Background: Orange juice (OJ) is rich in polyphenols with anti-inflammatory and antioxidant properties. After myocardial infarction (MI), complex changes occur in cardiac structure and function, which is known as cardiac remodeling (CR). Oxidative stress and inflammation can modulate this process. We hypothesized that the consumption of OJ attenuates the CR after MI.
Objectives: To evaluate the influence of OJ on CR after MI by analysis of functional, morphological, oxidative stress, inflammation, and energy metabolism variables.
Methods: A total of 242 male rats weighing 200-250 g were submitted to a surgical procedure (coronary artery ligation or simulated surgery). Seven days after surgery, survivors were assigned to one of the four groups 1) SM, sham animals with water and maltodextrin (n= 20); 2) SOJ, sham animals with OJ (n= 20); 3) IM, infarcted animals with water and maltodextrin (n= 40); and 4) IOJ, infarcted animals with OJ (n = 40). Statistical analysis was performed by the two-way ANOVA supplemented by Holm-Sidak. Results are presented as mean ± standard deviation, the level of significance adopted was 5%.
Results: After 3 months, MI led to left ventricular (LV) hypertrophy, with systolic and diastolic dysfunction, and increased oxidative stress and inflammatory mediators. OJ intake reduced LV cavity and improved systolic and diastolic function. The OJ animals presented lower activity of glutathione peroxidase and higher expression of heme-oxygenase-1 (HO-1).
Conclusion: OJ attenuated CR in infarcted rats and HO-1 may be play an important role in this process.
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http://dx.doi.org/10.36660/abc.20190397 | DOI Listing |
Methamphetamine (METH) is a highly addictive and dangerous drug that mainly affects neurotransmitters in the brain and leads to feelings of alertness and euphoria. The METH use can lead to addiction, which has become a worldwide problem, resulting in a slew of public health and safety issues. Recent studies showed that chronic METH use can lead to neurotoxicity, neuro-inflammation and oxidative stress which can lead to neuronal injury.
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Division of Food and Nutrition and Human Ecology Research Institute, Chonnam National University, Gwangju, Republic of Korea.
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View Article and Find Full Text PDFAutism Res
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School of Public Health, Hubei University of Medicine, Shiyan, China.
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View Article and Find Full Text PDFArch Pharm (Weinheim)
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Department of Pharmacognosy, University Institute of Pharma Sciences, Chandigarh University, Mohali, Punjab, India.
Alzheimer's disease (AD) is a prevalent neurological illness that affects over 80% of aged adults globally in cases of dementia. Although the exact pathophysiological causes of AD remain unclear, its pathogenesis is primarily driven by several distinct biochemical alterations: (i) the accumulation of toxic Aβ plaques, (ii) the hyperphosphorylation of tau proteins, (iii) oxidative stress resulting in cell death, and (iv) an imbalance between the two main neurotransmitters, glutamate and acetylcholine (ACh). Currently, there are very few medications available and no treatment.
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