scholarly journals Neuroprotective effect of Citrus unshiu immature peel and nobiletin inhibiting hydrogen peroxide-induced oxidative stress in HT22 murine hippocampal neuronal cells

2015 ◽  
Vol 11 (44) ◽  
pp. 284 ◽  
Author(s):  
InYoung Choi ◽  
HyunWoo Cho ◽  
SuYoung Jung ◽  
GyeongHwan Lee ◽  
JungHee Cho
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Neuroprotective Effect ◽  
Neuronal Cells ◽  
Citrus Unshiu

scholarly journals GLP-1 Analogue Liraglutide Attenuates Mutant Huntingtin-Induced Neurotoxicity by Restoration of Neuronal Insulin Signaling

2018 ◽  
Author(s):  
Ching-Chi Chang ◽  
Tzu-Chin Lin ◽  
Hsiao-Li Ho ◽  
Chien-Yin Kuo ◽  
Hsin-Hua Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stress Reduction ◽  
Insulin Signaling ◽  
Neuroprotective Effect ◽  
Neuronal Cells ◽  
Epidemiologic Studies ◽  
Cag Repeat ◽  
Coding Region ◽  
Endogenous Antioxidant

Huntington's disease (HD) is a progressive and fatal neurodegenerative disease caused by CAG repeat expansion in the coding region of huntingtin (HTT) protein. The accumulation of mutant HTT (mHTT) contributes to neurotoxicity by causing autophagy defects and oxidative stress that ultimately lead to neuronal death. Interestingly, epidemiologic studies have demonstrated that the prevalence of type-2 diabetes, a metabolic disease mainly caused by defective insulin signaling, is higher in patients with HD than in healthy controls. Although the precise mechanisms of mHTT-mediated toxicity remain unclear, the blockade of brain insulin signaling may initiate or exacerbate mHTT-induced neurodegeneration. In this study, we used an in vitro HD model to investigate whether neuronal insulin signaling is involved in mHTT-mediated neurotoxicity. Our results demonstrated that mHTT overexpression significantly impairs insulin signaling and causes apoptosis in neuronal cells. However, treatment with liraglutide, a GLP-1 analogue, markedly restores insulin sensitivity and enhances cell viability. This neuroprotective effect may be attributed to the contribution of the upregulated expression of genes associated with endogenous antioxidant pathways to oxidative stress reduction. In addition, liraglutide stimulates autophagy through AMPK activation, which attenuates the accumulation of HTT aggregates within neuronal cells. Our findings collectively suggest that liraglutide can rescue impaired insulin signaling caused by mHTT and that GLP-1 may potentially reduce mHTT-induced neurotoxicity in the pathogenesis of HD.

Neuroprotective Effect of 3-[(4-Chlorophenyl)selanyl]-1-methyl-1H-indole on Hydrogen Peroxide-Induced Oxidative Stress in SH-SY5Y Cells

2021 ◽  
Author(s):  
Angela Maria Casaril ◽  
Natália Segatto ◽  
Lucas Simões ◽  
Júlia Paschoal ◽  
Micaela Domingues ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Neuroprotective Effect

scholarly journals Protective Effects and Mechanism of Hyperoside in PC12 Cells Against Oxidative Stress Injury Induced by Hydrogen Peroxide

2021 ◽  
Vol 16 (5) ◽  
pp. 1934578X2110151
Author(s):  
Yan Feng ◽  
Dongxu Wang ◽  
Qi Wang ◽  
Zhifeng Li ◽  
Shi-Lin Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Neurodegenerative Diseases ◽  
Pc12 Cells ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Natural Antioxidants ◽  
Protective Effects ◽  
Stress Injury ◽  
Stress Damage

As the aging phenomenon continues to increase, the incidence of neurodegenerative diseases continues to increase annually. As one of the significant contributive factors of neurodegenerative diseases, oxidative stress damage has received extensive attention in recent years. Oxidative stress plays an important role in neuronal damage through various apoptotic mechanisms related to neurodegenerative diseases. The use of natural antioxidants to combat oxidative stress may be a useful approach in delaying disease progression. In this study, we explored the neuroprotective effect of hyperoside on rat pheochromoma (PC12) cells. Specifically, the antioxidant effect and mechanism of hyperoside in hydrogen peroxide (H2O2)-induced cellular cytotoxicity were investigated. Our results showed that hyperoside could significantly increase the survival rate of rat PC12 cells when exposed to H2O2. In addition, hyperoside regulated the expression of genes and proteins in the corresponding pathways by up-regulating the phosphatidylinositol-3-kinase (PI3K), protein kinase B (Akt), and light chain 3β (LC3B) pathways and down-regulating the nuclear factor-ᴋ-gene binding (NF-κB), Bcl2-associated X (Bax), cysteinyl aspartate specific proteinase 3 (Caspase 3), and P62 pathways, thereby inhibiting cell apoptosis. Therefore, hyperoside can effectively inhibit H2O2-induced oxidative stress damage by regulating inflammation, autophagy, and apoptosis-related pathways.

scholarly journals Neuroprotective effect of Aster yomena (Kitam.) Honda against hydrogen peroxide-induced oxidative stress in SH-SY5Y cells

2020 ◽  
Vol 63 (3) ◽  
pp. 283-290
Author(s):  
Min Jeong Kim ◽  
Ji Hyun Kim ◽  
Sanghyun Lee ◽  
Eun Ju Cho ◽  
Hyun Young Kim
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Neuroprotective Effect

Metformin alleviates hydrogen peroxide-induced inflammation and oxidative stress via inhibiting P2X7R signaling in spinal cord tissue cells neurons

2020 ◽  
Author(s):  
Gang Wang ◽  
Shurui Chen ◽  
Zhenya Shao ◽  
Yankun Li ◽  
Wei Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Spinal Cord ◽  
Purinergic Receptor ◽  
Neuroprotective Effect ◽  
Spinal Cord Tissue ◽  
Spinal Cord Neurons ◽  
Oxidative Effects ◽  
And Oxidative Stress

Metformin, the first medication that is often prescribed for the treatment of Type-2 Diabetes Mellitus (T2DM), was recently found to be neuroprotective. To study the mechanism underlying the neuroprotective effect of metformin, we pre-treated primary spinal cord neurons with 50 µM or 100 µM µM metformin for 2 hours prior to treatment with hydrogen peroxide (H2O2) for up to 48 hours. Our results showed that H2O2 increased the expression of purinergic receptor P2X7 (P2X7R) in spinal cord neurons, which promoted the downstream pro-inflammatory cytokines release and oxidative stress. We found that metformin could reverse these pro-inflammatory and pro-oxidative effects of H2O2. Besides, P2X7R knockdown by siRNA suppressed H2O2-induced proinflammatory cytokine release and oxidative stress response. In conclusion, our results show that metformin can alleviate H2O2-induced inflammation and oxidative stress via modulating the P2X7R signaling pathway.

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