Selenium deficiency inhibits micRNA-146a to promote ROS-induced inflammation via regulation of the MAPK pathway in the head kidney of carp

Gao, Xuejiao; Tang, Bin; Liang, Huihuang; Li, Yi; Zou, Wei

doi:10.1016/j.fsi.2019.05.039

Cited by 36 publications

(9 citation statements)

References 34 publications

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“…Mitochondria are the main sources of energy for aerobic respiration. Numerous studies found that the abnormal aerobic respiratory chain in mitochondria could lead to O 2 − accumulation, further resulting in an imbalance between oxidative and antioxidative responses [20,21]. In the present study, Se deficiency caused swelling in mitochondria, strongly suggesting that the aerobic respiratory chain in mitochondria might be destroyed and induce O 2 − accumulation, which gives rise to excessive activation of the oxidative response.…”

Section: Discussionsupporting

confidence: 46%

Selenium Deficiency Causes Inflammatory Injury in the Bursa of Fabricius of Broiler Chickens by Activating the Toll-like Receptor Signaling Pathway

Bai

Zhang

Liu

et al. 2021

Biol Trace Elem Res

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The aim of our study was to observe the effect of selenium (Se) deficiency on inflammatory injury in the bursa of Fabricius of broiler chickens and to determine the role of the Toll-like receptor (TLR)/myeloid differential protein-88 (MyD88)/nuclear factor-κB (NF-κB) signaling pathway during this process. Here, we revealed that severe inflammatory injury occurred in the broiler bursa of Fabricius with Se deficiency via histopathology. Moreover, the ultrastructural pathological results showed that the nuclear, mitochondrial, endoplasmic reticulum and cytomembrane structures were damaged to varying degrees. Additionally, interleukin-2 (IL-2), interleukin-6 (IL-6), and interferon (IFN-γ) mRNA expression was markedly upregulated in the broiler bursa of Fabricius with Se deficiency. Furthermore, TLR, toll-interleukin-1 receptor domain-containing adapter-inducing interferon-β (TRIF), MyD88, and NF-κB mRNA expression was also markedly elevated in the broiler bursa of Fabricius with Se deficiency. The above results suggested that Se deficiency increases the expression of numerous proinflammatory cytokines and is probably due to the activation of the TLR/MyD88/NF-κB signaling pathway, which causes inflammatory injury in the bursa of Fabricius of broiler chickens. Our findings provide a theoretical reference for further studying the underlying mechanism of Se deficiency-induced inflammatory injury in the bursa of Fabricius of broiler chickens.

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Section: Discussionsupporting

confidence: 46%

Selenium Deficiency Causes Inflammatory Injury in the Bursa of Fabricius of Broiler Chickens by Activating the Toll-like Receptor Signaling Pathway

Bai

Zhang

Liu

et al. 2021

Biol Trace Elem Res

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“…In this regard, reduced ROS and H 2 O 2 levels in colitic rats receiving QT-NPs indicated lowered lipid peroxidation and reduced free radical content. This was conceivably due to the fact that QT-NPs can depress the generation of ROS [ 32 , 76 ] by increasing cellular proficiency against oxidative stress with a consequent decline in lipid peroxidation and elevated numbers of healthy cells [ 77 ]. Accordingly, quercetin and resveratrol as naturally therapeutic molecules can hinder ROS, prevent the pro-oxidative damage, and cure oxidative stress-related diseases [ 78 ].…”

Section: Discussionmentioning

confidence: 99%

Therapeutic Potential of Quercetin Loaded Nanoparticles: Novel Insights in Alleviating Colitis in an Experimental DSS Induced Colitis Model

et al. 2022

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Oxidative stress is considered the main etiologic factor involved in inflammatory bowel disease (IBD). Integration of nanocarriers for natural therapeutic agents with antioxidant and anti-inflammatory potential is a novel promising candidate for curing IBD. Herein, the colonic antioxidant and anti-inflammatory effects of different concentrations of quercetin nanoparticles (QT-NPs) were evaluated using a dextran sulfate sodium (DSS)-induced colitis model. Following colitis induction, the efficacy and mechanistic actions of QT-NPs were evaluated by assessing lesion severity, molecular aids controlling oxidative stress and inflammatory response, and histopathological and immunohistochemistry examination of colonic tissues. Administration of QT-NPs, especially at higher concentrations, significantly reduced the disease activity index and values of fecal calprotectin marker compared to the colitic group. Colonic oxidant/antioxidant status (ROS, H2O2, MDA, SOD, CAT, GPX and TAC) was restored after treatment with higher concentrations of QT-NPs. Moreover, QT-NPs at levels of 20 mg/kg and, to a lesser extent, 15 mg/kg reduced Nrf2 and HO-1 gene expression, which was in line with decreasing the expression of iNOS and COX2 in colonic tissues. Higher concentrations of QT-NPs greatly downregulated pro-inflammatory cytokines; upregulated genes encoding occludin, MUC-2 and JAM; and restored the healthy architectures of colonic tissues. Taken together, these data suggest that QT-NPs could be a promising alternative to current IBD treatments.

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“…Selenium is involved in regulating ROS levels and redox balance in all tissues ( Bizerea et al., 2018 ), a large number of studies have shown that ROS is an important target for tissue damage caused by Se deficiency ( Gao et al., 2019 ). found that Se deficiency could stimulate ROS-induced inflammation.…”

Section: Discussionmentioning

confidence: 99%

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

et al. 2021

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Selenium (Se) deficiency can seriously affect the small intestine of swine, and cause diarrhea in swine. However, the specific mechanism of Se deficiency-induced swine diarrhea has rarely been reported. Here, to explore the damage of Se deficiency on the calcium homeostasis and autophagy mechanism of swine, in vivo and in vitro models of swine intestinal Se deficiency were established. Twenty-four pure line castrated male Yorkshire pigs (45 d old, 12.50 ± 1.32 kg, 12 full-sibling pairs) were divided into 2 equal groups and fed Se-deficient diet (0.007 mg Se/kg) as the Se-deficiency group, or fed Se-adequate diet (0.3 mg Se/kg) as the control group for 16 weeks. The intestinal porcine enterocyte cell line (IPEC-J2) was divided into 2 groups, and cultured by Se-deficient medium as the Se-deficient group, or cultured by normal medium as the control group. Morphological observations showed that compared with the control group, intestinal cells in the Se-deficiency group were significantly damaged, and autophagosomes increased. Autophagy staining and cytoplasmic calcium staining results showed that in the Se-deficiency group, autophagy increased and calcium homeostasis was destroyed. According to the reactive oxygen species (ROS) staining results, the percentage of ROS in the Se-deficiency group was higher than that in the control group in the in vitro model. Compared with the control group, the protein and mRNA expressions of autophagy-calcium-related genes including Beclin 1 , microtubule-associated proteins 1A ( LC3-1 ), microtubule-associated proteins 1B ( LC3-2 ), autophagy-related protein 5 ( ATG5 ), autophagy-related protein 12 ( ATG12 ), autophagy-related protein 16 ( ATG16 ), mammalian target of rapamycin ( mTOR ), calmodulin-dependent protein kinase kinase β ( CAMKK-β ), adenosine 5′-monophosphate-activated protein kinase ( AMPK ), sarco(endo)plasmic reticulum Ca 2+ -ATPase ( SERCA ), and calpain in the Se-deficiency group were significantly increased which was consistent in vivo and in vitro ( P < 0.05). Altogether, our results indicated that Se deficiency could destroy the calcium homeostasis of the swine small intestine to trigger cell autophagy and oxidative stress, which was helpful to explain the mechanism of Se deficiency-induced diarrhea in swine.

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Selenium deficiency inhibits micRNA-146a to promote ROS-induced inflammation via regulation of the MAPK pathway in the head kidney of carp

Cited by 36 publications

References 34 publications

Selenium Deficiency Causes Inflammatory Injury in the Bursa of Fabricius of Broiler Chickens by Activating the Toll-like Receptor Signaling Pathway

Selenium Deficiency Causes Inflammatory Injury in the Bursa of Fabricius of Broiler Chickens by Activating the Toll-like Receptor Signaling Pathway

Therapeutic Potential of Quercetin Loaded Nanoparticles: Novel Insights in Alleviating Colitis in an Experimental DSS Induced Colitis Model

Calcium overload and reactive oxygen species accumulation induced by selenium deficiency promote autophagy in swine small intestine

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