scholarly journals Neuroprotective Effects of Methyl 3,4-dihydroxybenzoate Against H2O2-Induced Apoptosis in RGC-5 Cells

2014 ◽  
Vol 125 (1) ◽  
pp. 51-58 ◽  
Author(s):  
Xing Zhou ◽  
Chao-Fen Su ◽  
Zheng Zhang ◽  
Chen-Yu Wang ◽  
Jin-Qi Luo ◽  
...  
Keyword(s):  
Neuroprotective Effects ◽  
Induced Apoptosis

scholarly journals Icariin Prevents Amyloid Beta-Induced Apoptosis via the PI3K/Akt Pathway in PC-12 Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Dongdong Zhang ◽  
Zhe Wang ◽  
Chenxia Sheng ◽  
Weijun Peng ◽  
Shan Hui ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Pc12 Cells ◽  
Amyloid Beta ◽  
Chinese Herb ◽  
Protective Effects ◽  
Amyloid Beta Protein ◽  
Neuroprotective Effects ◽  
Pi3k Inhibitor Ly294002 ◽  
Induced Apoptosis

Icariin is a prenylated flavonol glycoside derived from the Chinese herbEpimedium sagittatumthat exerts a variety of pharmacological activities and shows promise in the treatment and prevention of Alzheimer’s disease. In this study, we investigated the neuroprotective effects of icariin against amyloid beta protein fragment 25–35 (Aβ25–35) induced neurotoxicity in cultured rat pheochromocytoma PC12 cells and explored potential underlying mechanisms. Our results showed that icariin dose-dependently increased cell viability and decreasedAβ25–35-induced apoptosis, as assessed by MTT assay and Annexin V/propidium iodide staining, respectively. Results of western blot analysis revealed that the selective phosphatidylinositol 3-kinase (PI3K) inhibitor LY294002 suppressed icariin-induced Akt phosphorylation, suggesting that the protective effects of icariin are associated with activation of the PI3K/Akt signaling pathway. LY294002 also blocked the icariin-induced downregulation of proapoptotic factors Bax and caspase-3 and upregulation of antiapoptotic factor Bcl-2 inAβ25–35-treated PC12 cells. These findings provide further evidence for the clinical efficacy of icariin in the treatment of Alzheimer’s disease.

scholarly journals Effects of Gastrodin against Lead-Induced Brain Injury in Mice Associated with the Wnt/Nrf2 Pathway

Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1805
Author(s):  
Chan-Min Liu ◽  
Zhi-Kai Tian ◽  
Yu-Jia Zhang ◽  
Qing-Lei Ming ◽  
Jie-Qiong Ma ◽  
...  
Keyword(s):  
Phenolic Glycoside ◽  
Related Factor ◽  
Protective Effects ◽  
Neuroprotective Effects ◽  
Nrf2 Pathway ◽  
Wnt Inhibitor ◽  
Research Findings ◽  
Anti Oxidant ◽  
Underlying Mechanisms ◽  
Induced Apoptosis

Gastrodin (GAS), the main phenolic glycoside extracted from Gastrodia elata Blume, exhibited potential neuroprotective properties. Here we examined the protective effects of GAS against lead(Pb)-induced nerve injury in mice, and explores its underlying mechanisms. Our research findings revealed that GAS improved behavioral deficits in Pb-exposed mice. GAS reduced the accumulation of p-tau and amyloid-beta (Aβ). GAS inhibited Pb-induced inflammation in the brain, as indicated by the decreased levels of pro-inflammatory cytokines, including tumor necrosis factor-a (TNF-α), cyclooxygenase-2 (COX-2). GAS increased the expression levels of NR2A and neurotrophin brain-derived neurotrophic factor (BDNF). GAS inhibited Pb-induced apoptosis of neurons in hippocampus tissue, as indicated by the decreased levels of pro-apoptotic proteins Bax and cleaved caspase-3. Furthermore, the neuroprotective effects of GAS were associated with inhibiting oxidative stress by modulating nuclear factor-erythroid 2-related factor 2 (Nrf2)-mediated antioxidant signaling. GAS supplement activated the Wnt/β-catenin signaling pathway and reduced the expression of Wnt inhibitor Dickkopf-1 (Dkk-1). Collectively, this study clarified that GAS exhibited neuroprotective property by anti-oxidant, anti-inflammatory and anti-apoptosis effects and its ability to regulate the Wnt/Nrf2 pathway.

scholarly journals Modulation of Apoptotic Cell Death and Neuroprotective Effects of Glutathione—L-Dopa Codrug Against H2O2-Induced Cellular Toxicity

Antioxidants ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 319 ◽  
Author(s):  
Sara Franceschelli ◽  
Paola Lanuti ◽  
Alessio Ferrone ◽  
Daniela Maria Pia Gatta ◽  
Lorenza Speranza ◽  
...  
Keyword(s):  
Cell Lines ◽  
Apoptotic Cell ◽  
Redox Status ◽  
Dependent Manner ◽  
Neuroprotective Effects ◽  
Standard Drug ◽  
Cellular Redox ◽  
Cellular Toxicity ◽  
Ros Formation ◽  
Induced Apoptosis

The L-3,4-dihydroxyphenylalanine (LD) is the gold standard drug currently used to manage Parkinson’s disease (PD) and to control its symptoms. However, LD could cause disease neurotoxicity due to the generation of pro-oxidant intermediates deriving from its autoxidation. In order to overcome this limitation, we have conjugated LD to the natural antioxidant glutathione (GSH) to form a codrug (GSH-LD). Here we investigated the effect of GSH-LD on H2O2-induced cellular toxicity in undifferentiated and differentiated lymphoma U-937 and dopaminergic neuroblastoma SH-SY5Y cell lines, used respectively as models to study the involvement of macrophages/microglia and dopaminergic neurons in PD. We analyzed the effect of GSH-LD on apoptosis and cellular oxidative stress, both considered strategic targets for the prevention and treatment of neurodegenerative diseases. Compared to LD and GSH, GSH-LD had a stronger effect in preventing hydrogen peroxide (H2O2) induced apoptosis in both cell lines. Moreover, GSH-LD was able to preserve cell viability, cellular redox status, gluthation metabolism and prevent reactive oxygen species (ROS) formation, in a phosphinositide 3-kinase (PI3K)/kinase B (Akt)-dependent manner, in a neurotoxicity cellular model. Our findings indicate that the GSH-LD codrug offers advantages deriving from the additive effect of LD and GSH and it could represent a promising candidate for PD treatment.

scholarly journals Improvement of Cerebral Ischemia-Reperfusion Injury via Regulation of Apoptosis by Exosomes Derived from BDNF-Overexpressing HEK293

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Lizong Wang ◽  
Jinghan Jiang ◽  
Taofeng Zhou ◽  
Xiang Xue ◽  
Yongjun Cao
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Hek293 Cells ◽  
Neuroprotective Effects ◽  
In Vivo Experiments ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Induced Apoptosis

Brain-derived neurotrophic factor (BDNF) provides neuroprotective effects towards therapeutic cerebral ischemia-reperfusion (I/R) injury. This view has been proposed by more and more evidence. However, due to the lack of permeability of the blood-brain barrier (BBB) as well as the brief half-life in serum, clinical application is not widespread. To study the participation of exosomes containing BDNF in I/R, we isolated exosomes from BDNF-overexpressing HEK293. The protective outcomes of exosomes in hypoxia/reoxygenation (H/R) experiments were determined by the use of SY-5Y cells. Exosome-BDNF therapy restrained H/R-induced apoptosis by inhibition of the reducing levels of oxidative stress and calcium ions in the cells while maintaining stable levels of mitochondrial membrane potential in brain cells damaged by I/R. We then constructed a cerebral I/R injury model using SD rats to find the function of BDNF in exosome-mediated neuroprotection. The in vivo experiments conducted established that exosomes from BDNF-overexpressing HEK293 cells improved cerebral I/R injury by concealing neuronal apoptosis. Findings gained demonstrated that BDNF is a part of preventing cerebral I/R injury due to exosome mediation by regulating the cellular internal environment and inhibiting apoptosis.

scholarly journals Vitamin D and 17β-estradiol upregulate each other's receptors and regulating the AMPK/NF-κB pathway to relieve depressive-like behaviors in female ovariectomized rats

2019 ◽  
Author(s):  
Wen-yuan Zhang ◽  
Yujin Guo ◽  
Ke-yi Wang ◽  
Pei Jiang
Keyword(s):  
Vitamin D ◽  
Neuronal Damage ◽  
Chronic Administration ◽  
Ovariectomized Rats ◽  
Neuroprotective Effects ◽  
Ovx Rats ◽  
Increased Risk ◽  
17Β Estradiol ◽  
Induced Apoptosis ◽  
Control Sham

Abstract Background: A deficiency of vitamin D (VD) or 17β-estradiol (E2) is associated with increased risk of mood disorders such as depression in menopausal females, but the mechanism underlying is still elusive. The present study aims to evaluate whether vitamin D and 17β-estradiol could relieve a depressive-like state through neuroinflammatory regulation in ovariectomized (OVX) rats. Methods: Female SD rats were randomly divided into four groups, namely, control (SHAM), OVX, OVX+VD, and OVX+E2. The treatment procedure was performed for 10 weeks until sacrifice. Results: The chronic administration of vitamin D and 17β-estradiol showed anti-depressive-like activity in the OVX rats. Additionally, vitamin D and 17β-estradiol upregulated each other's receptors, including VDR, ERα, and ERβ in the hippocampus of OVX rats. Vitamin D and 17β-estradiol showed neuroprotective effects by decreasing OVX-induced apoptosis and neuronal damage, regulating the AMPK/NF-κB signaling pathway, and reducing the proinflammatory cytokines (IL-1β, IL-6, and TNFα), as well as iNOS and COX-2 in the hippocampus of OVX rats. Conclusions: The present study demonstrated that vitamin D and 17β-estradiol could upregulate each other's receptors and regulate the AMPK/NF-κB pathway to relieve the OVX-induced depressive-like state. The results should stimulate translational research towards the vitamin D potential for prevention or treatment of menopause-related depression.

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