scholarly journals Effects of Panthenol and N-Acetylcysteine on Changes in the Redox State of Brain Mitochondria under Oxidative Stress In Vitro

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1699
Author(s):  
Dmitry S. Semenovich ◽  
Egor Yu. Plotnikov ◽  
Oksana V. Titko ◽  
Elena P. Lukiyenko ◽  
Nina P. Kanunnikova
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Redox Potential ◽  
Brain Mitochondria ◽  
Neuroprotective Activity ◽  
Protective Effects ◽  
Glutathione System ◽  
Mitochondrial Energy Metabolism ◽  
The Brain

The glutathione system in the mitochondria of the brain plays an important role in maintaining the redox balance and thiol–disulfide homeostasis, whose violations are the important component of the biochemical shifts in neurodegenerative diseases. Mitochondrial dysfunction is known to be accompanied by the activation of free radical processes, changes in energy metabolism, and is involved in the induction of apoptotic signals. The formation of disulfide bonds is a leading factor in the folding and maintenance of the three-dimensional conformation of many specific proteins that selectively accumulate in brain structures during neurodegenerative pathology. In this study, we estimated brain mitochondria redox status and functioning during induction of oxidative damage in vitro. We have shown that the development of oxidative stress in vitro is accompanied by inhibition of energy metabolism in the brain mitochondria, a shift in the redox potential of the glutathione system to the oxidized side, and activation of S-glutathionylation of proteins. Moreover, we studied the effects of pantothenic acid derivatives—precursors of coenzyme A (CoA), primarily D-panthenol, that exhibit high neuroprotective activity in experimental models of neurodegeneration. Panthenol contributes to the significant restoration of the activity of enzymes of mitochondrial energy metabolism, normalization of the redox potential of the glutathione system, and a decrease in the level of S-glutathionylated proteins in brain mitochondria. The addition of succinate and glutathione precursor N-acetylcysteine enhances the protective effects of the drug.

scholarly journals Energy metabolism and redox status of the glutathione system in experimental brain ischemia and its correction by metabolic neuroprotectors

2021 ◽  
Vol 18 (3) ◽  
pp. 274-283
Author(s):  
O. V. Titko ◽  
E. P. Lukiyenko ◽  
E. F. Raduta ◽  
D. S. Semenovich ◽  
A. A. Vasilevich ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Redox Potential ◽  
Carotid Arteries ◽  
Free Radical Oxidation ◽  
Pentose Phosphate ◽  
Oxidation Products ◽  
Glutathione System ◽  
Corrective Effect ◽  
The Brain

The changes in the parameters of oxidative stress, energy metabolism, and redox potential of the glutathione system in the rat brain following cerebral ischemia were studied. To correct metabolic disorders, the pantothenic acid derivatives were used in combination with precursors of glutathione biosynthesis and selenium substances.Cerebral ischemia was modeled by ligating the both common carotid arteries in rats for 2 h. Drugs were administered i.p. in the following doses: panthenol – 400 mg/kg, N-acetylcysteine – 150, nanoselen – 1 mg/kg, three times: 1 h before ligation of the carotid arteries, at the time of ligation and 1 hour after ligation. We showed that the development of oxidative stress caused by ischemia is accompanied by the changes in the parameters of energy metabolism and the pentose phosphate pathway in the cerebral hemispheres. Simultaneously, there are a decrease in the GSH level, an increase in the GSSG content, a decrease in the GSH/GSSG ratio, and the activation of enzymes of redox transformations of glutathione.The redox potential of the glutathione system decreases and shifts towards oxidation, while the level of S-glutathionylated proteins increases. Thus, the value of the GSH/GSSG ratio and the protein glutathionylation intensity are the sensitive indicators of the redox potential in the brain tissue and can be used as markers of the extent of changes in the redox balance. The panthenol injection to animals leads to a decrease in the content of free radical oxidation products, violations of oxidative phosphorylation and restoration of thiol-disulfide balance in the brain. When panthenol is administered together with N-acetylcysteine and nanoselen, the corrective effect of panthenol is enhanced.

scholarly journals Homeoprotein neuroprotection of embryonic neuronal cells

2019 ◽  
Author(s):  
Stephanie E. Vargas Abonce ◽  
Mélanie Leboeuf ◽  
Alain Prochiantz ◽  
Kenneth L. Moya
Keyword(s):  
Oxidative Stress ◽  
Ganglion Cells ◽  
Neuronal Cells ◽  
Neuroprotective Activity ◽  
Live Cells ◽  
Protective Effects ◽  
Striatal Neurons ◽  
Dna Breaks ◽  
Embryonic Neurons

ABSTRACTMost homeoprotein transcription factors have a highly conserved internalization domain used in intercellular transfer. Internalization of homeoproteins ENGRAILED1 or ENGRAILED2 promotes the survival of adult dopaminergic cells, whereas that of OTX2 protects adult retinal ganglion cells. Here we characterize the in vitro neuroprotective activity of several homeoproteins in response to H2O2. Protection is observed with ENGRAILED1, ENGRAILED2, OTX2, GBX2 and LHX9 on midbrain and striatal embryonic neurons whereas cell-permeable c-MYC shows no protective effects. Therefore, five homeoproteins belonging to 3 different classes (ANTENNAPEDIA, PAIRED and LIM) share the ability to protect embryonic neurons from midbrain and striatum. Because midbrain and striatal neurons do not express the same repertoire of the 4 proteins, a lack of neuronal specificity together with a general protective activity can be proposed. In contrast, hEN1 and GBX2 exerted no protection on non-neuronal cells including mouse embryo fibroblasts, macrophages or HeLa cells. For the 4 proteins, protection against cell-death correlated with a reduction in the number of H2O2-induced DNA break foci in midbrain and striatal neurons. In conclusion, within the limit of the number of cell types and homeoproteins tested, homeoprotein protection against oxidative stress-induced DNA breaks and death is specific to neurons but shows no homeoprotein or neuronal type specificity.SIGNIFICANCE STATEMENTHomeoproteins are DNA binding proteins regulating gene expression throughout life. Many of them transfer between cells and are thus internalized by live cells. This has allowed for their use as therapeutic proteins in animal models of Parkinson disease and glaucoma. Part of their therapeutic activity is through a protection against neuronal death. Here we show that internalized homeoproteins from three different classes protect embryonic ventral midbrain and striatal neurons from oxidative stress, both at the level of DNA damage and survival. The interest of this finding is that it lends weight to the possibility that many homeoproteins play a role in neuroprotection through shared mechanisms involving, in particular, DNA protection against stress-induced breaks.

Oxidative stress in the brain of nicotine-induced toxicity: protective role of Andrographis paniculata Nees and vitamin E

2009 ◽  
Vol 34 (2) ◽  
pp. 124-135 ◽  
Author(s):  
Subhasis Das ◽  
N. Gautam ◽  
Sankar Kumar Dey ◽  
Tarasankar Maiti ◽  
Somenath Roy
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vitamin E ◽  
Body Mass ◽  
Brain Mitochondria ◽  
Brain Regions ◽  
Protective Role ◽  
Andrographis Paniculata ◽  
Protective Effects ◽  
The Brain

Mitochondria are the crossroads of several crucial cellular activities; they produce considerable quantities of superoxide radical and hydrogen peroxide, which can damage important macromolecules. Nicotine affects a variety of cellular processes, from induction of gene expression to modulation of enzymatic activities. The aim of this study was to elucidate the protective effects of andrographolide (ANDRO) aqueous extract (AE-Ap) of Andrographis paniculata, and vitamin E on nicotine-induced brain mitochondria. In this investigation, nicotine (1 mg·kg body mass–1·day–1) was treated, for the period of 7 days, simultaneously with 2 A. paniculata products, ANDRO and AE-Ap (250 mg·kg body mass–1·day–1); and vitamin E (50 mg·kg body mass–1·day–1) was supplemented in different group of male Wistar rats. The activities of mitochondrial electron transport chain (Mito–ETC) complexes (I, II, III), nitric oxide production, superoxide anion, catalase, glutathione reductase, glutathione peroxidase, glutathione-S-transferase, and concentrations of reduced glutathione and oxidized glutathione were measured in discrete regions of brain (the cerebral hemisphere, cerebellum, diencephalons, and brain stem). The study revealed that nicotine inhibits the Mito–ETC complexes and produces nitric oxide, which suppressed the mitochondrial oxidative stress scavenger system in different brain regions. In these circumstances, lipid peroxidation and protein oxidation were noted in different discrete regions of brain mitochondria. ANDRO, AE-Ap, and vitamin E showed the protective potentiality against nicotine toxicity. The analysis of such alterations is important in determining the basis of normal dysfunction in the brain associated with nicotine toxicity, which could be ameliorated by A. paniculata and vitamin E, and may help to develop therapeutic means against nicotine-induced disorders.

scholarly journals RNA-Seq Profiling to Investigate the Mechanism of Qishen Granules on Regulating Mitochondrial Energy Metabolism of Heart Failure in Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Hao He ◽  
Changxiang Li ◽  
Xiangyu Lu ◽  
Yanqin Li ◽  
Xuan Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Energy Metabolism ◽  
Cardiac Function ◽  
Mitochondrial Dysfunction ◽  
Structural Integrity ◽  
Mitochondrial Morphology ◽  
Rna Seq ◽  
Mitochondrial Energy Metabolism ◽  
Myocardial Oxidative Stress

Background. Qishen granules (QSG) are a frequently prescribed formula with cardioprotective properties prescribed to HF for many years. RNA-seq profiling revealed that regulation on cardiac mitochondrial energy metabolism is the main therapeutic effect. However, the underlying mechanism is still unknown. In this study, we explored the effects of QSG on regulating mitochondrial energy metabolism and oxidative stress through the PGC-1α/NRF1/TFAM signaling pathway. RNA-seq technology revealed that QSG significantly changed the differential gene expression of mitochondrial dysfunction in myocardial ischemic tissue. The mechanism was verified through the left anterior descending artery- (LAD-) induced HF rat model and oxygen glucose deprivation/recovery- (OGD/R-) established H9C2 induction model both in vivo and in vitro. Echocardiography and HE staining showed that QSG could effectively improve the cardiac function of rats with myocardial infarction in functionality and structure. Furthermore, transcriptomics revealed QSG could significantly regulate mitochondrial dysfunction-related proteins at the transcriptome level. The results of electron microscopy and immunofluorescence proved that the mitochondrial morphology, mitochondrial membrane structural integrity, and myocardial oxidative stress damage can be effectively improved after QSG treatment. Mechanism studies showed that QSG increased the expression level of mitochondrial biogenesis factor PGC-1α/NRF1/TFAM protein and regulated the balance of mitochondrial fusion/fission protein expression. QSG could regulate mitochondrial dysfunction in ischemia heart tissue to protect cardiac function and structure in HF rats. The likely mechanism is the adjustment of PGC-1α/NRF1/TFAM pathway to alleviate oxidative stress in myocardial cells. Therefore, PGC-1α may be a potential therapeutic target for improving mitochondrial dysfunction in HF.

scholarly journals Alleviation of Oxidative Stress in Dental Pulp Cells Following 4-Hexylresorcinol Administration in a Rat Model

2021 ◽  
Vol 11 (8) ◽  
pp. 3637
Author(s):  
Jun-Ho Chang ◽  
Dae-Won Kim ◽  
Seong-Gon Kim ◽  
Tae-Woo Kim
Keyword(s):  
Oxidative Stress ◽  
Dental Pulp ◽  
Therapeutic Effects ◽  
Protective Effects ◽  
Mandibular Incisor ◽  
Tnf Α ◽  
Total Antioxidant ◽  
Pulp Cells ◽  
Pre Treatment

Damaged dental pulp undergoes oxidative stress and 4-hexylresorcinol (4HR) is a well-known antioxidant. In this study, we aimed to evaluate the therapeutic effects of a 4HR ointment on damaged dental pulp. Pulp cells from rat mandibular incisor were cultured and treated with 4HR or resveratrol (1–100 μM). These treatments (10–100 μM) exerted a protective effect during subsequent hydrogen peroxide treatments. The total antioxidant capacity and glutathione peroxidase activity were significantly increased following 4HR or resveratrol treatment (p < 0.05), while the expression levels of TNF-α and IL1β were decreased following the exposure to 4HR pre-treatment in an in vitro model. Additionally, the application of 4HR ointment in an exposed dental pulp model significantly reduced the expression of TNF-α and IL1β (p < 0.05). Conclusively, 4HR exerted protective effects against oxidative stress in dental pulp tissues through downregulating TNF-α and IL1β.

Effects of hydrogen as adjuvant treatment for unstable angina

2021 ◽  
pp. 153537022110091
Author(s):  
Yanhong Si ◽  
Hua Tian ◽  
Bingqing Dong ◽  
Ying Zhang ◽  
Yuanyuan Wen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Unstable Angina ◽  
Water Intake ◽  
Adjuvant Treatment ◽  
Umbilical Vein ◽  
Pure Water ◽  
Atherosclerotic Cardiovascular Disease ◽  
Protective Effects ◽  
Water Addition

Oxidative stress and inflammation are closely related to atherosclerotic cardiovascular disease. It is established that hydrogen has significant protective effects on many diseases as a potential antioxidative and anti-inflammatory agent. The purpose of this study is to evaluate the effect of hydrogen on unstable angina in vitro and in vivo. An atherosclerosis model in vitro was constructed by ox-LDL-induced injury of human umbilical vein endothelial cells and in vitro testing indicated hydrogen inhibited ox-LDL-induced oxidative stress and inflammatory response by down-regulating LOX-1/NF-kB signaling pathway. Subsequently, the attenuating effect of hydrogen-rich water intake on unstable angina was further confirmed in clinic. Forty hospitalized subjects with unstable angina were enrolled and consumed either 1000–1200 mL/d hydrogen-rich water or the same amount of placebo pure water in addition to conventional drugs for three months. Clinical analysis showed hydrogen-rich water intake relieved angina symptoms in unstable angina patients. Serum analysis showed that hydrogen-rich water addition resulted in more effective reductions of total-cholesterol, low-density lipoprotein-cholesterol, and apolipoprotein B levels compared with conventional treatment. These results support that hydrogen as adjuvant treatment has a beneficial effect on unstable angina.

Chemical constituents isolated fromPaeonia lactifloraroots and their neuroprotective activity against oxidative stress in vitro

2009 ◽  
Vol 24 (5) ◽  
pp. 1138-1140 ◽  
Author(s):  
Seung Hyun Kim ◽  
Mi Kyeong Lee ◽  
Ki Yong Lee ◽  
Sang Hyun Sung ◽  
Jinwoong Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chemical Constituents ◽  
Neuroprotective Activity

Protective effects of lipoic acid against acrylamide-induced neurotoxicity: involvement of mitochondrial energy metabolism and autophagy

2017 ◽  
Vol 8 (12) ◽  
pp. 4657-4667 ◽  
Author(s):  
Ge Song ◽  
Zhigang Liu ◽  
Luanfeng Wang ◽  
Renjie Shi ◽  
Chuanqi Chu ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Lipoic Acid ◽  
Redox Status ◽  
Protective Effects ◽  
Mitochondrial Energy Metabolism

Lipoic acid (LA) suppressed acrylamide (ACR)-induced inflammation, redox status disturbance, autophagy, and apoptosis mediated by mitochondria in the SH-SY5Y cells.

The protective effects of carvacrol and thymol against paracetamol–induced toxicity on human hepatocellular carcinoma cell lines (HepG2)

2016 ◽  
Vol 35 (12) ◽  
pp. 1252-1263 ◽  
Author(s):  
SS Palabiyik ◽  
E Karakus ◽  
Z Halici ◽  
E Cadirci ◽  
Y Bayir ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Cytokines ◽  
Hepg2 Cells ◽  
Folk Medicine ◽  
Hepatoprotective Activity ◽  
High Dose ◽  
Protective Effects ◽  
And Oxidative Stress ◽  
Pro Inflammatory Cytokines

Acetaminophen (APAP) overdose could induce liver damage and lead to acute liver failure. The treatment of APAP overdoses could be improved by new therapeutic strategies. Thymus spp., which has many beneficial effects and has been used in folk medicine, is one such potential strategy. In the present study, the hepatoprotective activity of the main constituents of Thymus spp., carvacrol and thymol, were evaluated in light of APAP-induced hepatotoxicity. We hoped to understand the hepatoprotective mechanism of these agents on the antioxidant system and pro-inflammatory cytokines in vitro. Dose-dependent effects of thymol and carvacrol (25, 50, and 100 µM) were tested on cultured HepG2 cells. N-Acetylcysteine (NAC) was tested as positive control. We showed that APAP inhibited HepG2 cell growth by inducing inflammation and oxidative stress. Incubating APAP-exposed HepG2 cells with carvacrol and thymol for 24 h ameliorated this inflammation and oxidative stress. We also evaluated alanine transaminase and lactate dehydrogenase levels of HepG2 cells. We found that thymol and carvacrol protected against APAP-induced toxicity in HepG2 cells by increasing antioxidant activity and reducing pro-inflammatory cytokines, such as tumor necrosis factor α and interleukin 1β. Taking together high-dose thymol and carvacrol treatment has an effect close to NAC treatment in APAP toxicity, but thymol has better treatment effect than carvacrol.

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