Anti-Inflammatory Effect of Ginsenoside Rg5 in Lipopolysaccharide-Stimulated BV2 Microglial Cells

Lee, Yu Young; Jin-Sun, Park; Jung, Jisun; Kim, Dong-Hyun; Kim, Hee-Sun

doi:10.3390/ijms14059820

Cited by 66 publications

(48 citation statements)

References 36 publications

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“…The transcription factor NF- κ B, widely expressed in the nervous system, plays a leading role in LPS-induced inflammatory responses [15]. In this study, we noted that NF- κ B activation was dramatically induced by LPS stimulation, while salidroside regulates microglial activation by inhibiting the I κ B α degradation and phosphorylation of I κ B α and p65, a subunit of NF- κ B.…”

Section: Discussionmentioning

confidence: 74%

Salidroside Reduces Cell Mobility via NF‐κB and MAPK Signaling in LPS‐Induced BV2 Microglial Cells

Zhu

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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The unregulated activation of microglia following stroke results in the production of toxic factors that propagate secondary neuronal injury. Salidroside has been shown to exhibit protective effects against neuronal death induced by different insults. However, the molecular mechanisms responsible for the anti-inflammatory activity of salidroside have not been elucidated clearly in microglia. In the present study, we investigated the molecular mechanism underlying inhibiting LPS-stimulated BV2 microglial cell mobility of salidroside. The protective effect of salidroside was investigated in microglial BV2 cell, subjected to stretch injury. Moreover, transwell migration assay demonstrated that salidroside significantly reduced cell motility. Our results also indicated that salidroside suppressed LPS-induced chemokines production in a dose-dependent manner, without causing cytotoxicity in BV2 microglial cells. Moreover, salidroside suppressed LPS-induced activation of nuclear factor kappa B (NF-κB) by blocking degradation of IκBα and phosphorylation of MAPK (p38, JNK, ERK1/2), which resulted in inhibition of chemokine expression. These results suggest that salidroside possesses a potent suppressive effect on cell migration of BV2 microglia and this compound may offer substantial therapeutic potential for treatment of ischemic strokes that are accompanied by microglial activation.

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Section: Discussionmentioning

confidence: 74%

Salidroside Reduces Cell Mobility via NF‐κB and MAPK Signaling in LPS‐Induced BV2 Microglial Cells

Zhu

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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“…In addition, elevated H 2 O 2 due to SOD upregulation leads to the activation of mitogen‐activated protein kinase (MAPK), which decreases the levels of the antiapoptotic factor Mcl1, resulting in apoptotic cell death . The transcription factor NF‐κB plays a leading role in the inflammatory response . TCDD activates MAPK, triggering subsequent redox imbalance through CYP1A1 expression .…”

Section: Discussionmentioning

confidence: 99%

Actein alleviates 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin‐mediated cellular dysfunction in osteoblastic MC3T3‐E1 cells

Choi

Suh

Jung

et al. 2017

Environmental Toxicology

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The environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is known to affect bone metabolism. We evaluated the protective effects of the triterpene glycoside actein from the herb black cohosh against TCDD-induced toxicity in MC3T3-E1 osteoblastic cells. We found that TCDD significantly reduced cell viability and increased apoptosis and autophagy in MC3T3-E1 osteoblastic cells (P < .05). In addition, TCDD treatment resulted in a significant increase in intracellular calcium concentration, mitochondrial membrane potential collapse, reactive oxygen species (ROS) production, and cardiolipin peroxidation, whereas pretreatment with actein significantly mitigated these effects (P < .05). The effects of TCDD on extracellular signal-related kinase (ERK), aryl hydrocarbon receptor, aryl hydrocarbon receptor repressor, and cytochrome P450 1A1 levels in MC3T3-E1 cells were significantly inhibited by actein. The levels of superoxide dismutase, ERK1, and nuclear factor kappa B mRNA were also effectively restored by pretreatment with actein. Furthermore, actein treatment resulted in a significant increase in alkaline phosphatase (ALP) activity and collagen content, as well as in the expression of genes associated with osteoblastic differentiation (ALP, type I collagen, osteoprotegerin, bone sialoprotein, and osterix). This study demonstrates the underlying molecular mechanisms of cytoprotection exerted by actein against TCDD-induced oxidative stress and osteoblast damage.

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Section: R E T R a C T E Dmentioning

confidence: 99%

“…Data have shown that activated microglia change their morphology, proliferate and enhance the expression of distinctive surface molecules such as CD40 and MHC II. Furthermore, activation of microglia results in the release of various proinflammatory cytokines such as IL1b, IL-18, TNF-a, and IL-6, as well as neurotoxic mediators like nitric oxide (NO), prostaglandin (PG) E2 and superoxide anion (Jana et al 2007;Lee et al 2013).It should be noted that many factors trigger pathological microglial activation. One such factor is experimental exposure to a primary component of endotoxin from Gramnegative bacteria cell walls, lipopolysaccharide (LPS) (Kettenmann et al 2011).…”

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confidence: 99%

Retracted: Anti‐inflammatory properties of tianeptine on lipopolysaccharide‐induced changes in microglial cells involve toll‐like receptor‐related pathways

Ślusarczyk

Trojan

Głombik

et al. 2016

Journal of Neurochemistry

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Accumulating evidence suggests that activation of microglia plays a key role in the pathogenesis of depression. Activated microglia produce a wide range of factors whose prolonged or excessive release may lead to brain disorders. Thus, the inhibition of microglial cells may be beneficial in the treatment of depressive diseases. Tianeptine is an atypical antidepressant drug with proven clinical efficacy, but its mechanism of action remains still not fully understood. In the present study, using microglial cultures we investigated whether tianeptine modifies microglial activation after lipopolysaccharide (LPS) stimulation and which intracellular pathways are involved in the activity of this antidepressant. Our study shows that tianeptine attenuated the LPS-evoked inflammatory activation of microglia by decreasing the expression of proinflammatory cytokines such as IL-1b, IL-18, IL-6 and tumor necrosis factor a (TNF-a), the release of nitric oxide (NO) and reactive oxygen species (ROS) as well as the expression of inducible nitric oxide synthase. Analyses of signaling pathways demonstrate that tianeptine led to the suppression of LPS-induced TLR4 expression and ERK1/2 phosphorylation. Furthermore, our study reveals the inhibitory impact of tianeptine on caspase-3-induced PKCd degradation and consequently on the activation of NF-jB factor in microglial cells. Taken together, present results show anti-inflammatory properties of tianeptine in microglial cultures stimulated by LPS. This study provides evidence that the inhibition of microglial activation may underlie the therapeutic activity of tianeptine. Keywords: antidepressant drugs, cytokines, inflammation, intracellular pathways, microglia, tianeptine. J. Neurochem. (2016) 136, 958-970. Increasing evidence indicates that microglia, the resident immune cells in the central nervous system (CNS), may be considered the main mediators of inflammation-associated disorders. These cells manage the innate and adaptive immune responses in various pathological processes including brain trauma, ischemia, stroke and infections, as well as during CNS repair (Graeber and Streit 2010;Yang et al. 2011). It has been observed that active microglia can clear Received September 29, 2015; revised manuscript received November 16, 2015; accepted November 17, 2015. Address correspondence and reprint requests to Agnieszka BastaKaim, Department of Experimental Neuroendocrinology, Polish Academy of Sciences, 12 Sme z tna St., 31-343 Krak ow, Poland. E-mail: basta@if-pan.krakow.plAbbreviations used: AP-1, activator protein-1; CD40, cluster of differentiation 40; DCFH, 2 0 ,7 0 -dichlorodihydrofluorescin; DCFH-DA, 2 0 ,7 0 -dichlorofluorescin diacetate; DMEM, Dulbecco's modified Eagle medium; FAM, fluorescein amidite; FBS, fetal bovine serum; HBSS, Hank's Balanced Salt Solution; HPA, hypothalamus-pituitary-adrenal; IL-18, interleukin 18; IL-1b, interleukin 1b; IL-6, interleukin 6; JNK, cJun N-terminal kinase; LDH, lactate dehydrogenase; MCP-1, monocyte chemoattractant protein-1;...

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Anti-Inflammatory Effect of Ginsenoside Rg5 in Lipopolysaccharide-Stimulated BV2 Microglial Cells

Cited by 66 publications

References 36 publications

Salidroside Reduces Cell Mobility via NF‐κB and MAPK Signaling in LPS‐Induced BV2 Microglial Cells

Salidroside Reduces Cell Mobility via NF‐κB and MAPK Signaling in LPS‐Induced BV2 Microglial Cells

Actein alleviates 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin‐mediated cellular dysfunction in osteoblastic MC3T3‐E1 cells

Retracted: Anti‐inflammatory properties of tianeptine on lipopolysaccharide‐induced changes in microglial cells involve toll‐like receptor‐related pathways

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