scholarly journals Protective effect of Rhus chinensis Mill. extract against liver cirrhosis in rats

2022 ◽  
Vol 20 (2) ◽  
pp. 365-368
Author(s):  
Zirong Pan ◽  
Qiang Cheng ◽  
Heyan Chen ◽  
Longhai Lin ◽  
Weijia Liao ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Liver Cirrhosis ◽  
Protective Effect ◽  
Rat Model ◽  
Plasma Concentrations ◽  
Alanine Transaminase ◽  
Model Group ◽  
Rhus Chinensis ◽  
And Oxidative Stress

Purpose: To study the effect of Rhus chinensis Mill. extract (RCME) on diethylnitrosamine (DEN)-induced liver cirrhosis in rats. Methods: RCME was obtained by extracting the dried Rhus chinensis Mill. in water. Liver cirrhosis rat model was prepared by injecting with DEN once a week for 8 weeks. After 8th-week of RCME treatment, biochemical index and oxidative stress were determined in DEN-induced liver cirrhosis in rats. Results: Compared with model group, plasma concentrations of alanine transaminase (ALT, 125.3 ± 4.1 U/L) and aspartate aminotransferase (AST, 152.4 ± 3.5 U/L) decreased significantly (p < 0.01) in the 8th week. Rhus chinensis Mill. extract (RCME) significantly decreased malondialdehyde (MDA, 0.18 ± 0.02 umol/L) and superoxide dismutase (SOD, 0.76 ± 0.05 U/mg protein) in DEN-induced liver cirrhosis in rats (p < 0.01) when compared with model group. Conclusion: RCME protects against diethylnitrosamine-induced liver cirrhosis in rats. However, further investigations are required to ascertain the plant extract’s suitability for the clinical management of liver cirrhosis.

scholarly journals Lycopene-Rich Extract from Red Guava (Psidium guajava L.) Decreases Plasma Triglycerides and Improves Oxidative Stress Biomarkers on Experimentally-Induced Dyslipidemia in Hamsters

Nutrients ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 393 ◽  
Author(s):  
Ana Karolinne da Silva Brito ◽  
Geovanni de Morais Lima ◽  
Luciana Melo de Farias ◽  
Lays Arnaud Rosal Lopes Rodrigues ◽  
Vanessa Brito Lira de Carvalho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Day Treatment ◽  
Plasma Concentrations ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Psidium Guajava ◽  
Atherogenic Index ◽  
Oxidative Stress Biomarkers ◽  
And Oxidative Stress

This work assessed the effects of a 28-day treatment with lycopene-rich extract (LRE) from red guava fruit (Psidium guajava L.) on the lipid profile and oxidative stress in an experimental model of dyslipidemia. Male hamsters (116.5 ± 2.16 g) were fed with the AIN 93G diet containing casein (20%), coconut fat (13.5%) and cholesterol (0.1%). The animals were divided into four groups: normolipidemic control (standard feed; NC, n = 7); hypercholesterolemic control (HC, n = 7); LRE 25 mg/kg/day (LRE-25, n = 7) and LRE 50 mg/kg/day (LRE-50, n = 9). After treatment, plasma concentrations of triglycerides (TG), total cholesterol (TC), low-density lipoprotein (LDL) cholesterol (LDL-c), high-density lipoprotein (HDL) cholesterol (HDL-c), malondialdehyde (MDA-p) and myeloperoxidase (MPO), as well as erythrocytic superoxide dismutase (SOD-e) and the atherogenic index, were determined. Malondialdehyde (MDA-h), catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD-h) levels were assessed. Feed intake (FI) and weight gain (WG) were also determined. The LRE-25 group presented significantly lower TG levels and atherogenic index than did the HC group (p < 0.05). Both LRE-25 and LRE-50 groups presented lower levels of MDA-p and MPO than did the HC group (p < 0.05). LRE demonstrated a promising effect against dyslipidemia and oxidative stress.

Protective Effect of Swertiamarin on Myocardial Injury Through Activation of Nrf2/HO-1 Pathway in Heart Failure Model of Rats

2020 ◽  
Vol 18 (3) ◽  
pp. 260-265
Author(s):  
Xu Lin ◽  
Zheng Xiaojun ◽  
Lv Heng ◽  
Mo Yipeng ◽  
Tong Hong
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Ejection Fraction ◽  
Protective Effect ◽  
Infarct Size ◽  
Rat Model ◽  
Left Ventricular ◽  
Related Factor ◽  
Nuclear Factor ◽  
Internal Dimension

The purpose of this study was to evaluate the protective effect of swertiamarin on heart failure. To this end, a rat model of heart failure was established via left coronary artery ligation. Infarct size of heart tissues was determined using triphenyl tetrazolium chloride staining. Echocardiography was performed to evaluate cardiac function by the determination of ejection fraction, left ventricular internal dimension in diastole and left ventricular internal dimension in systole. The effect of swertiamarin on oxidative stress was evaluated via enzyme-linked immunosorbent assay. The mechanism was evaluated using western blot. Administration of swertiamarin reduced the infarct size of heart tissues in rat models with heart failure. Moreover, swertiamarin treatment ameliorated the cardiac function, increased ejection fraction and fractional shortening, decreased left ventricular internal dimension in diastole and left ventricular internal dimension in systole. Swertiamarin improved oxidative stress with reduced malondialdehyde, while increased superoxide dismutase, glutathione, and GSH peroxidase. Furthermore, nuclear-factor erythroid 2-related factor 2, heme oxygenase and NAD(P)H dehydrogenase (quinone 1) were elevated by swertiamarin treatment in heart tissues of rat model with heart failure. Swertiamarin alleviated heart failure through suppression of oxidative stress response via nuclear-factor erythroid 2-related factor 2/heme oxygenase-1 pathway providing a novel therapeutic strategy for heart failure.

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.

Fetuin-A exerts a protective effect against experimentally induced intestinal ischemia/reperfusion by suppressing autophagic cell death

2021 ◽  
pp. 153537022199520
Author(s):  
Nanees F El-Malkey ◽  
Amira E Alsemeh ◽  
Wesam MR Ashour ◽  
Nancy H Hassan ◽  
Husam M Edrees
Keyword(s):  
Oxidative Stress ◽  
Rat Model ◽  
Intestinal Ischemia ◽  
Ischemia Reperfusion ◽  
Protective Role ◽  
Beclin 1 ◽  
Male Rats ◽  
Fetuin A ◽  
Intestinal Ischemia Reperfusion ◽  
And Oxidative Stress

Intestinal tissue is highly susceptible to ischemia/reperfusion injury in many hazardous health conditions. The anti-inflammatory and antioxidant glycoprotein fetuin-A showed efficacy in cerebral ischemic injury; however, its protective role against intestinal ischemia/reperfusion remains elusive. Therefore, this study investigated the protective role of fetuin-A supplementation against intestinal structural changes and dysfunction in a rat model of intestinal ischemia/reperfusion. We equally divided 72 male rats into control, sham, ischemia/reperfusion, and fetuin-A-pretreated ischemia/reperfusion (100 mg/kg/day fetuin-A intraperitoneally for three days prior to surgery and a third dose 1 h prior to the experiment) groups. After 2 h of reperfusion, the jejunum was dissected and examined for spontaneous contractility. A jejunal homogenate was used to assess inflammatory and oxidative stress enzymes. Staining of histological sections was carried out with hematoxylin, eosin and Masson’s trichrome stain for evaluation. Immunohistochemistry was performed to detect autophagy proteins beclin-1, LC3, and p62. This study found that fetuin-A significantly improved ischemia/reperfusion-induced mucosal injury by reducing the percentage of areas of collagen deposition, increasing the amplitude of spontaneous contraction, decreasing inflammation and oxidative stress, and upregulating p62 expression, which was accompanied by beclin-1 and LC3 downregulation. Our findings suggest that fetuin-A treatment can prevent ischemia/reperfusion-induced jejunal structural and functional changes by increasing antioxidant activity and regulating autophagy disturbances observed in the ischemia/reperfusion rat model. Furthermore, fetuin-A may provide a protective influence against intestinal ischemia/reperfusion complications.

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.

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