Rutin activates the MAPK pathway and BDNF gene expression on beta-amyloid induced neurotoxicity in rats

Moghbelinejad, Sahar; Nassiri‐Asl, Marjan; Farivar, Taghi Naserpour; Abbasi, Esmail; Sheikhi, Mehdi; Taghiloo, Mina; Farsad, Farzaneh; Samimi, Amir; Hajiali, Farid

doi:10.1016/j.toxlet.2013.10.010

Cited by 104 publications

(49 citation statements)

References 45 publications

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“…In the present study, it was demonstrated that treatment with rutin increased p-Akt protein expression levels in CHD model pigs. This is in agreement with a study by Moghbelinejad et al (41), which indicated that rutin may be protective against the neurotoxic effects of amyloid β on memory in rats through actions on ERK and PI3K/Akt.…”

Section: Discussionsupporting

confidence: 93%

Rutin inhibits coronary heart disease through ERK1/2 and Akt signaling in a porcine model

Yao

Zhao

et al. 2017

Exp Ther Med

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Abstract.Rutin has a variety of pharmacological actions, including radical reactivity, and protective activity against lipid peroxidation, viruses and acute pancreatitis; thus, it may be used as a treatment for many diseases. The present study aimed to investigate whether rutin inhibits coronary heart disease through extracellular signal-regulated kinase (ERK) 1/2 and Akt signaling in a porcine model. Male Chinese miniature pigs were randomly divided into four groups: A sham group, a coronary heart disease (CHD) model group, a group receiving 15 mg/kg rutin for 8 weeks following CHD modeling and a group receiving 45 mg/kg rutin for 8 weeks following CHD modeling. The results suggested that treatment with rutin suppressed the reduction in left ventricular ejection fraction and increase in systolic internal diameter that occurred in CHD model pigs. Rutin administration reduced the infarct size of the myocardium, attenuated LVEF, increased LVID and inhibited urine protein concentration, BUN and Scr expression levels in CHD model pigs. Results from western blot analysis demonstrated that in CHD pigs treated with 45 mg/kg rutin, the CHD-associated increases in transforming growth factor β1 and SMAD2 expression and reductions in phosphorylated (p)-ERK1/2 and p-Akt expression were attenuated. The present study suggests that rutin inhibits coronary heart disease through ERK1/2 and Akt signaling pathways in a porcine model.

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Section: Discussionsupporting

confidence: 93%

Rutin inhibits coronary heart disease through ERK1/2 and Akt signaling in a porcine model

Yao

Zhao

et al. 2017

Exp Ther Med

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“…Rutin (3,3,4,5,, a flavonol found in buckwheat, passion flower, apple, and tea, significantly increased levels of extracellular signalregulated kinase (ERK)-1, CREB, and BDNF gene expression in the hippocampus of rats (Moghbelinejad et al, 2014). Chronic stress-induced depression decreases BDNF and phosphorylated CREB levels in the hippocampus and frontal cortex in rats, and curcumin treatment prevents the suppression of BDNF levels (Xu et al, 2006b).…”

Section: B Trophic Signaling Pathwaysmentioning

confidence: 99%

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

et al. 2014

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“…The neuroprotective effects of rutin, a flavonoid have been reported in beta amyloid induced neurotoxicity in rats [153] . Flavonoid induced decreased acetylcholinesterase activity has also been suggested in experimental model of AD [154][155][156][157] . Study in cellular model of AD has showed that flavonoid offered protection through antioxidation, mitochondrion protection and MAPK signal inactivation [158] .…”

Section: Evidences For the Beneficial Use Of Antioxidants In Neurodegmentioning

confidence: 89%

Antioxidants as a preventive therapeutic option for age related neurodegenerative diseases

Singh

2015

Ther Targets Neurol Dis

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Neurodegenerative diseases: an overview -Neurodegenerative disease term illustrate a range of conditions in which primarily neurons get affected or die. Neurons are the building blocks of the central and peripheral nervous system. Neurons could not reproduce or replace themselves with age therefore, when they get damaged or die they cannot be replaced and lead to specific neurodegenerative disease. Few evidences for the presence of stem cells are reported [1] but still it is not understood whether damaged neuron could regenerate or not. The Parkinson's, Alzheimer's, and Huntington's diseases are the most prevalent age related neurodegenerative diseases of central nervous system involving death of specific neuronal population. The treatment of these neurodegenerative diseases might involve the re-supplementation of specific neuronal population with the help of stem cells but researchers and clinicians did not get noticeable success in this approach yet. Millions of people each year are getting affected by these neurodegenerative diseases and the incidences are increasing further significantly with the extended life expectancy. It has been reported by World Health Organisation (2006) that the number of older people of more than 65 years age are expected to increase to approximately 1 billion in 2030 worldwide. Developing countries like India and China will see the largest increase in numbers of aged persons. Therefore the percentage of aged population in developing countries would increase from 59% to 71% worldwide [2] . Since occurrence of most of the neurodegenerative Advances in our understanding for neurodegenerative mechanisms have increased significantly in last few decades. But still no novel disease modifying therapy has been developed which could prevent the disease progression and drawn our attention towards the development of new alternative therapy. The major obstacle for the development of disease therapy is incomplete knowledge about neurodegenerative mechanisms. Due to the insufficient information about neurodegenerative mechanisms no standard diagnostic tests for the detection of neurodegenerative disease could be develop to date, causes delayed diagnosis and disease worsening. So far the exploratory reports and clinical data have suggested the involvement of oxidative stress, mitochondrial impairment and apoptosis as major neurodegenerative mechanisms. Investigations have elicited that once initiated the degeneration of neurons could not be arrested therefore in the scarcity of curative therapy we should approach for the preventive neurodegenerative therapy. Since oxidative stress has noteworthy involvement in neuronal death solely, and in connection to other death pathways therefore, antioxidants as preventive therapeutics might provide beneficial effects in age related neurodegenerative diseases. With this hypothesis in this review we are discussing about the use of antioxidants as a preventive treatment of neurodegenerative diseases. Such therapies may work in the preventive phase or in curati...

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Rutin activates the MAPK pathway and BDNF gene expression on beta-amyloid induced neurotoxicity in rats

Cited by 104 publications

References 45 publications

Rutin inhibits coronary heart disease through ERK1/2 and Akt signaling in a porcine model

Rutin inhibits coronary heart disease through ERK1/2 and Akt signaling in a porcine model

Adaptive Cellular Stress Pathways as Therapeutic Targets of Dietary Phytochemicals: Focus on the Nervous System

Antioxidants as a preventive therapeutic option for age related neurodegenerative diseases

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