scholarly journals The New Inhibitor of Monoamine Oxidase, M30, has a Neuroprotective Effect Against Dexamethasone-Induced Brain Cell Apoptosis

2010 ◽  
Vol 4 ◽  
Author(s):  
Shakevia Johnson ◽  
Shawna Tazik ◽  
Deyin Lu ◽  
Chandra Johnson ◽  
Moussa B. H. Youdim ◽  
...  
Keyword(s):  
Monoamine Oxidase ◽  
Cell Apoptosis ◽  
Neuroprotective Effect ◽  
Brain Cell

scholarly journals Artemisinin attenuated oxidative stress and apoptosis by inhibiting autophagy in MPP+-treated SH-SY5Y cells

2021 ◽  
Vol 28 (1) ◽  
Author(s):  
Junqiang Yan ◽  
Hongxia Ma ◽  
Xiaoyi Lai ◽  
Jiannan Wu ◽  
Anran Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Membrane Potential ◽  
Protein Expression ◽  
Mitochondrial Membrane Potential ◽  
Western Blotting ◽  
Cell Apoptosis ◽  
Mitochondrial Membrane ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects

Abstract Background Parkinson’s disease (PD) is the second most common neurodegenerative disease after Alzheimer's disease. The oxidative stress is an important component of the pathogenesis of PD. Artemisinin (ART) has antioxidant and neuroprotective effects. The purpose of this study is to explore the neuroprotective effect of ART on 1-methyl-4-phenyliodine iodide (MPP +)-treated SH-SY5Y cells and underlying mechanism. Methods We used MPP+-treated SH-SY5Y cells to study the neuroprotective effect of ART. Cell viability was measured by MTT assay after incubating the cells with MPP+ and/or ART for 24 h. DCFH-DA was used to detect the level of intracellular reactive oxygen species (ROS), and WST-8 was used to detect the level of superoxide dismutase (SOD). The level of intracellular reduced glutathione (GSH) was detected with 5,5΄-dithiobis-(2-nitrobenzoic acid), and the level of malondialdehyde (MDA) was assessed based on the reaction of MDA and thiobarbituric acid. A mitochondrial membrane potential detection kit (JC-1) was used to detect changes in the mitochondrial membrane potential (MMP), and an Annexin V-FITC cell apoptosis kit was used to detect cell apoptosis. The expression levels of caspase-3, cleaved caspase-3 and the autophagy-related proteins LC3, beclin-1, and p62 were detected by Western blotting. In addition, to verify the change in autophagy, we used immunofluorescence to detect the expression of LC3 and p62. Results No significant cytotoxicity was observed at ART concentrations up to 40 μM. ART could significantly increase the viability of SH-SY5Y cells treated with MPP+ and reduce oxidative stress damage and apoptosis. In addition, the Western blotting and immunofluorescence results showed that MPP+ treatment could increase the protein expression of beclin1 and LC3II/LC3I and decrease the protein expression of p62, indicating that MPP+ treatment could induce autophagy. Simultaneous treatment with ART and MPP+ could decrease the protein expression of beclin1 and LC3II/LC3I and increase the protein expression of p62, indicating that ART could decrease the level of autophagy induced by MPP+. Conclusion Our results indicate that ART has a protective effect on MPP+-treated SH-SY5Y cells by the antioxidant, antiapoptotic activities and inhibition of autophagy. Our findings may provide new hope for the prevention and treatment of PD.

Dexamethasone reduces brain cell apoptosis and inhibits inflammatory response in rats with intracerebral hemorrhage

2014 ◽  
Vol 93 (1) ◽  
pp. 178-188 ◽  
Author(s):  
I-Neng Lee ◽  
Wan-Chun Cheng ◽  
Chiu-Yen Chung ◽  
Ming-Hsueh Lee ◽  
Martin Hsiu-Chu Lin ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Intracerebral Hemorrhage ◽  
Cell Apoptosis ◽  
Brain Cell

scholarly journals Brain cell apoptosis inhibition by butylphthalide in Alzheimer's disease model in rats

2017 ◽  
Vol 13 (6) ◽  
pp. 2771-2774 ◽  
Author(s):  
Fu-Xia Song ◽  
Li Wang ◽  
Hong Liu ◽  
Ying-Li Wang ◽  
Yong Zou
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Apoptosis ◽  
Disease Model ◽  
Brain Cell ◽  
Apoptosis Inhibition

scholarly journals Diazoxide Attenuates Postresuscitation Brain Injury in a Rat Model of Asphyxial Cardiac Arrest by Opening Mitochondrial ATP-Sensitive Potassium Channels

2016 ◽  
Vol 2016 ◽  
pp. 1-6 ◽  
Author(s):  
Haidong Wu ◽  
Peng Wang ◽  
Yi Li ◽  
Manhui Wu ◽  
Jiali Lin ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Brain Injury ◽  
Cell Apoptosis ◽  
Brain Cell ◽  
Vehicle Group ◽  
Control Group ◽  
Tunel Staining ◽  
Sham Operation ◽  
Sprague Dawley ◽  
Mitokatp Channels

Objective. We investigated whether and how diazoxide can attenuate brain injury after cardiopulmonary resuscitation (CPR) by selective opening of mitochondrial ATP-sensitive potassium (mitoKATP) channels.Methods. Adult male Sprague-Dawley rats with induced cerebral ischemia (n=10per group) received an intraperitoneal injection of 0.1% dimethyl sulfoxide (1 mL; vehicle group), diazoxide (10 mg/kg; DZ group), or diazoxide (10 mg/kg) plus 5-hydroxydecanoate (5 mg/kg; DZ + 5-HD group) 30 min after CPR. The control group (sham group,n=5) underwent sham operation, without cardiac arrest. Mitochondrial respiratory control rate (RCR) was determined. Brain cell apoptosis was assessed using TUNEL staining. Expression of Bcl-2, Bax, and protein kinase C epsilon (PKCε) in the cerebral cortex was determined by Western blotting and immunohistochemistry.Results. The neurological deficit scores (NDS) in the vehicle group decreased significantly at 24 h and 48 h after CPR. Diazoxide significantly improved NDS and mitochondrial RCR after CPR at both time points; 5-HD cotreatment abolished these effects. Diazoxide decreased TUNEL-positive cells following CPR, upregulated Bcl-2 and PKCε, downregulated Bax, and increased the Bcl-2/Bax ratio; 5-HD cotreatment reversed these effects.Conclusions. Diazoxide attenuates postresuscitation brain injury, protects mitochondrial function, inhibits brain cell apoptosis, and activates the PKC pathway by opening mitoKATP channels.

scholarly journals Calreticulin Binds to Fas Ligand and Inhibits Neuronal Cell Apoptosis Induced by Ischemia-Reperfusion Injury

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Beilei Chen ◽  
Zhengzheng Wu ◽  
Jun Xu ◽  
Yun Xu
Keyword(s):  
Reperfusion Injury ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Fas Ligand ◽  
Ischemia Reperfusion Injury ◽  
Early Stage ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Neuronal Cell ◽  
Caspase 8

Background. Calreticulin (CRT) can bind to Fas ligand (FasL) and inhibit Fas/FasL-mediated apoptosis of Jurkat T cells. However, its effect on neuronal cell apoptosis has not been investigated.Purpose. We aimed to evaluate the neuroprotective effect of CRT following ischemia-reperfusion injury (IRI).Methods. Mice underwent middle cerebral artery occlusion (MCAO) and SH-SY5Y cells subjected to oxygen glucose deprivation (OGD) were used as models for IRI. The CRT protein level was detected by Western blotting, and mRNA expression of CRT, caspase-3, and caspase-8 was measured by real-time PCR. Immunofluorescence was used to assess the localization of CRT and FasL. The interaction of CRT with FasL was verified by coimmunoprecipitation. SH-SY5Y cell viability was determined by MTT assay, and cell apoptosis was assessed by flow cytometry. The measurement of caspase-8 and caspase-3 activity was carried out using caspase activity assay kits.Results. After IRI, CRT was upregulated on the neuron surface and bound to FasL, leading to increased viability of OGD-exposed SH-SY5Y cells and decreased activity of caspase-8 and caspase-3.Conclusions. This study for the first time revealed that increased CRT inhibited Fas/FasL-mediated neuronal cell apoptosis during the early stage of ischemic stroke, suggesting it to be a potential protector activated soon after IRI.

scholarly journals Acupuncture at Baihui and Dazhui reduces brain cell apoptosis in heroin readdicts

2014 ◽  
Vol 9 (2) ◽  
pp. 164 ◽  
Author(s):  
Xiaoge Song ◽  
Xiaorong Hou ◽  
Rongjun Zhang ◽  
Hang Lv ◽  
Xinghui Cai ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Brain Cell

scholarly journals Endosulfan Increases IL-1β, IL-6, IL-17, and TNF-α Production in Pregnant Rats and Causes Fetal Brain Cell Apoptosis

2019 ◽  
Vol 17 (2) ◽  
pp. 103-112
Author(s):  
Sri ANDARINI ◽  
Asmika MADJRI ◽  
Hidayat SUJUTI ◽  
Romi ROMI ◽  
Adi Surya PRATAMA ◽  
...  
Keyword(s):  
Cell Apoptosis ◽  
Organic Pollutant ◽  
Fetal Brain ◽  
Annexin V ◽  
Negative Control ◽  
Brain Cell ◽  
Rat Serum ◽  
Pregnant Rats ◽  
Group I ◽  
Tnf Α

Endosulfan is a persistent organic pollutant commonly used as an insecticide in Indonesia. It has been reported to cause teratogenic effects, i.e., to decrease humoral activity, produce inflammation, and induce apoptosis in various type of cells. This study investigated the effect of endosulfan on the expression of IL-1β, IL-6, IL-17, and TNF-α in rats (Rattus norvegicus), as well as the incidence of fetal brain cell apoptosis. This experiment was carried out on pregnant rats divided into 4 groups: negative control (I), endosulfan: 1 mg/kg (II), 10 mg/kg (III), and 50 mg/kg (IV). The solution of endosulfan was given daily during the 20-day test period. Rat serum was collected for the measurement of IL-1β, IL-6, IL-17, and TNF-α using the ELISA kit. Fetal rat brains were taken and stained with Annexin V for apoptosis detection. The proinflammatory cytokine levels in Groups II, III, and IV were higher than in Group I, with significant increases of IL-1β (p = 0.016), IL-6 (p = 0.009), IL-17 (p < 0.001), and TNF-α (p < 0.001). The intensity of Annexin V in 4 groups of rats showed that the incidence of apoptosis increased with increasing endosulfan doses. In conclusion, the administration of endosulfan in pregnant rats increased the expression of IL-1β, IL-6, IL-17, and TNF-α and triggered apoptosis in fetal brain cells.

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