Abstract
We show that down-regulation of circular ribonucleic acid 0001588 with small interfering-circular ribonucleic acid 0001588 mimics promoted caspase-3 and caspase-9 activity levels, increased lactate dehydrogenase activity levels, and reduced cell growth of in vitro model. Circular ribonucleic acid 0001588 plasmids increased circular ribonucleic acid 0001588 expressions and promoted cell growth and reduced activity levels of lactate dehydrogenase, caspase-3, and caspase-9 activity levels in vitro model of Alzheimer's disease. Then, circular ribonucleic acid 0001588 down-regulation also promoted reactive oxygen species production and oxidative stress (malonaldehyde), and reduced superoxide dismutase, glutathione, and glutathione peroxidase levels by suppressing of silent information regulator 1/nuclear factor erythroid 2-related factor 2/heme oxygenase-1 in vitro. However, over-expression of circular ribonucleic acid 0001588 reduced reactive oxygen species production and malonaldehyde levels and increased superoxide dismutase, glutathione, and levels via activation signal pathway of silent information regulator 1/nuclear factor erythroid 2-related factor 2/heme oxygenase-1 signaling pathway by miR-211-5p up-regulation in vitro. Over-expression of miR-211-5p attenuated the role of circular ribonucleic acid 0001588 on Alzheimer's disease-induced oxidative stress. Also, activation of the silent information regulator 1 pathway attenuated the antioxidative effects of circular ribonucleic acid 0001588 down-regulation on oxidative stress by activating silent information regulator 1/nuclear factor erythroid 2-related factor 2/heme oxygenase-1 in vitro. In conclusion, our findings indicated that circular ribonucleic acid 0001588 induced the silent information regulator 1/nuclear factor erythroid 2-related factor 2-dependent heme oxygenase-1 pathway to prevent oxidative stress by miR-211-5p in the rat model or in vitro model of a sporadic type of Alzheimer's disease. Therefore, the expression of the circular ribonucleic acid 0001588 gene was inhibited in rodent Alzheimer's disease model.
Highlights
Alzheimer's disease (AD) is a severe central neurodegeneration disorder related to aging, which has become one of the leading death causes following tumor and angiocardiopathy (Magro et al, 2015)
We analyzed the functions of circRNA 0001588 in a rat model of AD
The MDA level was increased, while the levels of superoxide dismutase (SOD), GSH, and GSH-px were reduced in AD model rats in comparison with the sham control group (Fig. 1E and 1H)
Summary
Alzheimer's disease (AD) is a severe central neurodegeneration disorder related to aging, which has become one of the leading death causes following tumor and angiocardiopathy (Magro et al, 2015). AD deterioration will deprive the patients of the ability of independent living (Cheng et al, 2016) It will cause complications and even death with disease aggravation (Li et al, 2013). Silent information regulator 1 (SIRT1) has been found to delay the pathogenesis and development of AD through anti-oxidative stress (Ak et al, 2015; Hsieh et al, 2009). It plays a vital character in the elimination of AD pathological deposits, anti-inflammation, anti-apoptosis, and neurotrophy (Hsieh et al, 2009). Circular HDAC9/miRNA-138 pathway has been demonstrated to regulate synaptic and amyloid precursor protein processing deficits in AD (Browne et al, 2010; Yang et al, 2019)
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