Caffeine suppresses lipopolysaccharide-stimulated BV2 microglial cells by suppressing Akt-mediated NF-κB activation and ERK phosphorylation

Kang, Chang‐Hee; Jayasooriya, Rajapaksha Gendara Prasad Tharanga; Dilshara, Matharage Gayani; Choi, Yung Hyun; Jeong, Yong-Kee; Kim, Nam Deuk; Kim, Gi‐Young

doi:10.1016/j.fct.2012.08.041

Cited by 70 publications

(49 citation statements)

References 29 publications

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“…To investigate whether the inhibition of NF-κB activation by SMEAF is mediated through the MAPKs pathway, the LPS-induced phosphorylation of various MAPK family proteins, particularly p38, JNK and ERK1/ 2, was assessed in BV-2 cells. Previous studies have demonstrated that the phosphorylation levels of ERK, JNK and p38 MAPKs were significantly elevated in activated microglia (Choi & Park, 2012;Kang et al, 2012;. In accordance with these previous findings, we found that LPS caused a significant increase in ERK, JNK and p38 MAPK levels of phosphorylation.…”

Section: Discussionsupporting

confidence: 94%

SMEAF attenuates the production of pro-inflammatory mediators through the inactivation of Akt-dependent NF-κB, p38 and ERK1/2 pathways in LPS-stimulated BV-2 microglial cells

Supriady

Kamarudin

Chan

et al. 2015

Journal of Functional Foods

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Section: Discussionsupporting

confidence: 94%

SMEAF attenuates the production of pro-inflammatory mediators through the inactivation of Akt-dependent NF-κB, p38 and ERK1/2 pathways in LPS-stimulated BV-2 microglial cells

Supriady

Kamarudin

Chan

et al. 2015

Journal of Functional Foods

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“…Although no previous studies have assessed the effects of caffeine on microglia in the developing brain, we show that high-dose caffeine does not lead to activation or proliferation of microglia in the developing ovine WM. Although this finding likely reflects the lack of overt WM injury, it is possible that caffeine may act directly on microglia via adenosine receptors to influence the production of neurotrophins (e.g., nerve growth factor (32)) and suppress pro-inflammatory mediators (33) as seen in the adult brain.…”

Section: Caffeine and Developing White Mattermentioning

confidence: 94%

Impact of daily high-dose caffeine exposure on developing white matter of the immature ovine brain

et al. 2014

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Background: Caffeine is widely used to treat apnea of prematurity, but the standard dosing regimen is not always sufficient to prevent apnea. Before higher doses of caffeine can be used, their effects on the immature brain need to be carefully evaluated. Our aim was to determine the impact of daily highdose caffeine administration on the developing white matter of the immature ovine brain. Methods: High-dose caffeine (25 mg/kg caffeine base loading dose; 20 mg/kg daily maintenance dose; n = 9) or saline (n = 8) were administered to pregnant sheep from 0.7 to 0.8 of term, equivalent to approximately 27-34 wk in humans. At 0.8 of term, the white and gray matter were assessed histologically and immunohistochemically. results: Daily caffeine administration led to peak caffeine concentration of 32 mg/l in fetal plasma at 1 h, followed by a gradual decline, with no effects on mean arterial pressure and heart rate. Initial caffeine exposure led to transient, mild alkalosis in the fetus but did not alter oxygenation. At necropsy, there was no effect of daily high-dose caffeine on brain weight, oligodendrocyte density, myelination, axonal integrity, microgliosis, astrogliosis, apoptosis, or neuronal density. conclusion: Daily high-dose caffeine administration does not appear to adversely affect the developing white matter at the microstructural level.

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“…Linagliptin, loxoprofen, and diclofenac sodium, the latter two being representative anti-inflammatory drugs, significantly inhibited LPS-stimulated IL-6 production to a similar extent. Caffeine also inhibited LPS-stimulated IL-6 production [24]. Both linagliptin and caffeine are drugs with xanthine-related skeletal system activity.…”

Section: Fig 1 Effects Of Linagliptin On Lipopolysaccharide (Lps)-inmentioning

confidence: 99%

“…Moreover, some studies reported that linagliptin decreased the risk of cardiovascular and cerebrovascular diseases, which are associated with systemic atherosclerosis and related prognostic factors [11][12][13]. We previously reported the anti-inflammatory effects of linagliptin in HD patients with diabetes [14] and, on the basis of reports from other groups, proposed three possible underlying mechanisms: increased GLP-1 activity (including an anti-diabetic effect) [15][16][17][18][19][20], inhibition of DPP-4 (CD26) [21][22][23], or xanthine-related skeletal system activity [24,25]. Therefore, linagliptin is a critical therapeutic drug for this patient population, for which inflammation is a prognosis-related factor [26].…”

Section: Introductionmentioning

confidence: 99%

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Linagliptin inhibits lipopolysaccharide-stimulated interleukin-6 production, intranuclear p65 expression, and p38 mitogen-activated protein kinase phosphorylation in human umbilical vein endothelial cells

et al. 2016

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Background: Linagliptin, the only bile-excreted dipeptidyl peptidase-4 (DPP-4) inhibitor, is a therapeutic drug for patients with diabetes receiving hemodialysis, for whom inflammation is a prognosis-related factor, because of its potential anti-inflammatory effects. Although the anti-inflammatory effects of linagliptin in vivo are reported, no study has described these effects in vitro. DPP-4 degrades glucagon-like peptide-1 (GLP-1), which is known to have anti-inflammatory properties. Since GLP-1 is a gut hormone secreted by intestinal L cells, in vivo examination of the GLP-1-independent anti-inflammatory effects of DPP-4 inhibitors is difficult. We evaluated the mitogen-activated protein kinase (MAPK)-dependent, GLP-1-independent, anti-inflammatory effects of linagliptin in lipopolysaccharide (LPS)-stimulated human umbilical vein endothelial cells (HUVECs) which do not secrete GLP-1. Furthermore, to determine whether linagliptin has unique pharmacological actions compared with other DPP-4 inhibitors, we assessed the anti-inflammatory effects of sitagliptin (a DPP-4 inhibitor without xanthine-related skeletal system activity), caffeine (a phosphodiesterase inhibitor), loxoprofen, and diclofenac sodium. Methods: HUVECs were cultured for 24 h at densities of 1-2 × 10 5 cells/mL. We pretreated HUVECs with or without linagliptin (1, 5, 10, 50, and 100 nM), 150 nM sitagliptin, 50 nM caffeine, 17 μM loxoprofen, or 1.3 μM diclofenac sodium for 1 h prior to incubation with LPS. The concentration of LPS used (1 μg/mL) was sufficient to induce an inflammatory response in HUVECs. Five hours after incubation with LPS, culture media was evaluated for interleukin (IL)-6 expression. Intranuclear p65 (a subunit of nuclear factor kappa-B (NFκB)) levels were measured 5 h after treatment with LPS and 50 nM linagliptin, while phosphorylated p38 MAPK levels were measured in the cytosolic fractions obtained 30 min after treatment with LPS and 50 nM linagliptin.

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Caffeine suppresses lipopolysaccharide-stimulated BV2 microglial cells by suppressing Akt-mediated NF-κB activation and ERK phosphorylation

Cited by 70 publications

References 29 publications

SMEAF attenuates the production of pro-inflammatory mediators through the inactivation of Akt-dependent NF-κB, p38 and ERK1/2 pathways in LPS-stimulated BV-2 microglial cells

SMEAF attenuates the production of pro-inflammatory mediators through the inactivation of Akt-dependent NF-κB, p38 and ERK1/2 pathways in LPS-stimulated BV-2 microglial cells

Impact of daily high-dose caffeine exposure on developing white matter of the immature ovine brain

Linagliptin inhibits lipopolysaccharide-stimulated interleukin-6 production, intranuclear p65 expression, and p38 mitogen-activated protein kinase phosphorylation in human umbilical vein endothelial cells

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