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Selenium downregulates oxidative stress-induced activation of leukotriene pathway in experimental rats with diabetic
B L Dhanya1, R P Swathy, M Indira
1Department of Biochemistry, University of Kerala, Kariavattom, Thiruvananthapuram, 695581, Kerala, India.
Insights
Selenium supplementation in diabetic rats reduced oxidative stress and inflammation, mitigating cardiac hypertrophy. This study elucidates selenium
Area of Science:
- Cardiovascular Research
- Endocrinology
- Nutritional Science
Background:
- Cardiac hypertrophy, a thickening of the heart's ventricle wall, increases morbidity and mortality.
- Diabetic complications, including cardiac hypertrophy, are significantly mediated by hyperglycemia-induced reactive oxygen species and inflammation.
- Selenium exhibits insulin-like and anti-inflammatory effects, but its molecular mechanism in diabetic cardiac hypertrophy remains unclear.
Purpose of the Study:
- To investigate the molecular mechanism of selenium's protective effects against diabetic cardiac hypertrophy.
- To evaluate the impact of sodium selenite on oxidative stress, inflammation, and cardiac function in a rat model of diabetes.
Main Methods:
- A 30-day study involving four groups of rats: control, sodium selenite-treated control, diabetic, and sodium selenite-treated diabetic.
- Assessment of antioxidant enzyme activities, serum glucose, glycated hemoglobin, high-sensitivity C-reactive protein, and lipid peroxidation products.
- Analysis of phospholipase activity, leukotriene pathway markers, and the expression of nuclear transcription factor κB (NFκB) and related inflammatory mediators.
Main Results:
- Selenium supplementation significantly decreased serum glucose, glycated hemoglobin, C-reactive protein, and lipid peroxidation.
- Selenium enhanced antioxidant enzyme activities and reduced phospholipase activity, leading to leukotriene pathway downregulation.
- Selenium inhibited NFκB activation and the expression of pro-inflammatory mediators, including lipoxygenase and cyclooxygenase.
Conclusions:
- Selenium, as sodium selenite, effectively reduces reactive oxygen species production and inhibits NFκB-mediated inflammation in diabetic cardiac hypertrophy.
- Selenium's anti-inflammatory and antioxidant actions downregulate the leukotriene pathway, offering a potential therapeutic strategy for diabetic heart disease.
Abstract:
Cardiac hypertrophy has been considered as an important risk factor of morbidity and mortality. It is characterized as thickening of ventricle wall of the heart and consequent reduction in the contracting ability of the heart to pump the blood. Hyperglycemia-induced reactive oxygen species act as major mediators of diabetic complications. Inflammation plays an essential role in the development of diabetic cardiac hypertrophy. Selenium has been shown to induce insulin-like and anti-inflammatory effects in human and experimental animals. But, its mechanism of action has not been elucidated. Hence, in order to probe into its mechanism at molecular level, we designed an experiment to study the effect of selenium as sodium selenite in streptozotocin-induced diabetic rats. The rats were divided into four groups and maintained as follows: (1) controls, (2) sodium selenite-treated controls, (3) diabetic, and (4) sodium selenite-treated diabetic rats. Duration of the experiment was 30 days. Selenium supplementation enhanced the streptozotocin-induced reduction in the activities of antioxidant enzymes, decreased the serum glucose level, glycated hemoglobin content, concentration of high-sensitivity C-reactive protein, levels of lipid peroxidation products, as well as inflammatory parameters. Decrease in the phospholipase activity by selenium supplementation also contributed to the downregulation of leukotriene pathway. It also downregulated the expressions of nuclear transcription factor κB (NFκB), lipoxygenase, cyclooxygenase, 5-lipoxygenase-activating protein, and receptor for leukotriene B4. Hence, selenium decreased the production of reactive oxygen species and inhibited the activation of NFκB-mediated transcription of pro-inflammatory mediators which resulted in the downregulation of leukotriene pathway in diabetic cardiac hypertrophy.
