scholarly journals PROTECTIVE EFFECT OF FOLIC ACID ON OXIDATIVE STRESS INDUCED BY METHIONINE OVERLOAD IN MALE MICE

2021 ◽  
Vol 21 (Suppliment-1) ◽  
pp. 1430-1434
Author(s):  
Tuqa Sabbar Rahi ◽  
Wifaq j. albazi ◽  
Ali K. Aljarah ◽  
Alaa Hussein AL-Safy
2010 ◽  
Vol 97 (1) ◽  
pp. 7-12 ◽  
Author(s):  
Nagat Aly ◽  
Kawther EL-Gendy ◽  
Fatma Mahmoud ◽  
Abdel Khalek El-Sebae

2020 ◽  
Vol 13 (2) ◽  
pp. 137-143
Author(s):  
Abeer M. Rababa’h ◽  
Samah A. Hussein ◽  
Omar F. Khabour ◽  
Karem H. Alzoubi

Background: Methotrexate is an antagonist of folic acid that has been shown to be genotoxic to healthy body cells via induction of oxidative stress. Cilostazol is a phosphodiesterase III inhibitor and a potent antioxidant drug. Objectives: To evaluate the potential protective effect of cilostazol on methotrexate genotoxicity. Results: Methotrexate significantly increased the frequency of CAs and SCEs (p < 0.0001) as compared to control cultures. This chromosomal damage induced by methotrexate was considerably decreased by pretreatment of the cells with cilostazol (P < 0.01). Moreover, the results showed that methotrexate resulted in a notable reduction (P < 0.01) in cells kinetic parameters, the mitotic index (MI) and the proliferative index (PI). Similarly, cilostazol significantly reduced the mitotic index, which could be related to the anti-proliferative effect (P < 0.01). Conclusion: Methotrexate is genotoxic, and cilostazol could prevent the methotrexate-induced chromosomal damage with no modulation of methotrexate-induced cytotoxicity.


2015 ◽  
Vol 54 (3) ◽  
pp. 433-444 ◽  
Author(s):  
Ankita Bhattacharjee ◽  
Shilpi K. Prasad ◽  
Swagata Pal ◽  
Bithin Maji ◽  
Alak K. Syamal ◽  
...  

2018 ◽  
Vol 24 (1) ◽  
pp. 53-59
Author(s):  
Jong Min Kim ◽  
Seon Kyeong Park ◽  
Jin Yong Kang ◽  
Seong-kyeong Bae ◽  
Ga-Hee Jeong ◽  
...  

2012 ◽  
Vol 32 (1) ◽  
pp. 88-91
Author(s):  
Zhi-yong WANG ◽  
Ling-zhen TANG ◽  
Tian-wen GAO

2020 ◽  
Vol 18 (3) ◽  
pp. 260-265
Author(s):  
Xu Lin ◽  
Zheng Xiaojun ◽  
Lv Heng ◽  
Mo Yipeng ◽  
Tong Hong

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.


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