Insulin is a potential antioxidant for diabetes-associated cognitive decline via regulating Nrf2 dependent antioxidant enzymes

Song, Ying; Ding, Wei; Bei, Yun; Xiao, Yan; Tong, Hai-Da; Wang, Libo; Ai, Li-Yao

doi:10.1016/j.biopha.2018.04.097

Cited by 60 publications

(30 citation statements)

References 27 publications

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“…This problem seems to be interesting and requires further research because in the scientific literature only a few data concerning this facet are present. Song et al [12], in studies examining the neuroprotective influence of insulin on apoptosis of PC12 cell line induced by H 2 O 2 , proved a positive result of incubating these with directly added insulin in growing concentrations (25,50, 100, and 200 mmol/L) and increased viability of cells despite the activity of a pro-apoptotic agent. Nampoothiri et al [25] proved the protective effect of insulin in the conditions of toxic activity of glutamate, using cells from the human neuroblastoma line (SH-SY5Y).…”

Section: Discussionmentioning

confidence: 99%

“…Due to insulin receptors in the CNS, its activity is twofold: it acts as a peptide hormone and as a neurotransmitter for the neurons [11]. Literature data indicate that peripheral hyperinsulinaemia directly influences the development of insulin resistance in the brain and, consequently, neuronal disturbances, and predisposes also to development of neurodegenerative disorders [9,12,13].…”

Section: Introductionmentioning

confidence: 99%

“…States of hyperglycaemia in combination with insulin resistance and hyperinsulinaemia, observed in individuals with impaired carbohydrate metabolism, are an important factor in further development of biochemical disturbances and the pathogenesis of clinical complications. They also predispose to the development of many neurodegenerative diseases, which has become an object of interest among many scientists [3,12,14]. Most of the literature to date concern the influence of individual, chemically pure substances (for example, glucose, insulin, glutathione solutions), which are conducted in vivo on animal models or in vitro on different cell lines [15,16].…”

Section: Introductionmentioning

confidence: 99%

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Ex vivo model for the assessment of the cytotoxicity of biological materialfrom patients with carbohydrate metabolism disturbances

Piwowar

Rorbach-Dolata

Głogowska

et al. 2019

pedm

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Ex vivo model for the assessment of the cytotoxicity of biological materialfrom patients with carbohydrate metabolism disturbances

Piwowar

Rorbach-Dolata

Głogowska

et al. 2019

pedm

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“…Intranasal insulin treatment in rats activated insulin signaling which Insulin treatment is the best therapeutic approach used since decades for treating insulin deficiency in diabetes. It is now being investigated in treating cognitive dysfunction in DM (Marissal-Arvy et al, 2018;Song et al, 2018). Other than insulin treatment there are antidiabetic drugs whose potential is being tested for treating cognitive impairment in diabetes.…”

Section: Insulinmentioning

confidence: 99%

Cognitive dysfunction: A growing link between diabetes and Alzheimer's disease

Jash

Gondaliya

Kirave

et al. 2019

Drug Development Research

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Diabetes mellitus (DM) is a gradually rising metabolic disease which is currently affecting millions of people worldwide. Diabetes is associated with various complications like nephropathy, neuropathy, retinopathy, diabetic foot, cognitive impairment, and many more. Evidence suggests that cognitive dysfunction is a rising complication of diabetes which adversely affects the brain of patients suffering from diabetes. Age‐related memory impairment is a complication having its major effect on people suffering from diabetes and Alzheimer's. Patients suffering from diabetes are at two times higher risk of developing cognitive dysfunction as compared with normal individuals. Multiple factors which are involved in diabetes related complications are found to play a role in the development of neurodegeneration in Alzheimer's. The problem of insulin deficiency and insulin resistance is well reported in diabetes but there are many studies which suggest dysregulation of insulin levels as a reason behind the development of Alzheimer's. As the link between diabetes and Alzheimer disease (AD) is deepening, there is a need to understand the plausible tie‐ins between the two. Emerging role of major factors like insulin imbalance, advanced glycation end products and micro‐RNA's involved in diabetes and Alzheimer's have been discussed here. This review helps in understanding the plausible mechanism underlying the pathophysiology of amyloid beta (Aβ) plaque formation and tau hyperphosphorylation as well provides information about studies carried out in this area of research. The final thought is to enhance the scientific knowledge on this correlation and develop future therapeutics to treat the same.

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“…Compared with other organs, human brain has a higher oxygen consumption and a lower antioxidant level; its membrane structure contains more oxidizable unsaturated fatty acids, which makes human brain more vulnerable to the oxidative damage. Edaravone (Ed) is a free‐radical scavenger and its neuroprotective effect, especially its effect against cerebral ischemia, has been widely proved in recent years . Interestingly, with the deepening study, plenty of biological activities or even new indications have been found.…”

Section: Introductionmentioning

confidence: 99%

Nrf2 mediates the protective effect of edaravone after chlorpyrifos‐induced nervous system toxicity

Shou

Bei

Song

et al. 2019

Environmental Toxicology

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We aim to confirm the impairment of chlorpyrifos (CPF) in PC12 cells, evaluate the protective effect of edaravone on CPF-induced injury, and try to unravel its underlying mechanism perspective from Nrf2 signaling pathway. Viability of PC12 cells treated with CPF and edaravone (Ed) were evaluated by MTT assay. Cell apoptosis was observed by the Hoechst 33342 stain. The level of reactive oxygen species (ROS), the content of malondialdehyde (MDA), and the activity of superoxide dismutase (SOD) were detected to evaluate the oxidative stress injury. The expression of Nrf2 was detected by Western blot; profoundly, RNA interference was conducted to construct Nrf2 gene knockdown PC12 cells and to uncover its underlying mechanism. MTT results showed CPF injured PC12 cells in a concentration-dependent manner. Increased ROS and MDA content, decreased total SOD activity, or even apoptosis were occurred in PC12 cells when treated with CPF. Interestingly, CPF-induced cell injury was conspicuously reversed after Ed administration. Nrf2 signaling pathway was activated after Ed treatment and the neuroprotective effect of Ed was not significant in cells after Nrf2 gene knockdown. In conclusion, Ed exerts neuroprotective effect on CPF-induced oxidative stress injury and its mechanism was correlated with the Nrf2 signaling pathway. K E Y W O R D S chlorpyrifos, edaravone, Nrf2, oxidative stress, PC12 cells

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Insulin is a potential antioxidant for diabetes-associated cognitive decline via regulating Nrf2 dependent antioxidant enzymes

Cited by 60 publications

References 27 publications

Ex vivo model for the assessment of the cytotoxicity of biological materialfrom patients with carbohydrate metabolism disturbances

Ex vivo model for the assessment of the cytotoxicity of biological materialfrom patients with carbohydrate metabolism disturbances

Cognitive dysfunction: A growing link between diabetes and Alzheimer's disease

Nrf2 mediates the protective effect of edaravone after chlorpyrifos‐induced nervous system toxicity

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