Impact of Selenium on the Leukotriene B4 Synthesis Pathway during Isoproterenol-Induced Myocardial Infarction in Experimental Rats

Panicker, Seema; Swathy, S.; John, Febi; Indira, M.

doi:10.1007/s10753-010-9291-3

Cited by 6 publications

(4 citation statements)

References 37 publications

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“…Similarly, Cr(pic)3 has been reported to decrease the levels of TNF-α by reducing the levels of ROS and subsequent NF-kB inhibition (32)(33)(34). Recently, Panicker et al (62) found that rats, when pretreated with selenium before the induction of MI, is efficient in blocking the leukotriene biosynthetic pathway, through inhibiting the expression of both lipooxygenase and leukotriene A4 hydrolase, the two key enzymes in the synthesis of proinflammatory mediator leukotriene B4. Our results provide evidence that Se, Cr (pic)3 and Zn play an important role as anti-inflammatory agents in a rat model of MI, and that Se may be the most potent cardioprotective agent of those tested elements.…”

Section: Discussionmentioning

confidence: 99%

Preventive Effects of Selenium Yeast, Chromium Picolinate, Zinc Sulfate and their Combination on Oxidative Stress, Inflammation, Impaired Angiogenesis and Atherogenesis in Myocardial Infarction in Rats

et al. 2014

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Purpose: Accumulating evidences suggest a critical role of trace metal dyshemostasis in oxidative stress and cardiac dysfunction after myocardial infarction (MI). This study investigated the cardioprotective effects of selenium yeast (Se), chromium picolinate Cr(pic)3, zinc sulfate (Zn) and their combination on isoproterenol (ISO)-induced MI. Methods: Rats were divided into six groups: normal control, ISO control, Se-pretreated (0.1 mg/kg), Cr(pic)3-pretreated (400 µg/kg), Zn-pretreated (30 mg/kg) and metal combination-pretreated groups. All metals were administered for 28 days and at the 27th day, MI was induced by subcutaneous injection of ISO (85 mg/kg) once for two consecutive days. Results: ISO control group showed hyperlipidemia, elevation of cardiac biomarkers and lipid peroxidation and increased immunostaining of p47 phox NADPH oxidase subunit in addition to decreased levels of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). Cardiac levels of tumor necrosis factor-α (TNF-α) were increased, while vascular endothelial growth factor (VEGF, the major angiogenic factor) was decreased. Pretreatment with Se normalized the cardiac enzymes, lipid peroxidation, GSH, SOD, CAT, GPx, TNF-α and VEGF (P<0.001) and reduced the immunostaining of p47 phox subunit. However, Se failed to correct the dyslipidemia. Cr(pic)3 significantly improved lipid profile (P<0.001) and all other biochemical deviations except for VEGF. Zn, but to lesser extent, reduced the oxidative damage and TNF-α levels and improved both dyslipidemia and angiogenesis. Combination therapy exhibited less prominent protection compared to individual metals. Conclusion: Daily supplementation with trace metals is promising for improving myocardial performance via preventing oxidative damage, induction of angiogenesis, anti-inflammatory and/or anti-hyperlipidemic mechanisms.This article is open to POST-PUBLICATION REVIEW. Registered readers (see “For Readers”) may comment by clicking on ABSTRACT on the issue’s contents page.

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Section: Discussionmentioning

confidence: 99%

Preventive Effects of Selenium Yeast, Chromium Picolinate, Zinc Sulfate and their Combination on Oxidative Stress, Inflammation, Impaired Angiogenesis and Atherogenesis in Myocardial Infarction in Rats

et al. 2014

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“…For example, Paniker et al explored the impact of fatty acid substrate availability and downstream eicosanoid enzymic expression ( 89 ) . In their study, sodium selenite (8 µg/100 g body weight) supplementation for 30 d in isoproterenol-induced myocardial infarction in rats decreased LOX activity, leukotriene A 4 hydrolase (LTA 4 H) expression, and LTB 4 production in monocytes ( 89 ) . Se supplementation also decreased the amount of NEFA in the heart which can serve as substrates for LOX enzymic pathways.…”

Section: Can Selemium and Selenoproteins Have An Impact On Inflammatimentioning

confidence: 99%

“…In addition to the antioxidant properties of selenoproteins, other possible mechanisms to explain Se's protective effects in an atherosclerosis disease model were examined. For example, Paniker et al explored the impact of fatty acid substrate availability and downstream eicosanoid enzymic expression ( 89 ) . In their study, sodium selenite (8 µg/100 g body weight) supplementation for 30 d in isoproterenol-induced myocardial infarction in rats decreased LOX activity, leukotriene A 4 hydrolase (LTA 4 H) expression, and LTB 4 production in monocytes ( 89 ) .…”

Section: Can Selemium and Selenoproteins Have An Impact On Inflammatimentioning

confidence: 99%

Regulation of inflammation by selenium and selenoproteins: impact on eicosanoid biosynthesis

2013

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Uncontrolled inflammation is a contributing factor to many leading causes of human morbidity and mortality including atherosclerosis, cancer and diabetes. Se is an essential nutrient in the mammalian diet that has some anti-inflammatory properties and, at sufficient amounts in the diet, has been shown to be protective in various inflammatory-based disease models. More recently, Se has been shown to alter the expression of eicosanoids that orchestrate the initiation, magnitude and resolution of inflammation. Many of the health benefits of Se are thought to be due to antioxidant and redox-regulating properties of certain selenoproteins. The present review will discuss the existing evidence that supports the concept that optimal Se intake can mitigate dysfunctional inflammatory responses, in part, through the regulation of eicosanoid metabolism. The ability of selenoproteins to alter the biosynthesis of eicosanoids by reducing oxidative stress and/or by modifying redox-regulated signalling pathways also will be discussed. Based on the current literature, however, it is clear that more research is necessary to uncover the specific beneficial mechanisms behind the anti-inflammatory properties of selenoproteins and other Se metabolites, especially as related to eicosanoid biosynthesis. A better understanding of the mechanisms involved in Se-mediated regulation of host inflammatory responses may lead to the development of dietary intervention strategies that take optimal advantage of its biological potency.

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“…The Ltb4 expression elevates in MI to stimulate the proinflammatory activity [28]. Moreover, the downregulation of Ltb4 has also been proven to inhibit MI [29], whereas its underlying mechanism in MIinduced cardiomyocyte apoptosis remains to be explored. According to the aforementioned findings, we hypothesized that the silencing of Ltb4r1 could potentially inhibit the progression of CHD-induced MI.…”

Section: Discussionmentioning

confidence: 99%

Constitutive activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway in mice with myocardial injury following acute myocardial infarction

Wang¹,

Wang²,

Wang³

2021

aging

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Coronary heart disease (CHD) with myocardial infarction (MI) being the manifestation of its advanced manifestation, remains the primary cause of mortality and disability worldwide. Aberrant expression of long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) can affect the occurrence of MI in CHD. The present study aimed to explore whether NEAT1 sponging with miR-22-3p affected MI in CHD and its related mechanism. We established that the NEAT1 and Ltb4r1 expressions were increased, while miR-22-3p expression was downregulated in MI mice following CHD. NEAT1 could competitively bind to miR-22-3p and positively regulate Ltb4r1 expression. Ltb4r1 was the downstream target of miR-22-3p. Moreover, silencing NEAT1 or downregulating Ltb4rl expression resulted in improved cardiac function, reduced infarct size, and declined levels of IL-1β, IL-6, and IL-18. Furthermore, silencing of NEAT1 also inhibited apoptosis by decreasing levels of Cleaved caspase-3 and Bax, and increasing Bcl-2 level through sponging miR-22-3p, resulting in reduced myocardial injury in CHD. Altogether, the activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway appears to aggravate myocardial injury following a MI, which suggested that this signaling may be a useful target for improved and more individualized treatments for MI.

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Impact of Selenium on the Leukotriene B4 Synthesis Pathway during Isoproterenol-Induced Myocardial Infarction in Experimental Rats

Cited by 6 publications

References 37 publications

Preventive Effects of Selenium Yeast, Chromium Picolinate, Zinc Sulfate and their Combination on Oxidative Stress, Inflammation, Impaired Angiogenesis and Atherogenesis in Myocardial Infarction in Rats

Preventive Effects of Selenium Yeast, Chromium Picolinate, Zinc Sulfate and their Combination on Oxidative Stress, Inflammation, Impaired Angiogenesis and Atherogenesis in Myocardial Infarction in Rats

Regulation of inflammation by selenium and selenoproteins: impact on eicosanoid biosynthesis

Constitutive activation of the NEAT1/miR-22-3p/Ltb4r1 signaling pathway in mice with myocardial injury following acute myocardial infarction

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