scholarly journals STUDY OF THE NEUROPROTECTIVE EFFECT OF ALPHA LIPOIC ACID ON ACRYLONITRILE INDUCED CELLULAR & MITOCHONDRIAL DYSFUNCTION BY ENHANCEMENT OF OXIDATIVE STRESS IN RAT HIPPOCAMPUS MAPPING.

2016 ◽  
Vol 4 (11) ◽  
pp. 1376-1385
Author(s):  
Kumar Sunil ◽  
◽  
SharmaAshish Kumar. ◽  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Lipoic Acid ◽  
Neuroprotective Effect ◽  
Rat Hippocampus ◽  
Alpha Lipoic Acid

scholarly journals Neurotherapeutic Effect of Inula britannica var. Chinensis against H2O2-Induced Oxidative Stress and Mitochondrial Dysfunction in Cortical Neurons

Antioxidants ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 375
Author(s):  
Jin Young Hong ◽  
Hyunseong Kim ◽  
Junseon Lee ◽  
Wan-Jin Jeon ◽  
Seung Ho Baek ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cortical Neurons ◽  
Inflammatory Diseases ◽  
Neuroprotective Effect ◽  
Neuroprotective Effects ◽  
Neuronal Viability ◽  
Inula Britannica ◽  
Oxidative Effects

Inula britannica var. chinensis (IBC) has been used as a traditional medicinal herb to treat inflammatory diseases. Although its anti-inflammatory and anti-oxidative effects have been reported, whether IBC exerts neuroprotective effects and the related mechanisms in cortical neurons remain unknown. In this study, we investigated the effects of different concentrations of IBC extract (5, 10, and 20 µg/mL) on cortical neurons using a hydrogen peroxide (H2O2)-induced injury model. Our results demonstrate that IBC can effectively enhance neuronal viability under in vitro-modeled reaction oxygen species (ROS)-generating conditions by inhibiting mitochondrial ROS production and increasing adenosine triphosphate level in H2O2-treated neurons. Additionally, we confirmed that neuronal death was attenuated by improving the mitochondrial membrane potential status and regulating the expression of cytochrome c, a protein related to cell death. Furthermore, IBC increased the expression of brain-derived neurotrophic factor and nerve growth factor. Furthermore, IBC inhibited the loss and induced the production of synaptophysin, a major synaptic vesicle protein. This study is the first to demonstrate that IBC exerts its neuroprotective effect by reducing mitochondria-associated oxidative stress and improving mitochondrial dysfunction.

scholarly journals Dual Specificity Phosphatase 6 Protects Neural Stem Cells from β-Amyloid-Induced Cytotoxicity through ERK1/2 Inactivation

Biomolecules ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 181 ◽  
Author(s):  
Wang Liao ◽  
Yuqiu Zheng ◽  
Wenli Fang ◽  
Shaowei Liao ◽  
Ying Xiong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Neural Stem Cells ◽  
Western Blot ◽  
Mitochondrial Dysfunction ◽  
Neuroprotective Effect ◽  
Dependent Manner ◽  
Dual Specificity Phosphatase ◽  
Cell Vitality ◽  
Dual Specificity

Alzheimer’s disease (AD) is a devastating neurodegenerative disease with limited treatment options and no cure. Beta-amyloid (Aβ) is a hallmark of AD that has potent neurotoxicity in neural stem cells (NSCs). Dual specificity phosphatase 6 (DUSP6) is a member of the mitogen-activated protein kinases (MAPKs), which is involved in regulating various physiological and pathological processes. Whether DUSP6 has a protective effect on Aβ-induced NSC injury remains to be explored. C17.2 neural stem cells were transfected with DUSP6-overexpressed plasmid. NSCs with or without DUSP6 overexpression were administrated with Aβ25–35 at various concentrations (i.e., 0, 2.5, 5 μM). DUSP6 expression after Aβ treatment was detected by Real-Time Polymerase Chain Reaction (RT-PCR) and Western blot and cell vitality was examined by the CCK8 assay. The oxidative stress (intracellular reactive oxygen species (ROS) and malondialdehyde (MDA)), endoplasmic reticulum stress (ER calcium level) and mitochondrial dysfunction (cytochrome c homeostasis) were tested. The expression of p-ERK1/2 and ERK1/2 were assayed by Western blot. Our results showed that Aβ decreased the expression of DUSP6 in a dose-dependent manner. The overexpression of DUSP6 increased the cell vitality of NSCs after Aβ treatment. Oxidative stress, ER stress, and mitochondrial dysfunction induced by Aβ could be restored by DUSP6 overexpression. Additionally, the Aβ-induced ERK1/2 activation was reversed. In summary, DUSP6 might have a neuroprotective effect on Aβ-induced cytotoxicity, probably via ERK1/2 activation.

Alpha-lipoic acid and coenzyme Q10 combination ameliorates experimental diabetic neuropathy by modulating oxidative stress and apoptosis

Life Sciences ◽  
2019 ◽  
Vol 216 ◽  
pp. 101-110 ◽  
Author(s):  
Nasrin Sadeghiyan Galeshkalami ◽  
Mohammad Abdollahi ◽  
Rezvan Najafi ◽  
Maryam Baeeri ◽  
Akram Jamshidzade ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Neuropathy ◽  
Lipoic Acid ◽  
Coenzyme Q10 ◽  
Alpha Lipoic Acid ◽  
Experimental Diabetic Neuropathy

Alpha-lipoic acid defends homocysteine-induced endoplasmic reticulum and oxidative stress in HAECs

2016 ◽  
Vol 80 ◽  
pp. 63-72 ◽  
Author(s):  
Huimin Hu ◽  
Changyuan Wang ◽  
Yue Jin ◽  
Qiang Meng ◽  
Qi Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Lipoic Acid ◽  
Alpha Lipoic Acid ◽  
And Oxidative Stress

scholarly journals The role of oxidative stress and effect of alpha-lipoic acid in reexpansion pulmonary edema – an experimental study

2010 ◽  
Vol 6 ◽  
pp. 848-853 ◽  
Author(s):  
Seyfettin Gumus ◽  
Orhan Yucel ◽  
Mehmet Gamsizkan ◽  
Ayse Eken ◽  
Omer Deniz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Experimental Study ◽  
Pulmonary Edema ◽  
Lipoic Acid ◽  
Alpha Lipoic Acid ◽  
Reexpansion Pulmonary Edema

scholarly journals Alpha-Lipoic Acid Protects Rat Kidney Against Oxidative Stress-Mediated DNA Damage and Apoptosis Induced by Lead

2015 ◽  
Vol 6 (1) ◽  
pp. 1-14 ◽  
Author(s):  
Samy Ali Hussein ◽  
Mohamed Ragaa R. Hassanein ◽  
Aziza Amin ◽  
Asmaa H. Mohammad Hussein
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Lipoic Acid ◽  
Rat Kidney ◽  
Alpha Lipoic Acid

scholarly journals Oxidative Stress in 5/6 Nephrectomized Rat Model: Effect of Alpha-Lipoic Acid

Renal Failure ◽  
2012 ◽  
Vol 34 (7) ◽  
pp. 907-914 ◽  
Author(s):  
Xiaofang Yu ◽  
Hong Liu ◽  
Jianzhou Zou ◽  
Jiaming Zhu ◽  
Xunhui Xu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipoic Acid ◽  
Rat Model ◽  
Alpha Lipoic Acid

Activity of Alpha-Lipoic Acid in the Protection against Oxidative Stress in Skin

2000 ◽  
pp. 43-51 ◽  
Author(s):  
M. Podda ◽  
T.M. Zollner ◽  
M. Grundmann-Kollmann ◽  
J.J. Thiele ◽  
L. Packer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipoic Acid ◽  
Alpha Lipoic Acid

Alpha-Lipoic Acid Prevents Atrial Electrical and Structural Remodeling via Inhibition of NADPH Oxidase in a Rabbit Rapid Atrial Pacing Model

2020 ◽  
Author(s):  
Lei Chen ◽  
Wensu Chen ◽  
Yao Zhang ◽  
Zhirong Wang
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Western Blot ◽  
Lipoic Acid ◽  
Right Atrial ◽  
Atrial Pacing ◽  
Alpha Lipoic Acid ◽  
Model Group ◽  
Structural Remodeling ◽  
Masson Staining

Abstract Background The pathogenesis of atrial fibrillation(AF) is complex, and the treatment method is still not satisfactory. A rapid atrial pacing (RAP) model was constructed to study the effects of alpha-lipoic acid (ALA) on electrical and structural remodeling, as well as its possible mechanism in rabbits.Methods A total of 30 rabbits were randomly divided into a sham-operated group (SHAM group), a rapid atrial pacing model group (RAP group) and an alpha-lipoic acid+rapid atrial pacing model group (ALA+RAP group). Their right atriums were paced at a speed of 600 beats/min for 12 h in the RAP and ALA+RAP groups, and the atrial effective refractory period (AERP) and AERP frequency adaptability were determined during the pace. In each group, malondialdehyde (MDA), superoxide dismutase (SOD) and reactive oxygen species (ROS) were detected to observe the effects of oxidative stress. The pathological structure of the atrial tissue was observed through HE and Masson staining. Ultrastructural changes in the atrial myocytes were observed by transmission electron microscopy (TEM), and the expression levels of Nox2 and Nox4 were detected by immunohistochemistry, western blot and ELISA.Results Through testing AERP and AERP frequency adaptability, it was found that in the early stage of rapid atrial pacing, AERP gradually shortened, while ALA injection could remarkably delay this process. Correspondingly, AERP frequency adaptability in the RAP group was reduced, and ALA could enhance it. HE staining showed that pathological changes in the ALA+RAP group were milder than those in the RAP group. And it was found that in the ALA+RAP group, the deposition of collagen in the endomysium was remarkably reduced via Masson staining. Ultrastructure injury in the ALA+RAP group showed various degrees of improvement compared with the RAP group. RAP was accompanied by an increase in oxidative stress levels, and ALA could effectively inhibit RAP-induced oxidative stress in vivo via detecting SOD, MDA and ROS. In addition, Western blot showed that the expression of NOX2 and NOX4 was upregulated in RAP group, but ALA intervention could inhibit their expression. Moreover, immunohistochemistry and ELISA also got similar results as Western blot.Conclusion ALA can inhibit atrial electrical remodeling and structural remodeling by reducing ROS production and alleviating oxidative stress injury induced by rapid right atrial pacing, and its mechanism may be related to inhibiting the activity of NADPH oxidase.

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