP-2,andβ-tubulin.Additionally,we confirmed and noted reduced levels of both total and p-Tau,as well as elevated levels of microtubule-associated protein 2,β-tubulin,synaptophysin,vesicular acetylcholine transporter,and the mitochondrial biogenesis protein-pe roxisome prolife rator-activated receptor-gamma coactivator-1α.In mTa u-expressed HT22 neurons,we observed DDQ enhanced the neurite characteristics and improved neurite development through increased synaptic outgrowth.Our findings conclude that mTa u-HT22(Alzheimer's disease)cells treated with DDQ have functional neurite developmental chara cteristics.The key finding is that,in mTa u-HT22 cells,DDQ preserves neuronal structure and may even enhance nerve development function with mTa u inhibition.
文摘Context:Trigonella foenum-graecum(TriFG)exhibits increased scavenger enzymatic activities and reduces the production of reactive oxygen species in diabetic rats.Objective:The present study was aimed to investigate the effect of TriFG on lipid peroxidation levels and antioxidant status in brain tissue of rats exposed to alloxan.Materials and Methods:Healthy male rats(180±10 g)were allocated into five groups.Animals in group 1 maintained on normal tap water served as controls and rats in groups 2,3,4,and 5 were treated as experimental groups.Rats in group 2 were intraperitoneally injected with alloxan(120 mg/kg BW)and treated as diabetic rats,whereas rats in groups 3 and 4 were maintained on same experimental regimen as that of rats in groups 1 and 2,respectively,and in addition,they were orally gavaged with herbal extracts of TriFG(0.25 g/kg BW).Diabetic rats treated with glibenclamide in group 5 were used as positive controls.Results and Discussion:Significant(P<0.001)increase in the antioxidant enzymes with a significant(P<0.001)decrease in the lipid peroxidation levels were observed in the brain tissue of diabetic rats treated with TriFG extract as compared to diabetic and glibenclamide-treated rats.No significant changes were observed in pro-and antioxidant levels in brain tissue of rats treated with TriFG extract alone when compared to normal rats.In diabetic rats,brain mitochondrial and cytosolic enzymes like succinate dehydrogenase,glutamate dehydrogenase,and glucose-6-phosphate dehydrogenase activity levels were significantly(P<0.05)decreased with reversely increased was observed in lactate dehydrogenase activity(P<0.05).Conclusions:The findings of the present study suggested that TriFG,through its antioxidant properties,protects brain tissue by mitigating oxidative stress induced by alloxan-exposed rats.TriFG extract significantly increased the antioxidant and oxidative properties in diabetic rats when compared with the control group rats.