Down-regulation of IL-6 production by astaxanthin via ERK-, MSK-, and NF-κB-mediated signals in activated microglia

Kim, Yeon Hyang; Koh, Hyung-Kon; Kim, Doo-Sik

doi:10.1016/j.intimp.2010.09.007

Cited by 76 publications

(68 citation statements)

References 33 publications

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“…Increased DNA binding activity of Rela/p65 is regarded as the key step in the onset of labor [18]. Moreover, the upregulation of Rela/p65 activity enhances gene transcription of proinflammatory cytokines including Il6 and Il8 [19][20][21], which are closely associated with the contraction of uterine smooth muscle and dilation of the cervix [22][23][24]. This study demonstrated that the regulatory role of the Nmb/Nmbr interaction on Rela/p65 and Il6 expression is blocked by siRNA-mediated Nmbr knockdown.…”

Section: Zhang Et Almentioning

confidence: 99%

“…Indeed, Rela/P65 and its associated inflammatory reactions are widely accepted to be a key feature of labor onset [19][20][21]. Downstream effectors in the Rela/P65 pathway, including Il6 and interleukin 1b (Il1b), have been shown to promote cervical ripening, uterine contraction, and acceleration of human parturition [22][23][24]. Therefore, it is hypothesized that Nmb/Nmbr regulates uterine smooth muscle contraction in parturition through regulation of the expression of and …”

Section: Introductionmentioning

confidence: 99%

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Neuromedin B and Its Receptor Influence the Activity of Myometrial Primary Cells In Vitro Through Regulation of Il6 Expression via the Rela/p65 Pathway in Mice1

Zhang

Fei

et al. 2012

Biology of Reproduction

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The neuromedin B receptor (Nmbr) is an important physiological regulator of spontaneous activities and stress responses through different cascades as well as its autocrine and paracrine effects. Previous studies have revealed that neuromedin B (Nmb) and its receptor signal via the Rela (also known as p65)/Il6 pathway in a mouse model of pregnancy. This study investigated the mechanism of Nmbr signaling via the Rela/p65-Il6 pathway and regulation of the concentration of intracellular free calcium ([Ca(2+)](i)) during the onset of labor in primary mouse myometrial cell cultures isolated from mice in term labor. Data demonstrated Nmbr agonist-mediated upregulation of the DNA binding activity of Rela/p65, Il6 expression, and [Ca(2+)](i) in a concentration-dependent manner. Furthermore, a significant correlation was observed between DNA binding activity of Rela/p65 and Il6 expression. Moreover, this up-regulation was blocked by Nmbr and Rela/p65 knockdown, achieved by RNA interference (RNAi) technology. No significant differences were identified in the inhibition of Il6 expression as a result of Nmbr or Rela/p65 knockdown. However, significant differences were observed between the [Ca(2+)](i) in Rela/p65-specific group and that in the Nmbr-specific small interfering RNA (siRNA)-treated groups. These data demonstrated that the Nmb/Nmbr interaction in pregnant myometrial primary cells in vitro predominantly influenced uterine activity through regulation of Il6 expression via the Rela/p65 pathway, although the effects of Nmbr on [Ca(2+)](i) involved several pathways that remain to be elucidated.

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Section: Zhang Et Almentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Neuromedin B and Its Receptor Influence the Activity of Myometrial Primary Cells In Vitro Through Regulation of Il6 Expression via the Rela/p65 Pathway in Mice1

Zhang

Fei

et al. 2012

Biology of Reproduction

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“…Astaxanthin also protected U937 cells from LPS-induced inflammatory and oxidative stress [19]. Astaxanthin inhibited LPS-stimulated IL-6 messenger RNA and protein in BV-2 microglial cells by suppressing ERK-, MSK-, and NF-kBemediated signals [20]. In the present study, treatment with astaxanthin significantly inhibited the elevation of TNF-a, IL-1b, and IL-6 levels at different time points caused by CLP; it is consistent with other reports that demonstrated the potent inhibitory effect of astaxanthin [18e20].…”

Section: Discussionmentioning

confidence: 94%

“…Previous studies have shown that astaxanthin can decrease inflammation by inhibiting reactive oxygen species (ROS)-induced nuclear factor kappa-B (NF-kB) activation [18], it also has therapeutic properties protecting U937 cells from LPS-induced inflammatory and oxidative stress [19]. Astaxanthin inhibited LPS-stimulated IL-6 messenger RNA and protein in BV-2 microglial cells by suppressing extracellular signal-regulated kinase (ERK-), mitogen-and stress-activated protein kinase (MSK-), and NF-kBemediated signals [20]. No evidence has been published, however, whether it has protective effects on sepsis mortality and associated organ dysfunction.…”

Section: Introductionmentioning

confidence: 99%

Protective effect of astaxanthin against multiple organ injury in a rat model of sepsis

Zhou

Gao

Xiao

et al. 2015

Journal of Surgical Research

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“…MAPKs are involved in cellular responses to a variety of stimuli such as pro-infl ammatory cytokines. They regulate cell function, including proliferation, gene expression, differentiation, cell survival, and apoptosis (32).…”

Section: Discussionmentioning

confidence: 99%

Astaxanthin effectiveness in preventing multiple sclerosis in animal model

Bidaran¹,

Ahmadi²,

Yaghmaei³

et al. 2018

BLL

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OBJECTIVE: The aim of the present study was to reveal the effect of therapeutic and prophylactic potential of astaxanthin in experimental autoimmune encephalomyelitis (EAE) as an acceptable model for the study of multiple sclerosis (MS). BACKGROUND: Astaxanthin has powerful antioxidant activities as well as several essential biological functions while multiple sclerosis prevention is highly regarded by researchers. METHODS: The astaxanthin potential in prevention of multiple sclerosis was examined in the chronic model of experimental autoimmune encephalomyelitis (EAE) by using female C57BL/6 mice induced with oligodendrocyte glycoprotein (MOG). Splenocytes were assessed to measure the levels of proinfl ammatory and antiinfl ammatory cytokines, proliferation rate and FoxP3+Treg cell frequency. Immunohistochemical examinations were performed on spinal cord and brain tissue. RESULTS: Astaxanthin reduced splenocytes proliferation index and proinfl ammatory cytokine levels, and vice versa increased the anti-infl ammatory cytokine levels. Immunohistochemical studies of the spinal cord and brain showed that the infi ltration with infl ammatory cells was highly confi ned in the central nervous system. Protective effects of astaxanthin were visible by assigning low score recording in clinical behavior and disease severity. CONCLUSION: Astaxanthin is a powerful tool for intervention in EAE on a model of multiple sclerosis, so it can be studied further to prevent and treat MS (Tab. 2, Fig. 3, Ref. 41). Text in PDF www.elis.sk.

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Down-regulation of IL-6 production by astaxanthin via ERK-, MSK-, and NF-κB-mediated signals in activated microglia

Cited by 76 publications

References 33 publications

Neuromedin B and Its Receptor Influence the Activity of Myometrial Primary Cells In Vitro Through Regulation of Il6 Expression via the Rela/p65 Pathway in Mice1

Neuromedin B and Its Receptor Influence the Activity of Myometrial Primary Cells In Vitro Through Regulation of Il6 Expression via the Rela/p65 Pathway in Mice1

Protective effect of astaxanthin against multiple organ injury in a rat model of sepsis

Astaxanthin effectiveness in preventing multiple sclerosis in animal model

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