Protective effect of hypoglycemic granule against diabetes‐induced liver injury by alleviating glycolipid metabolic disorder and oxidative stress

2020 ◽  
Vol 121 (5-6) ◽  
pp. 3221-3234 ◽  
Author(s):  
Xiaosong Yang ◽  
Pengjie Zhang ◽  
Feixue Zhang ◽  
Zhiqiang Ke ◽  
Qingjie Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Protective Effect ◽  
Metabolic Disorder ◽  
And Oxidative Stress

Acetaminophen-induced liver injury and oxidative stress: protective effect of propofol

2009 ◽  
Vol 26 (7) ◽  
pp. 548-553 ◽  
Author(s):  
Georgia G Kostopanagiotou ◽  
Agni D Grypioti ◽  
Paraskevi Matsota ◽  
Michael G Mykoniatis ◽  
Constantinos A Demopoulos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Protective Effect ◽  
And Oxidative Stress

scholarly journals Antia, a Natural Antioxidant Product, Attenuates Cognitive Dysfunction in Streptozotocin-Induced Mouse Model of Sporadic Alzheimer’s Disease by Targeting the Amyloidogenic, Inflammatory, Autophagy, and Oxidative Stress Pathways

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Nesrine S. El Sayed ◽  
Mamdooh H. Ghoneum
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Neurodegenerative Diseases ◽  
Protective Effect ◽  
Cognitive Dysfunction ◽  
Protective Role ◽  
Sporadic Alzheimer’S Disease ◽  
Stat3 Pathway ◽  
And Oxidative Stress

Background. Many neurodegenerative diseases such as Alzheimer’s disease are associated with oxidative stress. Therefore, antioxidant therapy has been suggested for the prevention and treatment of neurodegenerative diseases. Objective. We investigated the ability of the antioxidant Antia to exert a protective effect against sporadic Alzheimer’s disease (SAD) induced in mice. Antia is a natural product that is extracted from the edible yamabushitake mushroom, the gotsukora and kothala himbutu plants, diosgenin (an extract from wild yam tubers), and amla (Indian gooseberry) after treatment with MRN-100. Methods. Single intracerebroventricular (ICV) injection of streptozotocin (STZ) (3 mg/kg) was used for induction of SAD in mice. Antia was injected intraperitoneally (i.p.) in 3 doses (25, 50, and 100 mg/kg/day) for 21 days. Neurobehavioral tests were conducted within 24 h after the last day of injection. Afterwards, mice were sacrificed and their hippocampi were rapidly excised, weighed, and homogenized to be used for measuring biochemical parameters. Results. Treatment with Antia significantly improved mice performance in the Morris water maze. In addition, biochemical analysis showed that Antia exerted a protective effect for several compounds, including GSH, MDA, NF-κB, IL-6, TNF-α, and amyloid β. Further studies with western blot showed the protective effect of Antia for the JAK2/STAT3 pathway. Conclusions. Antia exerts a significant protection against cognitive dysfunction induced by ICV-STZ injection. This effect is achieved through targeting of the amyloidogenic, inflammatory, and oxidative stress pathways. The JAK2/STAT3 pathway plays a protective role for neuroinflammatory and neurodegenerative diseases such as SAD.

Reduction of doxorubicin-induced cytotoxicity and mitochondrial damage by betanin in rat isolated cardiomyocytes and mitochondria

2021 ◽  
pp. 096032712110228
Author(s):  
AA Hafez ◽  
Z Jamali ◽  
S Samiei ◽  
S Khezri ◽  
A Salimi
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Bioactive Compound ◽  
Isolated Cardiomyocytes ◽  
Cardiac Inflammation ◽  
Flow Cytometric ◽  
Significant Toxicity ◽  
Ros Formation ◽  
Gene Regulatory ◽  
And Oxidative Stress

Doxorubicin (DOX) is an anticancer drug which is used for treatment of several types of cancers. But the clinical use of doxorubicin is limited because of its cardiotoxicity and cardiomyopathy. Mitochondrial-dependent oxidative stress and cardiac inflammation appear to be involved in doxorubicin-induced cardiotoxicity. Betanin as a bioactive compound in Beetroot ( Beta vulgaris L.) displays anti-radical, antioxidant gene regulatory and cardioprotective activities. In this current study, we investigated the protective effect of betanin on doxorubicin-induced cytotoxicity and mitochondrial-dependent oxidative stress in isolated cardiomyocytes and mitochondria. Isolated cardiomyocytes and mitochondria were treated with three concentrations of betanin (1, 5 and 10 µM) and doxorubicin (3.5 µM) for 6 h. The parameters of cellular and mitochondrial toxicity were analyzed using biochemical and flow cytometric methods. Our results showed a significant toxicity in isolated cardiomyocytes and mitochondria in presence of doxorubicin which was related to reactive oxygen species (ROS) formation, increase in malondialdehyde (MDA), increase in oxidation of GSH to GSSG, lysosomal/mitochondrial damages and mitochondrial swelling. While betanin pretreatment reverted doxorubicin-induced cytotoxicity and oxidative stress in isolated cardiomyocytes and mitochondria. These results suggest that betanin elicited a typical protective effect on doxorubicin-induced cytotoxicity and oxidative stress. It is possible that betanin could be used as a useful adjuvant in combination with doxorubicin chemotherapy for reduction of cardiotoxicity and cardiomyopathy.

scholarly journals Protective effect of a hydroethanolic extract from Bowdichia virgilioides on muscular damage and oxidative stress caused by strenuous resistance training in rats

2014 ◽  
Vol 11 (1) ◽  
Author(s):  
Jymmys Lopes dos Santos ◽  
Rafaela Eugênia Arce Dantas ◽  
Clésio Andrade Lima ◽  
Silvan Silva de Araújo ◽  
Elis Cristiane Valença de Almeida ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Resistance Training ◽  
Protective Effect ◽  
Hydroethanolic Extract ◽  
Muscular Damage ◽  
And Oxidative Stress

scholarly journals The severity of rat liver injury by fructose and high fat depends on the degree of respiratory dysfunction and oxidative stress induced in mitochondria

2019 ◽  
Vol 18 (1) ◽  
Author(s):  
Claudia Isabel García-Berumen ◽  
Omar Ortiz-Avila ◽  
Manuel Alejandro Vargas-Vargas ◽  
Bricia A. del Rosario-Tamayo ◽  
Clotilde Guajardo-López ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Rat Liver ◽  
High Fat ◽  
Respiratory Dysfunction ◽  
And Oxidative Stress

scholarly journals Curcumin Attenuates Oxaliplatin-Induced Liver Injury and Oxidative Stress by Activating the Nrf2 Pathway

2020 ◽  
Vol Volume 14 ◽  
pp. 73-85 ◽  
Author(s):  
Yulei Lu ◽  
Shengming Wu ◽  
Bangde Xiang ◽  
Lequn Li ◽  
Youzhi Lin
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Nrf2 Pathway ◽  
And Oxidative Stress

scholarly journals The Late-Stage Protective Effect of Mito-TEMPO against Acetaminophen-Induced Hepatotoxicity in Mouse and Three-Dimensional Cell Culture Models

Antioxidants ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 965
Author(s):  
Mohammad Abdullah-Al-Shoeb ◽  
Kenta Sasaki ◽  
Saori Kikutani ◽  
Nanami Namba ◽  
Keiichi Ueno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Culture ◽  
Liver Injury ◽  
Protective Effect ◽  
Acute Liver Injury ◽  
Three Dimensional ◽  
3D Cell Culture ◽  
Cell Culture Model ◽  
Culture Model ◽  
Apap Hepatotoxicity

An overdose of acetaminophen (APAP), the most common cause of acute liver injury, induces oxidative stress that subsequently causes mitochondrial impairment and hepatic necroptosis. N-acetyl-L-cysteine (NAC), the only recognized drug against APAP hepatotoxicity, is less effective the later it is administered. This study evaluated the protective effect of mitochondria-specific Mito-TEMPO (Mito-T) on APAP-induced acute liver injury in C57BL/6J male mice, and a three dimensional (3D)-cell culture model containing the human hepatoblastoma cell line HepG2. The administration of Mito-T (20 mg/kg, i.p.) 1 h after APAP (400 mg/kg, i.p.) injection markedly attenuated the APAP-induced elevated serum transaminase activity and hepatic necrosis. However, Mito-T treatment did not affect key factors in the development of APAP liver injury including the activation of c-jun N-terminal kinases (JNK), and expression of the transcription factor C/EBP homologous protein (CHOP) in the liver. However, Mito-T significantly reduced the APAP-induced increase in the hepatic oxidative stress marker, nitrotyrosine, and DNA fragmentation. Mito-T markedly attenuated cytotoxicity induced by APAP in the HepG2 3D-cell culture model. Moreover, liver regeneration after APAP hepatotoxicity was not affected by Mito-T, demonstrated by no changes in proliferating cell nuclear antigen formation. Therefore, Mito-T was hepatoprotective at the late-stage of APAP overdose in mice.

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