Selenium incorporated guar gum nanoparticles safeguard mitochondrial bioenergetics during ischemia reperfusion injury in H9c2 cardiac cells

Soumya, Rema Sreenivasan; Prathapan, A.; Raj, P. Salin; Vineetha, Vadavanath Prabhakaran; Raghu, Kozhiparambil Gopalan

doi:10.1016/j.ijbiomac.2017.08.172

Cited by 16 publications

(9 citation statements)

References 47 publications

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“…When we investigated mitochondrial respiration in heart tissue from exercised mice, no differences were identified. Previous studies have demonstrated that administration of selenium improves mitochondrial respiration in a range of cell types, including heart cells [ 28 , 29 ]. It is possible that the increased mRNA expression of selenoproteins is a compensatory response to early-life selenium deficiency and is providing some degree of protection against mitochondrial dysfunction in the heart.…”

Section: Discussionmentioning

confidence: 99%

Selenium Deficiency during Pregnancy in Mice Impairs Exercise Performance and Metabolic Function in Adult Offspring

2022

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Selenium deficiency during the perinatal period programs metabolic dysfunction in offspring. Postnatal exercise may prevent the development of programmed metabolic disease. This study investigated the impact of selenium deficiency on offspring exercise behavior and whether this improved metabolic health. Female C57BL/6 mice were randomly allocated to control (NormalSe, >190 μg/Se/kg, n = 8) or low-selenium (LowSe, <50 μg/Se/kg, n = 8) diets from four weeks before mating. Male offspring were weaned at postnatal day (PN) twenty-four and placed on a normal chow diet. At PN60, mice were placed in cages with bi-directional running wheels and monitored until PN180. LowSe offspring had a reduced average weekly running speed and distance (p < 0.05). LowSe offspring exhibited glucose intolerance, with increased peak blood glucose (p < 0.05) and area under the curve following an intra-peritoneal injection of glucose (p < 0.05). Furthermore, mRNA expression of several selenoproteins within cardiac and skeletal muscle were increased in LowSe offspring (p < 0.05). The results indicated that selenium deficiency during development reduces exercise behavior. Furthermore, exercise does not prevent programmed glucose intolerance in low-selenium offspring. This highlights that exercise may not be the optimal intervention for metabolic disease in offspring impacted by selenium deficiency in early life.

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Section: Discussionmentioning

confidence: 99%

Selenium Deficiency during Pregnancy in Mice Impairs Exercise Performance and Metabolic Function in Adult Offspring

2022

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“…In addition to SERCA/PLN/PKA C‐α, defective mitochondria also contribute to intracellular calcium overload . Mitochondria are known for its involvement in the regulation of calcium mobilization through the uniporter in the cell.…”

Section: Discussionmentioning

confidence: 99%

High glucose induced calcium overload via impairment of SERCA/PLN pathway and mitochondrial dysfunction leads to oxidative stress in H9c2 cells and amelioration with ferulic acid

Raj

Swapna

Raghu

2019

Fundamemntal Clinical Pharma

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Oxidative stress and associated complications are the major pathological concerns of diabetic cardiomyopathy (DC). We aim to elucidate the mechanisms by which high glucose (HG) induced alteration in calcium homeostasis and evaluation of the beneficial effect of two concentrations (10 and 25 μm) of ferulic acid (FA). HG was induced in H9c2 cardiomyoblast by treating with glucose (33 mm) for 48 h, and FA was co‐treated. Intracellular calcium ([Ca2+]i) overload was found increased significantly with HG. For elucidation of mechanism, the SERCA pathway and mitochondrial integrity (transmembrane potential and permeability transition pore) were explored. Then, we assessed oxidative stress, and cell injury with brain natriuretic peptide (BNP), atrial natriuretic peptide (ANP), and lactate dehydrogenase (LDH) release. HG caused significant [Ca2+]i overload through downregulation of SERCA2/1, pPLN, and pPKA C‐α; and upregulation of PLN and PKA C‐α and alteration in the integrity of mitochondria with HG. The [Ca2+]i overload in turn caused oxidative stress via generation of reactive oxygen species, lipid peroxidation, and protein carbonylation. This resulted in cell injury which was evident with significant release of BNP, ANP, and LDH. FA co‐treatment was effective to mitigate all pathological changes caused by HG. From the overall results, we conclude that [Ca2+]i overload via SERCA pathway and altered mitochondrial integrity is the main cause for oxidative stress during HG. Based on our result, we report that FA could be an attractive nutraceutical for DC.

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“…A previous study found that sodium selenite pretreatment reduced I/R induced cardiac injury in rats 30 .…”

Section: Introductionmentioning

confidence: 92%

Selenomethionine Alleviates Intestinal Ischemia Reperfusion Injury by Inhibiting Mitochondrion-mediated Apoptosis in Mice 

Liu

Mou

et al. 2020

Preprint

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The mechanism of supplement selenomethionine (SeMet) mitigates ischemia reperfusion (I/R)- damage remains to be elucidated in the intestinal tissues of mice. In this study, a model of intestinal I/R injury was established. The levels of redox factors, such as the activities of glutathione peroxidase-1(Gpx1), catalase (CAT), superoxide dismutase (SOD) and malondialdehyde (MDA) content, were detected using ELISA assays in the intestinal tissues of mice. Several apoptosis-related markers (cytochrome c (Cyt-c), Bcl-2, Bax, and caspase-3) were detected using qPCR and Western blot. The results showed that SeMet alleviated I/R damage by increasing the activities of Gpx1, CAT, SOD and reducing MDA content. Our data demonstrated that SeMet reduced I/R induced mitochondrial damage and inhibited the expression of Cyt-c. SeMet also increased the Bcl-2 /Bax ratio and reduced the expression of Bax and caspase-3 in the mice intestinal tissues. Thus our data reveals that I/R could lead to increased apoptosis, and SeMet alleviated I/ R-induced apoptosis via maintaining REDOX homeostasis and attenuating mitochondrial pathway in the mice intestinal tissues.

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Selenium incorporated guar gum nanoparticles safeguard mitochondrial bioenergetics during ischemia reperfusion injury in H9c2 cardiac cells

Cited by 16 publications

References 47 publications

Selenium Deficiency during Pregnancy in Mice Impairs Exercise Performance and Metabolic Function in Adult Offspring

Selenium Deficiency during Pregnancy in Mice Impairs Exercise Performance and Metabolic Function in Adult Offspring

High glucose induced calcium overload via impairment of SERCA/PLN pathway and mitochondrial dysfunction leads to oxidative stress in H9c2 cells and amelioration with ferulic acid

Selenomethionine Alleviates Intestinal Ischemia Reperfusion Injury by Inhibiting Mitochondrion-mediated Apoptosis in Mice

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Selenium incorporated guar gum nanoparticles safeguard mitochondrial bioenergetics during ischemia reperfusion injury in H9c2 cardiac cells

Cited by 16 publications

References 47 publications

Selenium Deficiency during Pregnancy in Mice Impairs Exercise Performance and Metabolic Function in Adult Offspring

Selenium Deficiency during Pregnancy in Mice Impairs Exercise Performance and Metabolic Function in Adult Offspring

High glucose induced calcium overload via impairment of SERCA/PLN pathway and mitochondrial dysfunction leads to oxidative stress in H9c2 cells and amelioration with ferulic acid

Selenomethionine&nbsp;Alleviates&nbsp;Intestinal Ischemia Reperfusion&nbsp;Injury&nbsp;by Inhibiting Mitochondrion-mediated Apoptosis&nbsp;in&nbsp;Mice&nbsp;

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Selenomethionine Alleviates Intestinal Ischemia Reperfusion Injury by Inhibiting Mitochondrion-mediated Apoptosis in Mice