Synergistic protective effect of folic acid and vitamin B12against nicotine-induced oxidative stress and apoptosis in pancreatic islets of the rat

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.

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Protective efficacy of folic acid and vitamin B12 against nicotine-induced toxicity in pancreatic islets of the rat

Interdisciplinary Toxicology ◽

10.1515/intox-2015-0016 ◽

2015 ◽

Vol 8 (2) ◽

pp. 103-111 ◽

Cited By ~ 3

Author(s):

Ankita Bhattacharjee ◽

Shilpi Kumari Prasad ◽

Swagata Pal ◽

Bithin Maji ◽

Alak Kumar Syamal ◽

...

Keyword(s):

Oxidative Stress ◽

Body Weight ◽

Folic Acid ◽

Vitamin B12 ◽

Pancreatic Islets ◽

Protective Efficacy ◽

Fasting Blood Glucose ◽

Pancreatic Tissue ◽

Tissue Sections ◽

Increased Risk

Abstract Although cigarette smoking is associated with insulin resistance and an increased risk for type 2 diabetes, few studies have examined the effect of nicotine on the adult endocrine pancreas. In this study, male Wister rats were treated with nicotine (3 mg/kg body weight/day) with or without supplementation of folic acid (36 μg/kg body weight/day) or vitamin B12 (0.63 μg/kg body weight/day) alone or in combination. Fasting blood glucose, insulin and HBA1C level and different oxidative and anti-oxidative stress parameters were measured and pancreatic tissue sections were stained with eosin-haematoxylene. Data were analysed by nonparametric statistics. The results revealed that nicotine induced prediabetes condition with subsequent damage to pancreatic islets in rats. Nicotine also caused oxidative stress in pancreatic tissue as evidenced by increased nitric oxide and malondialdehyde level and decreased superoxide dismutase, catalase and reduced glutathione level. Compared to vitamin B12 supplementation, folic acid blunted the nicotine-induced toxicity in pancreatic islets with higher efficacy. Further, folic acid and vitamin B12 in combination were able to confer significant protection on pancreatic islets against nicotine induced toxicity. These results suggest that supplementation of folic acid and vitamin B12 in combination may be a possible strategy of detoxification against nicotine-induced toxicity in pancreatic islets of the rat.

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Protective effect of folic acid against oxidative stress produced in 21-day postpartum rats by maternal-ethanol chronic consumption during pregnancy and lactation period

Free Radical Research ◽

10.1080/10715760100300011 ◽

2001 ◽

Vol 34 (1) ◽

pp. 1-8 ◽

Cited By ~ 57

Author(s):

M.J. Cano ◽

A. Ayala ◽

M.L. Murillo ◽

O. Carreras

Keyword(s):

Oxidative Stress ◽

Folic Acid ◽

Protective Effect ◽

Lactation Period ◽

Pregnancy And Lactation

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Antioxidant Activity and Protective Effect against Oxidative Stress on Hippocampal HT22 Cells of Tea Seed Oil

The Korean Tea Society ◽

10.29225/jkts.2018.24.1.53 ◽

2018 ◽

Vol 24 (1) ◽

pp. 53-59

Author(s):

Jong Min Kim ◽

Seon Kyeong Park ◽

Jin Yong Kang ◽

Seong-kyeong Bae ◽

Ga-Hee Jeong ◽

...

Keyword(s):

Oxidative Stress ◽

Antioxidant Activity ◽

Protective Effect ◽

Seed Oil ◽

Ht22 Cells ◽

Tea Seed Oil

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Protective effect of DJ-1 against oxidative stress: an advance

Academic Journal of Second Military Medical University ◽

10.3724/sp.j.1008.2012.00088 ◽

2012 ◽

Vol 32 (1) ◽

pp. 88-91

Author(s):

Zhi-yong WANG ◽

Ling-zhen TANG ◽

Tian-wen GAO

Keyword(s):

Oxidative Stress ◽

Protective Effect

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

Current Topics in Nutraceutical Research ◽

10.37290/ctnr2641-452x.18:260-265 ◽

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.

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