Neuroprotective effect of propofol on necrosis and apoptosis following oxygen–glucose deprivation—Relationship between mitochondrial membrane potential and mode of death

2006 ◽  
Vol 1099 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Takehiko Iijima ◽  
Tatsuya Mishima ◽  
Kimio Akagawa ◽  
Yasuhide Iwao
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Neuroprotective Effect ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Mode Of Death

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.

scholarly journals Overexpression of Mitochondrial Hsp70/Hsp75 Protects Astrocytes against Ischemic Injury in vitro

2007 ◽  
Vol 28 (5) ◽  
pp. 1009-1016 ◽  
Author(s):  
Ludmila A Voloboueva ◽  
Melissa Duan ◽  
YiBing Ouyang ◽  
John F Emery ◽  
Christian Stoy ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Mitochondrial Membrane Potential ◽  
Heat Shock Protein 70 ◽  
Mitochondrial Membrane ◽  
Ischemic Injury ◽  
Glucose Deprivation ◽  
Hsp70 Family

Mitochondrial heat shock protein 70 (mtHsp70/Hsp75/Grp75/mortalin/TRAP-1/PBP74) is an essential mitochondrial chaperone and a member of the heat shock protein 70 (HSP70) family. Although many studies have shown the protective properties of overexpression of the cytosolic inducible member of the HSP70 family, Hsp72, few studies have investigated the protective potential of Hsp75 against ischemic injury. Mitochondria are one of the primary targets of ischemic injury in astrocytes. In this study, we analyzed the effects of Hsp75 overexpression on cellular levels of reactive oxygen species (ROS), mitochondrial membrane potential, ATP levels, and viability during the ischemia-like conditions of oxygen-glucose deprivation (OGD) or glucose deprivation (GD) in primary astrocytic cultures. We show that Hsp75 overexpression decreases ROS production and preserves mitochondrial membrane potential during GD, and preserves ATP levels and cell viability during OGD. These findings indicate that Hsp75 can provide protection against ischemia-like in vitro injury and suggest that it should be further studied as a potential candidate for protection against ischemic injury.

scholarly journals Neuroprotective Effects of Hesperidin, a Plant Flavanone, on Rotenone-Induced Oxidative Stress and Apoptosis in a Cellular Model for Parkinson’s Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Kuppusamy Tamilselvam ◽  
Nady Braidy ◽  
Thamilarasan Manivasagam ◽  
Musthafa Mohamed Essa ◽  
Nagarajan Rajendra Prasad ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Neuroprotective Effect ◽  
Neuroblastoma Cell ◽  
Ros Generation ◽  
Enzymatic Antioxidants ◽  
Neuroprotective Effects ◽  
Human Neuroblastoma ◽  
Cyt C

Rotenone a widely used pesticide that inhibits mitochondrial complex I has been used to investigate the pathobiology of PD bothin vitroandin vivo. Studies have shown that the neurotoxicity of rotenone may be related to its ability to generate reactive oxygen species (ROS), leading to neuronal apoptosis. The current study was carried out to investigate the neuroprotective effects of hesperidin, a citrus fruit flavanol, against rotenone-induced apoptosis in human neuroblastoma SK-N-SH cells. We assessed cell death, mitochondrial membrane potential, ROS generation, ATP levels, thiobarbituric acid reactive substances, reduced glutathione (GSH) levels, and the activity of catalase, superoxide dismutase (SOD) and glutathione peroxidase (GPx) using well established assays. Apoptosis was determined in normal, rotenone, and hesperidin treated cells, by measuring the protein expression of cytochrome c (cyt c), caspases 3 and 9, Bax, and Bcl-2 using the standard western blotting technique. The apoptosis in rotenone-induced SK-N-SH cells was accompanied by the loss of mitochondrial membrane potential, increased ROS generation, the depletion of GSH, enhanced activities of enzymatic antioxidants, upregulation of Bax, cyt c, and caspases 3 and 9, and downregulation of Bcl-2, which were attenuated in the presence of hesperidin. Our data suggests that hesperidin exerts its neuroprotective effect against rotenone due to its antioxidant, maintenance of mitochondrial function, and antiapoptotic properties in a neuroblastoma cell line.

scholarly journals Neuroprotective Effect of Tea Polyphenols on Oxyhemoglobin Induced Subarachnoid Hemorrhage in Mice

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Haizhen Mo ◽  
Ying Chen ◽  
Liyong Huang ◽  
Hao Zhang ◽  
Juxiang Li ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Subarachnoid Hemorrhage ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Neuroprotective Effect ◽  
Tea Polyphenols ◽  
Early Event ◽  
Atp Content ◽  
Neuroprotective Effects

Tea polyphenols are of great benefit to the treatment of several neurodegenerative diseases. In order to explore the neuroprotective effects of tea polyphenols and their potential mechanisms, an establishedin vivosubarachnoid hemorrhage (SAH) model was used and alterations of mitochondrial function, ATP content, and cytochromec(cytc) in cerebral cortex were detected. This study showed that the alteration of mitochondrial membrane potential was an early event in SAH progression. The trend of ATP production was similar to that of mitochondrial membrane potential, indicating that the lower the mitochondrial membrane potential, lesser the ATP produced. Due to mitochondrial dysfunction, more cytcwas released in the SAH group. Interestingly, the preadministration of tea polyphenols significantly rescued the mitochondrial membrane potential to basal level, as well as the ATP content and the cytclevel in the brain cortex 12 h after SAH. After pretreatment with tea polyphenols, the neurological outcome was also improved. The results provide strong evidence that tea polyphenols enhance neuroprotective effects by inhibiting polarization of mitochondrial membrane potential, increasing ATP content, and blocking cytcrelease.

scholarly journals Electrophysiological Activity and Survival Rate of Rats Nervous Tissue Cells Depends on D/H Isotopic Composition of Medium

Molecules ◽  
2021 ◽  
Vol 26 (7) ◽  
pp. 2036
Author(s):  
Stanislav Kozin ◽  
Vladimir Skrebitsky ◽  
Rodion Kondratenko ◽  
Alexander Kravtsov ◽  
Elena Butina ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Membrane Potential ◽  
Mitochondrial Membrane Potential ◽  
Temperature Stress ◽  
Incubation Medium ◽  
Mitochondrial Membrane ◽  
Glucose Deprivation ◽  
Deuterium Content ◽  
Oxygen Species ◽  
Cell Energy

The deuterium content modification in an organism has a neuroprotective effect during the hypoxia model, affecting anxiety, memory and stress resistance. The aim of this work was to elucidate the possible mechanisms of the medium D/H composition modification on nerve cells. We studied the effect of an incubation medium with a 50 ppm deuterium content compared to a medium with 150 ppm on: (1) the activity of Wistar rats’ hippocampus CA1 field neurons, (2) the level of cultured cerebellar neuron death during glucose deprivation and temperature stress, (3) mitochondrial membrane potential (MMP) and the generation of reactive oxygen species in cultures of cerebellar neurons. The results of the analysis showed that the incubation of hippocampal sections in a medium with a 50 ppm deuterium reduced the amplitude of the pop-spike. The restoration of neuron activity was observed when sections were returned to the incubation medium with a 150 ppm deuterium content. An environment with a 50 ppm deuterium did not significantly affect the level of reactive oxygen species in neuron cultures, while MMP decreased by 16–20%. In experiments with glucose deprivation and temperature stress, the medium with 50 ppm increased the death of neurons. Thus, a short exposure of nerve cells in the medium with 50 ppm deuterium acts as an additional stressful factor, which is possibly associated with the violation of the cell energy balance. The decrease in the mitochondrial membrane potential, which is known to be associated with ATP synthesis, indicates that this effect may be associated with the cell energy imbalance. The decrease in the activity of the CA1 field hippocampal neurons may reflect reversible adaptive changes in the operation of fast-reacting ion channels.

scholarly journals Circ_0030235 knockdown protects H9c2 cells against OGD/R-induced injury via regulation of miR-526b

PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e11482
Author(s):  
Yuquan Zhang ◽  
Shuzhu Liu ◽  
Limin Ding ◽  
Dawei Wang ◽  
Qiangqiang Li ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Cell Viability ◽  
Mitochondrial Membrane Potential ◽  
Mitochondrial Membrane ◽  
Cell Injury ◽  
Glucose Deprivation ◽  
Luciferase Reporter ◽  
Circular Rnas ◽  
H9c2 Cells ◽  
Related Factors

Backgrounds Acute myocardial infarction (MI) is the common clinical manifestation of coronary heart disease. Circular RNAs (circRNAs) act key roles in cardiomyocytes growth and angiogenesis. However, their functions in MI are not entirely clear. This research intended to investigate the role and underlying mechanisms of circ_0030235 in H9c2 cells. Methods H9c2 cells were conducted to oxygen glucose deprivation/reperfusion (OGD/R) inducement to establish the MI model. Circ_0030235 and miR-526b expression was tested and altered by qRT-PCR and transfection. Cell viability, apoptosis and reactive oxygen species (ROS) injury were tested by CCK-8 assay, TUNEL assay kit, and ROS Detection Assay Kit, respectively. Assessment of cell injury-related factors was performed by employing ELISA, Mitochondrial Viability Staining and the JC-1-Mitochondrial Membrane Potential Assay Kit. The relationship between circ_0030235 and miR-526b was analyzed by dual luciferase reporter assay. The expression of key proteins was analyzed by western blot. Results Circ_0030235 was highly expressed in OGD/R-induced H9c2 cells. OGD/R inducement cell viability, while accelerated apoptosis. Besides, the level ROS, cell injury-related factors, mitochondrial membrane potential were notably elevated by OGD/R inducement, while mitochondrial viability was remarkably declined. Whereas, these impacts were all noticeably remitted by circ_0030235 knockdown. miR-526b was a target of circ_0030235. Circ_0030235 knockdown-induced impacts were all notably abrogated by miR-526b inhibition, including the activating impacts on PI3K/AKT and MEK/ERK pathways. Conclusions This research implied that circ_0030235 knockdown might remit OGD/R-induced impacts via activation of PI3K/AKT and MEK/ERK pathways and regulation of miR-526b.

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