scholarly journals ANTIOXIDANT AND HEPATOPROTECTIVE EFFECT OF SWERTIA CHIRATA ON HYPOXIA-INDUCED OXIDATIVE STRESS IN WISTAR RATS

2019 ◽  
Vol 12 (1) ◽  
pp. 76
Author(s):  
Kritika Kaushal ◽  
Harvinder Singh ◽  
Anil Kant Thakur
Keyword(s):  
Oxidative Stress ◽  
Liver Function ◽  
Wistar Rats ◽  
Hepatic Damage ◽  
Ros Generation ◽  
Dependent Manner ◽  
Traditional Use ◽  
Hydroalcoholic Extract ◽  
Swertia Chirata ◽  
Liver Functions

Objective: Swertia chirata has been used in traditional and folklore medicine to treat several ailments such as hepatic disorders. However, the mechanistic and experimental justification to its traditional use is lacking. The present study was aimed to investigate the hepatoprotective potential of S. chirata during hypoxia (HYP)-induced hepatic damage in Wistar rats and to determine the underlying mechanism.Methods: Hydroalcoholic extract of S. chirata was prepared using Soxhlet extraction. Animals were divided into six groups (n=5). Animals in the HYP groups were subjected to HYP for 3 days (10% O2) to induce oxidative stress and hepatic damage. 50 and 100 mg/kg extract treatments were provided orally once daily for 7 days after which animals were sacrificed, and biochemical investigations for oxidative stress, liver function tests, and hepatic histopathology were performed.Results: HYP-induced marked oxidative stress as indicated by the significantly elevated mitochondrial ROS generation, lipid peroxidation, glutathione, and depleted catalase levels. Liver function test indicated hepatic damage as the levels of serum glutamic-oxaloacetic transaminase, serum glutamic pyruvic transaminase, and aspartate transaminase were significantly elevated in HYP animals. S. chirata treatment alleviated oxidative stress and improved liver functions in a dose-dependent manner. Liver histopathology confirmed the marked hepatic damage induced by HYP and revealed that S. chirata efficiently rescued liver from hypoxic damage.Conclusion: Hydroalcoholic extract of S. chirata is a potent hepatoprotective intervention which was associated with its potential to alleviate oxidative stress and improve liver functions. Moreover, it could find clinical application as a safer and alternative remedy for liver ailments.

scholarly journals ANTIOXIDANT AND HEPATOPROTECTIVE EFFECT OF SWERTIA CHIRATA ON HYPOXIA-INDUCED OXIDATIVE STRESS IN WISTAR RATS

2019 ◽  
Vol 12 (1) ◽  
pp. 76
Author(s):  
Kritika Kaushal ◽  
Harvinder Singh ◽  
Anil Kant Thakur
Keyword(s):  
Oxidative Stress ◽  
Liver Function ◽  
Wistar Rats ◽  
Hepatic Damage ◽  
Ros Generation ◽  
Dependent Manner ◽  
Traditional Use ◽  
Hydroalcoholic Extract ◽  
Swertia Chirata ◽  
Liver Functions

Objective: Swertia chirata has been used in traditional and folklore medicine to treat several ailments such as hepatic disorders. However, the mechanistic and experimental justification to its traditional use is lacking. The present study was aimed to investigate the hepatoprotective potential of S. chirata during hypoxia (HYP)-induced hepatic damage in Wistar rats and to determine the underlying mechanism.Methods: Hydroalcoholic extract of S. chirata was prepared using Soxhlet extraction. Animals were divided into six groups (n=5). Animals in the HYP groups were subjected to HYP for 3 days (10% O2) to induce oxidative stress and hepatic damage. 50 and 100 mg/kg extract treatments were provided orally once daily for 7 days after which animals were sacrificed, and biochemical investigations for oxidative stress, liver function tests, and hepatic histopathology were performed.Results: HYP-induced marked oxidative stress as indicated by the significantly elevated mitochondrial ROS generation, lipid peroxidation, glutathione, and depleted catalase levels. Liver function test indicated hepatic damage as the levels of serum glutamic-oxaloacetic transaminase, serum glutamic pyruvic transaminase, and aspartate transaminase were significantly elevated in HYP animals. S. chirata treatment alleviated oxidative stress and improved liver functions in a dose-dependent manner. Liver histopathology confirmed the marked hepatic damage induced by HYP and revealed that S. chirata efficiently rescued liver from hypoxic damage.Conclusion: Hydroalcoholic extract of S. chirata is a potent hepatoprotective intervention which was associated with its potential to alleviate oxidative stress and improve liver functions. Moreover, it could find clinical application as a safer and alternative remedy for liver ailments.

scholarly journals HYDROALCOHOLIC EXTRACT OF SWERTIA CHIRATA AND SWERTIA CORDATA ATTENUATES HYPOXIA-MEDIATED MEMORY DYSFUNCTION BY IMPROVING NEURONAL SURVIVAL IN WISTAR RATS

2019 ◽  
pp. 356-362
Author(s):  
KRITIKA KAUSHAL ◽  
HARVINDER SINGH ◽  
ANIL KANT
Keyword(s):  
Oxidative Stress ◽  
Passive Avoidance ◽  
Active Avoidance ◽  
Wistar Rats ◽  
Neuronal Damage ◽  
Memory Dysfunction ◽  
Hydroalcoholic Extract ◽  
Memory Functions ◽  
Swertia Chirata ◽  
The Brain

Objective: Swertia chirata and Swertia cordata have been used in traditional and folk medicines to treat several mental disorders. However, the mechanistic and experimental justification to its traditional use is lacking. The present study was aimed to investigate the neuromodulatory potential of S. chirata and S. cordata during hypoxia-induced neuronal damage in Wistar rats and to determine the underlying mechanism. Methods: Animals were divided into six groups (n=5). Hypoxia was inflicted by subjecting animals to the atmosphere having 10% O2 for 3 days. Animals were administered 100 mg/kg hydroalcoholic extract of S. chirata and S. cordata orally once daily for 7 days, after which motor coordination (Rotarod test) and memory functions (active avoidance test and passive avoidance test) were evaluated. Animals were sacrificed and biochemical investigations for oxidative stress and histopathology were performed. Results: Subjecting animals to hypoxia resulted in marked memory dysfunction, and extract treatments improved memory functions in active avoidance and passive avoidance task. Hypoxiainduced the marked oxidative stress as indicated by the significantly elevated reactive oxygen species and lipid peroxidation and depleted catalase and glutathione levels in the hippocampus. S. chirata and S. cordata treatment alleviated oxidative stress in the hippocampus region of the brain. Brain histopathology confirmed that hypoxia resulted in significant neuronal damage and extract treatment efficiently rescued neurons from hypoxic damage. Overall, S. chirata extract treatment was observed to have better neuromodulatory effect than S. cordata during hypoxia. Conclusion: Hypoxia induced memory dysfunction by inflicting neuronal damage and oxidative stress in the hippocampus region of the brain. The hydroalcoholic extract of S. chirata and S. cordata improved memory functions in hypoxic animals by alleviating hippocampal oxidative stress and by improving neuronal morphology and survival.

Abstract 107: Apocynin Attenuates Isoproterenol-induced Myocardial Injury: Implications For Targeting Nadph Oxidase In Myocardial Fibrogenesis

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Yu Chen ◽  
Jingang Cui ◽  
Qinbo Yang ◽  
Chenglin Jia ◽  
Minqi Xiong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nadph Oxidase ◽  
Myocardial Fibrosis ◽  
Myocardial Injury ◽  
Oxidase Inhibitor ◽  
Ros Generation ◽  
Dependent Manner ◽  
Expression Of Genes ◽  
Therapeutic Development ◽  
Myocardial Injuries

Myocardial fibrosis results from cardiac injuries caused by various pathophysiological mechanisms including myocardial infarction, leading to destruction of myocardial architecture and progressive cardiac dysfunction. Oxidative stress is likely involved in myocardial ischemic injury and the subsequent tissue remodeling mediated by myocardial fibrogenesis. Our current study aimed to evaluate the implication of NADPH oxidase in overproduction of reactive oxygen species and its contribution to the pathogenesis of myocardial fibrogenesis after ischemic injuries. The effects of Apocynin, a selective NADPH oxidase inhibitor, were evaluated in the mouse model of isoproterenol-induced myocardial injury by histopathological approaches and whole-genome gene expression profiling. The results demonstrated that Apocynin was able to inhibit the development of ISO-induced myocardial necrotic lesions and fibrogenesis in a dose-dependent manner. Moreover, the preventive effects of Apocynin on myocardial injuries were associated with suppressed expression of genes implicated in inflammation responses and extracellular matrix, which were remarkably upregulated by isoproterenol administration. In summary, o ur study provides proof-of-concept for the involvement of NADPH oxidase-mediated ROS generation in myocardial ischemic injuries and fibrogenesis, which will benefit the mechanism-based therapeutic development targeting NADPH oxidase and oxidative stress in treating myocardial fibrosis and related disorders.

scholarly journals 17β-Estradiol Modulates SIRT1 and Halts Oxidative Stress-Mediated Cognitive Impairment in a Male Aging Mouse Model

Cells ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 928 ◽  
Author(s):  
Mehtab Khan ◽  
Rahat Ullah ◽  
Shafiq Ur Rehman ◽  
Shahid Ali Shah ◽  
Kamran Saeed ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cognitive Impairment ◽  
Mouse Model ◽  
Memory Impairment ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ros Generation ◽  
Dependent Manner ◽  
Molecular Docking Study ◽  
17Β Estradiol

Oxidative stress has been considered the main mediator in neurodegenerative disease and in normal aging processes. Several studies have reported that the accumulation of reactive oxygen species (ROS), elevated oxidative stress, and neuroinflammation result in cellular malfunction. These conditions lead to neuronal cell death in aging-related neurodegenerative disorders such as Alzheimer’s disease (AD) and Parkinson’s disease. Chronic administration of d-galactose (d-gal) for a period of 10 weeks causes ROS generation and neuroinflammation, ultimately leading to cognitive impairment. In this study, we evaluated the estrogen receptor α (ERα)/silent mating type information regulation 2 homolog 1 (SIRT1)-dependent antioxidant efficacy of 17β-estradiol against d-gal-induced oxidative damage-mediated cognitive dysfunction in a male mouse model. The results indicate that 17β-estradiol, by stimulating ERα/SIRT1, halts d-gal-induced oxidative stress–mediated JNK/NF-ҡB overexpression, neuroinflammation and neuronal apoptosis. Moreover, 17β-estradiol ameliorated d-gal-induced AD-like pathophysiology, synaptic dysfunction and memory impairment in adult mouse brains. Interestingly, inhibition of SIRT1 with Ex527 (a potent and selective SIRT1 inhibitor) further enhanced d-gal-induced toxicity and abolished the beneficial effect of 17β-estradiol. Most importantly, for the first time, our molecular docking study reveals that 17β-estradiol allosterically increases the expression of SIRT1 and abolishes the inhibitory potential of d-ga. In summary, we can conclude that 17β-estradiol, in an ERα/SIRT1-dependent manner, abrogates d-gal-induced oxidative stress–mediated memory impairment, neuroinflammation, and neurodegeneration in adult mice.

scholarly journals Protective effects of delphinidin against H2O2–induced oxidative injuries in human retinal pigment epithelial cells

2019 ◽  
Vol 39 (8) ◽  
Author(s):  
Timin Ni ◽  
Wanju Yang ◽  
Yiqiao Xing
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Retinal Pigment Epithelial ◽  
Retinal Pigment ◽  
Retinal Pigment Epithelial Cells ◽  
Age Related Macular Degeneration ◽  
Ros Generation ◽  
Dependent Manner ◽  
Pigment Epithelial ◽  
Age Related

Abstract Age-related macular degeneration (AMD) is now one of the leading causes of blindness in the elderly population and oxidative stress-induced damage to retinal pigment epithelial (RPE) cells occurs as part of the pathogenesis of AMD. In the present study, we evaluated the protective effect of delphinidin (2-(3,4,5-trihydroxyphenyl) chromenylium-3,5,7-triol) against hydrogen peroxide (H2O2)-induced toxicity in human ARPE-19 cells and its molecular mechanism. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay and flow cytometry demonstrated that pretreatment of ARPE-19 cells with delphinidin (25, 50, and 100 μg/ml) significantly increased cell viability and reduced the apoptosis from H2O2 (0.5 mM)-induced oxidative stress in a concentration-dependent manner, which was achieved by the inhibition of Bax, cytochrome c, and caspase-3 protein expression and enhancement of Bcl-2 protein. The same tendency was observed in ARPE-19 cells pre-treated with 15 mM of N-acetylcysteine (NAC) before the addition of H2O2. Furthermore, pre-incubation of ARPE-19 cells with delphinidin markedly inhibited the intracellular reactive oxygen species (ROS) generation and Nox1 protein expression induced by H2O2. Moreover, the decreased antioxidant enzymes activities of superoxide dismutase (SOD), catalase (CAT), and glutathione-peroxidase (GSH-PX) and elevated (MDA) level in H2O2-treated cells were reversed to the normal standard by the addition of delphinidin, which was regulated by increasing nuclear Nrf2 protein expression in ARPE-19 cells. Our results suggest that delphinidin effectively protects human ARPE-19 cells from H2O2-induced oxidative damage via anti-apoptotic and antioxidant effects.

scholarly journals ANG II promotes autophagy in podocytes

2010 ◽  
Vol 299 (2) ◽  
pp. C488-C496 ◽  
Author(s):  
Anju Yadav ◽  
Sridevi Vallabu ◽  
Shitij Arora ◽  
Pranay Tandon ◽  
Divya Slahan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ros Generation ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Ang Ii ◽  
Electron Microscopic ◽  
Glomerular Filtration Barrier ◽  
Filtration Barrier ◽  
Microscopic Studies ◽  
Autophagic Process

Podocytes are an integral and important constituent of the glomerular filtration barrier (GFB) and are exposed to a higher concentrations of ANG II in diseased states; consequently, podocytes may accumulate oxidized proteins and damaged mitochondria. In the present study, we evaluated the effect of ANG II on the podocyte autophagic process, which is likely to be triggered in order to degrade unwanted proteins and damaged organelles. To quantitate the occurrence of autophagy, electron microscopic studies were carried out on control and ANG II-treated conditionally immortalized mouse podocytes (CIMPs). ANG II-treated cells showed a fivefold greater number of autophagosomes/field compared with control cells. This proautophagic effect of ANG II was inhibited by pretreatment with 3-methyladenine, an inhibitor of autophagy. ANG II also enhanced podocyte expression of autophagic genes such as LC3-2 and beclin-1. Since oxidative stress is often associated with the induction of autophagy, we examined the effect of ANG II on podocyte reactive oxygen species (ROS) generation. ANG II enhanced podocyte ROS generation in a time-dependent manner. To determine whether there is a causal relationship between ANG II-induced oxidative stress and induction of autophagy, we evaluated the effect of antioxidants on ANG II-induced autophagy. As expected, the proautophagic effect of ANG II was inhibited by antioxidants. We conclude that ANG II promotes podocyte autophagy through the generation of ROS.

scholarly journals Osthole Attenuates Bleomycin-Induced Pulmonary Fibrosis by Modulating NADPH Oxidase 4-Derived Oxidative Stress in Mice

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Lijun Fang ◽  
Wei Wang ◽  
Jiazheng Chen ◽  
Anju Zuo ◽  
Hongmei Gao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pulmonary Fibrosis ◽  
Lung Fibroblasts ◽  
Ros Generation ◽  
Dependent Manner ◽  
Active Constituent ◽  
Concentration Dependent Manner ◽  
Nadph Oxidase 4 ◽  
Tgf Β1

Idiopathic pulmonary fibrosis (IPF) is a chronic progressive lung disease characterized by the extensive accumulation of myofibroblasts and collagens. However, the exact mechanism that underlies this condition is unclear. Growing evidence suggests that NADPH oxidases (NOXs), especially NOX4-derived oxidative stress, play an important role in the development of lung fibrosis. Bleomycin (BLM) is a tumor chemotherapeutic agent, which has been widely employed to establish IPF animal models. Osthole (OST) is an active constituent of the fruit of Cnidium ninidium. Here, we used an in vivo mouse model and found that OST suppressed BLM-induced body weight loss, lung injury, pulmonary index increase, fibroblast differentiation, and pulmonary fibrosis. OST also significantly downregulated BLM-induced NOX4 expression and oxidative stress in the lungs. In vitro, OST could inhibit TGF-β1-induced Smad3 phosphorylation, differentiation, proliferation, collagen synthesis, NOX4 expression, and ROS generation in human lung fibroblasts in a concentration-dependent manner. Moreover, NOX4 overexpression could prevent the above effects of OST. We came to the conclusion that OST could significantly attenuate BLM-induced pulmonary fibrosis in mice, via the mechanism that involved downregulating TGF-β1/NOX4-mediated oxidative stress in lung fibroblasts.

scholarly journals Octadecaneuropeptide prevents toxicity induced by 6-hydroxydopamine in cultured rat astrocyte: involvement of the endogenous antioxidant systems and the intrinsic apoptotic pathway

2018 ◽  
Author(s):  
Hadhemi Kaddour ◽  
Yosra Hamdi ◽  
David Vaudry ◽  
Jérôme Leprince ◽  
Hubert Vaudry ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Apoptotic Cell ◽  
Antioxidant Systems ◽  
Mitochondrial Activity ◽  
Ros Generation ◽  
Potential Candidate ◽  
Dependent Manner ◽  
Antioxidant Defences ◽  
Apoptotic Pathway

AbstractOxidative stress, associated with various neurodegenerative diseases, induces imbalance in ROS generation, impairs cellular antioxidant defences and finally triggers both neurons and astroglial cell death by apoptosis. Astrocytes specifically synthesize and release endozepines, a family of regulatory peptides, including the octadecaneuropeptide (ODN). We have previously reported that ODN is a potent neuroprotective agent that prevents 6-OHDA-induced apoptotic neuronal death. The purpose of the present study was to investigate the potential glioprotective effect of ODN on 6-OHDA-induced oxidative stress and cell death in cultured rat astrocytes. Incubation of astrocytes with graded concentrations of ODN (10−14 to 10−8 M) inhibited 6-OHDA-evoked cell death in a concentration- and time-dependent manner. In addition, ODN prevented the decrease of mitochondrial activity and caspase-3 activation induced by 6-OHDA. Toxin-treated cells exhibited high level of ROS associated with a generation of H2O2 and O2°-and a reduction of both SOD and catalase activities. Co-treatment of astrocytes with low concentrations of ODN dose dependently blocked 6-OHDA-evoked ROS production and inhibition of antioxidant enzymes activities. Taken together, these data demonstrate that ODN is a potent glioprotective agent that prevents 6-OHDA-induced oxidative stress and apoptotic cell death. ODN is thus a potential candidate to delay neuronal damages in various pathological conditions involving oxidative neurodegeneration.

scholarly journals Oxidative Stress and Mitogen-Activated Protein Kinase Pathways Involved in Cadmium-Induced BRL 3A Cell Apoptosis

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Zhang Yiran ◽  
Jiang Chenyang ◽  
Wang Jiajing ◽  
Yuan Yan ◽  
Gu Jianhong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitogen Activated Protein Kinase ◽  
Ros Generation ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Nuclear Condensation ◽  
Concentration Dependent Manner ◽  
P38 Inhibitor ◽  
Mapk Pathways ◽  
Induced Apoptosis

In this study, BRL 3A cells were treated with different Cd concentrations (0, 10, 20, and 40 μmol/L) for 12 h and preincubated with or without N-acetyl-L-cysteine (NAC) (2 mmol/L) for 30 min, and cells were treated with Cd (0 and 20 μmol/L), pretreated with p38 inhibitor (SB203580), JNK (c-Jun NH2-terminal kinases) inhibitor (SP600125), and extracellular signal-regulated kinase (ERK) inhibitor (U0126) for 30 min, and then treated with 20 μmol/L Cd for 12 h. Cd decreased cell viability, SOD, and GSH-Px activity in a concentration-dependent manner. Increased MDA level, ROS generation, nuclear condensation, shrinkage, and fragmentation in cell morphology were inhibited by NAC. Cd-induced apoptosis was attenuated by pretreatment with SB203580, SP600125, and U0126. The results of western blot showed that NAC preincubation affected Cd-activated MAPK pathways, p38 and ERK phosphorylation. Cd treatment elevated the mRNA levels of Bax and decreased the mRNA levels of Bcl-2, respectively. The same effect was found in their protein expression levels. These results suggest that oxidative stress and MAPK pathways participate in Cd-induced apoptosis and that the balance between pro- and antiapoptotic genes (Bax and Bcl-2) is important in Cd-induced apoptosis.

scholarly journals EVALUATION OF ANTIDEPRESSANT ACTIVITY OF ETHANOLIC EXTRACT OF LAGERSTROEMIA SPECIOSA LEAVES IN ALBINO WISTAR RATS

2019 ◽  
pp. 68-74
Author(s):  
VANITA KANASE ◽  
SUNITA VISHWAKARMA
Keyword(s):  
Oxidative Stress ◽  
Normal Saline ◽  
Restraint Stress ◽  
Wistar Rats ◽  
Ethanolic Extract ◽  
Antidepressant Activity ◽  
Control Group ◽  
Dependent Manner ◽  
Lagerstroemia Speciosa ◽  
Dose Dependent

Objective: The objective of the study was to evaluate the antidepressant activity of ethanolic extract of dried leaves of Lagerstroemia speciosa L. (EELS) on acute restraint stress (ARS)-induced depression-like behavior and biochemical alterations in albino Wistar rats. Methods: Thirty rats were randomly divided into five experimental groups. Group-I (normal control) rats received normal saline (2.0 ml/kg, p.o.) daily for 14 days; Group-II (stress control) rats received normal saline (2.0 ml/kg, p.o.) daily for 14 days and subjected to restraint stress on the 13th day. Group-III (standard drug-treated) rats received imipramine (15 mg/kg, p.o.) daily for 14 days and subjected to restraint stress on the 13th day. Groups-IV and V rats were treated with EELS (100 mg/kg and 300 mg/kg, p.o.) daily for 14 days subjected to ARS on the 13th day. Stress-like behavior was assessed by subjecting the rats to behavioral paradigms such as tail-suspension test (TST) and open field test (OFT), 40 min post-restraint stress procedure. Pretest of 10 min for forced swim test (FST) was also given to each rat simultaneously. Then, 23.5 h later, the relevant samples were administered and the main test performed 30 min later. Oxidative stress parameters such as superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and extent of lipid peroxidation (LPO) were analyzed in restraint stress-induced animals and control group, following FST on the 15th day. Statistical Analysis: Expression of data was done as a mean standard error of the mean. The normally distributed data were subjected to one-way analysis of variance followed by Dunnett’s test. *p<0.05 was considered statistically significant. Results: It was observed that L. speciosa L. showed a significant dose-dependent decrease in duration of immobility time in TST and FST when compared with the control group in a dose-dependent manner. The results of OFT also showed a dose-dependent increase in locomotor activity. In addition to behavioral tests, EELS also normalized oxidative stress markers such as CAT, SOD, MDA, and LPO in a dose-dependent manner. Conclusion: The results suggest that the ethanolic extract of L. speciosa L. leaves possesses significant antidepressant property, may be recommended as a supplement for the antidepressant activity.

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