Selenium prevents interferon-gamma induced activation of TRPM2 channel and inhibits inflammation, mitochondrial oxidative stress, and apoptosis in microglia

Akyuva, Yener; Nazıroğlu, Mustafa; Yıldızhan, Kenan

doi:10.1007/s11011-020-00624-0

Cited by 30 publications

(17 citation statements)

References 68 publications

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“…The anti-gliomagenic and neuroprotective effect of Se appeared to have a role in regulation of calcium channels, in particular, transient receptor potential (TRP) cationic channels (Figure 2), including TRP melastin 2 (TRPM2) and vanilloid 1 (TRPV1) (Ataizi et al, 2019;Ertilav et al, 2019;Naziroglu et al, 2020;Akyuva et al, 2021). The involvement of TRPM2 channel FIGURE 2 | Schematic model for the potential of selenium on glioblastoma cells.…”

Section: Selenium Effects In Glioblastoma Cellsmentioning

confidence: 99%

“…Interestingly, Naziroglu's group reported that Se-species stimulate glioblastoma cell death by increasing the mitochondrial ROS generation and the intracellular free calcium concentration through enhanced TRPM2 activation (Ertilav et al, 2019). Nonetheless, protective effects were observed in non-malignant cells such as neurons or microglia cells (Ataizi et al, 2019;Ertilav et al, 2019;Akyuva et al, 2021), suggesting a cellular specificity and higher affinity of Se-species on apoptosis and oxidative stress to glioma cells (Yakubov et al, 2014;Hazane-Puch et al, 2016;Harmanci et al, 2017;Yakubov, 2019). It has been previously reported that low doses of organic and inorganic forms of Se-species have antioxidant properties in malignant cell lines, but there are apoptotic effects with high dose applications (Uguz et al, 2009;Harmanci et al, 2017).…”

Section: Selenium Effects In Glioblastoma Cellsmentioning

confidence: 99%

“…It is plausible that a disturbance of NF-κB in microglia/macrophages by Se supplementation can lead to a decrease of the local immune suppression and may also affect the expression of cell survival factors such as interleukin-6 (IL-6), tumor necrosis factor alpha (TNFα), MIF, COX-2, and PGE2 (Xin et al, 2010;Fujita et al, 2011;Li et al, 2018;Liang et al, 2018;Cheng et al, 2020). Recently, it has been shown that Se is able to suppress the proinflammatory activity, and mitochondrial stress via inhibition of calcium channels such as TRPM2 channel (Akyuva et al, 2021). Additional supplements of selenoproteins were also associated with an increasement of migration and phagocytosis properties of microglial cells (Meng et al, 2019).…”

Section: Selenium and Glioma-associated Microgliamentioning

confidence: 99%

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Therapeutic Potential of Selenium in Glioblastoma

et al. 2021

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Little progress has been made in the long-term management of malignant brain tumors, leaving patients with glioblastoma, unfortunately, with a fatal prognosis. Glioblastoma remains the most aggressive primary brain cancer in adults. Similar to other cancers, glioblastoma undergoes a cellular metabolic reprogramming to form an oxidative tumor microenvironment, thereby fostering proliferation, angiogenesis and tumor cell survival. Latest investigations revealed that micronutrients, such as selenium, may have positive effects in glioblastoma treatment, providing promising chances regarding the current limitations in surgical treatment and radiochemotherapy outcomes. Selenium is an essential micronutrient with anti-oxidative and anti-cancer properties. There is additional evidence of Se deficiency in patients suffering from brain malignancies, which increases its importance as a therapeutic option for glioblastoma therapy. It is well known that selenium, through selenoproteins, modulates metabolic pathways and regulates redox homeostasis. Therefore, selenium impacts on the interaction in the tumor microenvironment between tumor cells, tumor-associated cells and immune cells. In this review we take a closer look at the current knowledge about the potential of selenium on glioblastoma, by focusing on brain edema, glioma-related angiogenesis, and cells in tumor microenvironment such as glioma-associated microglia/macrophages.

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Section: Selenium Effects In Glioblastoma Cellsmentioning

confidence: 99%

Section: Selenium Effects In Glioblastoma Cellsmentioning

confidence: 99%

Section: Selenium and Glioma-associated Microgliamentioning

confidence: 99%

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Therapeutic Potential of Selenium in Glioblastoma

et al. 2021

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“…On the other hand, essential elements play key roles in the related molecular mechanisms of metabolism, enzyme activity, and anti-inflammatory cytokines. Akyuva et al reported that Se decreased the inflammation of microglia [ 26 ]. Another study evaluated the restoration of plasma Zn concentrations, leading to a decrease in oxidative stress in hemodialysis patients [ 27 ].…”

Section: Introductionmentioning

confidence: 99%

Use of Generalized Weighted Quantile Sum Regressions of Tumor Necrosis Factor Alpha and Kidney Function to Explore Joint Effects of Multiple Metals in Blood

Luo

Yang³

et al. 2022

IJERPH

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Exposure to heavy metals could lead to adverse health effects by oxidative reactions or inflammation. Some essential elements are known as reactors of anti-inflammatory enzymes or coenzymes. The relationship between tumor necrosis factor alpha (TNF-α) and heavy metal exposures was reported. However, the interaction between toxic metals and essential elements in the inflammatory response remains unclear. This study aimed to explore the association between arsenic (As), cadmium (Cd), lead (Pb), cobalt (Co), copper (Cu), selenium (Se), and zinc (Zn) in blood and TNF-α as well as kidney function. We enrolled 421 workers and measured the levels of these seven metals/metalloids and TNF-α in blood; kidney function was calculated by CKD-EPI equation. We applied weighted quantile sum (WQS) regression and group WQS regression to assess the effects of metal/metalloid mixtures to TNF-α and kidney function. We also approached the relationship between metals/metalloids and TNF-α by generalized additive models (GAM). The relationship of the exposure–response curve between Pb level and TNF-α in serum was found significantly non-linear after adjusting covariates (p < 0.001). Within the multiple-metal model, Pb, As, and Zn were associated with increased TNF-α levels with effects dedicated to the mixture of 50%, 31%, and 15%, respectively. Grouped WQS revealed that the essential metal group showed a significantly negative association with TNF-α and kidney function. The toxic metal group found significantly positive associations with TNF-α, serum creatinine, and WBC but not for eGFR. These results suggested Pb, As, Zn, Se, and mixtures may act on TNF-α even through interactive mechanisms. Our findings offer insights into what primary components of metal mixtures affect inflammation and kidney function during co-exposure to metals; however, the mechanisms still need further research.

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“…According to our present study, kaempferol may be an antioxidant with a good prospect that helps reduce inflammatory response and oxidative stress, thus improving SOP. Moreover, accumulating studies have revealed that the expressions of core targets, including AKT1 [ 58 ], TNF [ 29 ], SRC [ 35 ], CASP3 [ 59 ], JUN [ 44 ], etc., make vital functions in regulating inflammatory response and oxidative stress. Therefore, we speculated that KP could regulate core targets' expressions and bone homeostasis by inflammatory response and oxidative stress in SOP patients, so as to anti-SOP.…”

Section: Discussionmentioning

confidence: 99%

Research on the Mechanism of Kaempferol for Treating Senile Osteoporosis by Network Pharmacology and Molecular Docking

Tang

Zhang

Zhao

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Kaempferol (KP), as a natural anti-inflammatory compound, has been reported to have curative effects on alleviating senile osteoporosis (SOP), which is an inflammation-related musculoskeletal disease, but the molecular mechanisms remain unclear due to scanty relevant studies. We predicted the targets of KP and SOP, and the common targets of them were subsequently used to carry out PPI analysis. Moreover, we adopted GO and KEGG enrichment analysis and molecular docking to explore potential mechanisms of KP against SOP. There were totally 152 KP-related targets and 978 SOP-related targets, and their overlapped targets comprised 68 intersection targets. GO enrichment analysis showed 1529 biological processes ( p < 0.05 ), which involved regulation of inflammatory response, oxidative stress, regulation of bone resorption and remodeling, osteoblast and osteoclast differentiation, etc. Moreover, KEGG analysis revealed 146 items including 44 signaling pathways ( p < 0.05 ), which were closely linked to TNF, IL-17, NF-kappa B, PI3K-Akt, MAPK, estrogen, p53, prolactin, VEGF, and HIF-1 signaling pathways. By means of molecular docking, we found that kaempferol is bound with the key targets’ active pockets through some connections such as hydrogen bond, pi-alkyl, pi-sigma, pi-pi Stacked, pi-pi T-shaped, and van der Waals, illustrating that kaempferol has close combination with the key targets. Collectively, various targets and pathways involve in the process of kaempferol treatment against SOP through regulating inflammatory response, oxidative stress, bone homeostasis, etc. Moreover, our study first reported that kaempferol may regulate core targets’ expression with involvement of inflammatory response, oxidative stress, and bone homeostasis, thus treating SOP.

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Selenium prevents interferon-gamma induced activation of TRPM2 channel and inhibits inflammation, mitochondrial oxidative stress, and apoptosis in microglia

Cited by 30 publications

References 68 publications

Therapeutic Potential of Selenium in Glioblastoma

Therapeutic Potential of Selenium in Glioblastoma

Use of Generalized Weighted Quantile Sum Regressions of Tumor Necrosis Factor Alpha and Kidney Function to Explore Joint Effects of Multiple Metals in Blood

Research on the Mechanism of Kaempferol for Treating Senile Osteoporosis by Network Pharmacology and Molecular Docking

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