Protective potential of IL-6 against trimethyltin-induced neurotoxicity in vivo

Tran, Hoang Yen Phi; Shin, Eun Joo; Nguyen, Xuan Khanh Thi; Chung, Yoon Hee; Jeong, Ji Hoon; Bach, Jae Hyung; Park, Dae-Hun; Yamada, Kiyofumi; Nabeshima, Toshitaka; Yoneda, Yukio; Kim, Hyoung Chun

doi:10.1016/j.freeradbiomed.2011.12.008

Cited by 59 publications

(44 citation statements)

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“…[14][15][16] Also, interleukin-6 exerts a neuroprotective effect by inhibiting excitotoxicity-induced oxidative stress via the transcriptional activation of genes involved in reducing glutathione synthesis. [17][18] Furthermore, interleukin-6 upregulation has been shown to be correlated with an improved outcome in children with severe traumatic brain injuries via endogenous neuroprotection. 19 The current study showed that the interleukin-6 concentration in the plasma of the febrile seizure patients was higher than that in those with severe acute encephalitis, suggesting that interleukin-6 plays a neuroprotective role in febrile seizures as a compensatory measure preventing further brain parenchymal damage.…”

Section: Discussionmentioning

confidence: 99%

Analysis of Plasma Multiplex Cytokines for Children With Febrile Seizures and Severe Acute Encephalitis

Huang

et al. 2013

J Child Neurol

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We investigated the plasma cytokine profiles of children with febrile seizures or severe acute encephalitis using multiplex cytometry to evaluate the role of cytokines in these diseases. Interleukin-6, -10, -12p70, -17A, -2, -4, -5, -9, -13, -22, and -1β, interferon-γ, and tumor necrosis factor-α were measured in the plasma from children with febrile seizures (n = 9) or severe acute encephalitis (n = 21). In multivariate analysis, interleukin-6 was significantly increased in the plasma of the febrile seizure patients compared to those with severe acute encephalitis, suggesting that interleukin-6 is activated during the acute stage of a febrile seizure. A lower plasma interleukin-6 concentration was significantly associated with severe acute encephalitis. The cytokine network may be deregulated in severe acute encephalitis via the persistence of an uncontrolled inflammatory state in the brain.

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Section: Discussionmentioning

confidence: 99%

Analysis of Plasma Multiplex Cytokines for Children With Febrile Seizures and Severe Acute Encephalitis

Huang

et al. 2013

J Child Neurol

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“…Nevertheless, inhibition of IL-6 signaling resulted in delayed PDAC progression from pancreatic intraepithelial neoplasia, and reduced primary tumor growth and recurrences in vivo [43, 44]. While it is unclear whether Nrf2 is a target gene of IL-6, Nrf2 nuclear translocation and transcriptional activity were significantly reduced in IL-6 knockout mice [45]. Activation of Nrf2 in PDAC may exert a positive feedback to further enhance IL-6 signaling, as there is a known ARE sequence within the promoter of IL-6 [46].…”

Section: Discussionmentioning

confidence: 99%

Soluble factors from stellate cells induce pancreatic cancer cell proliferation via Nrf2-activated metabolic reprogramming and ROS detoxification

Looi

Subramaniam

et al. 2016

Oncotarget

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Pancreatic stellate cells (PSC), a prominent stromal cell, contribute to the progression of pancreatic ductal adenocarcinoma (PDAC). We aim to investigate the mechanisms by which PSC promote cell proliferation in PDAC cell lines, BxPC-3 and AsPC-1. PSC-conditioned media (PSC-CM) induced proliferation of these cells in a dose- and time-dependent manner. Nrf2 protein was upregulated and subsequently, its transcriptional activity was increased with greater DNA binding activity and transcription of target genes. Downregulation of Nrf2 led to suppression of PSC-CM activity in BxPC-3, but not in AsPC-1 cells. However, overexpression of Nrf2 alone resulted in increased cell proliferation in both cell lines, and treatment with PSC-CM further enhanced this effect. Activation of Nrf2 pathway resulted in upregulation of metabolic genes involved in pentose phosphate pathway, glutaminolysis and glutathione biosynthesis. Downregulation and inhibition of glucose-6-phosphate-dehydrogenase with siRNA and chemical approaches reduced PSC-mediated cell proliferation. Among the cytokines present in PSC-CM, stromal-derived factor-1 alpha (SDF-1α) and interleukin-6 (IL-6) activated Nrf2 pathway to induce cell proliferation in both cells, as shown with neutralization antibodies, recombinant proteins and signaling inhibitors. Taken together, SDF-1α and IL-6 secreted from PSC induced PDAC cell proliferation via Nrf2-activated metabolic reprogramming and ROS detoxification.

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“…The MDA level was measured using HPLC-UV/VIS detection system (model LC-20AT and SPD-20A, Shimadzu, Kyoto, Japan) as described by Richard et al [52] with slight modifications [49, 53]. Briefly, each hippocampal tissue was homogenized in PBS, and 0.1 ml of this homogenate (or standard solutions prepared daily from 1,1,3,3-tetra-methoxypropane) and 0.75 ml of the working solution (thiobarbituric acid 0.37% and perchloric acid 6.4%, 2:1, v : v ) were mixed and heated to 95 °C for 1 h. After cooling (10 min in ice water bath), the flocculent precipitate was removed by centrifugation at 3200 × g for 10 min.…”

Section: Methodsmentioning

confidence: 99%

“…Results are expressed as nanomoles of DNPH incorporated/mg protein [49, 53] based on the extinction coefficient for aliphatic hydrazones at 21 mM −1 ·cm −1 .…”

Section: Methodsmentioning

confidence: 99%

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YY-1224, a terpene trilactone-strengthened Ginkgo biloba, attenuates neurodegenerative changes induced by β-amyloid (1-42) or double transgenic overexpression of APP and PS1 via inhibition of cyclooxygenase-2

Chung

Shin

et al. 2017

J Neuroinflammation

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Background Ginkgo biloba has been reported to possess free radical-scavenging antioxidant activity and anti-inflammatory properties. In our pilot study, YY-1224, a terpene trilactone-strengthened extract of G. biloba, showed anti-inflammatory, neurotrophic, and antioxidant effects.ResultsWe investigated the pharmacological potential of YY-1224 in β-amyloid (Aβ) (1-42)-induced memory impairment using cyclooxygenase-2 (COX-2) knockout (−/−) and APPswe/PS1dE9 transgenic (APP/PS1 Tg) mice. Repeated treatment with YY-1224 significantly attenuated Aβ (1-42)-induced memory impairment in COX-2 (+/+) mice, but not in COX-2 (−/−) mice. YY-1224 significantly attenuated Aβ (1-42)-induced upregulation of platelet-activating factor (PAF) receptor gene expression, reactive oxygen species, and pro-inflammatory factors. In addition, YY-1224 significantly inhibited Aβ (1-42)-induced downregulation of PAF-acetylhydrolase-1 (PAF-AH-1) and peroxisome proliferator-activated receptor γ (PPARγ) gene expression. These changes were more pronounced in COX-2 (+/+) mice than in COX-2 (−/−) mice. YY-1224 significantly attenuated learning impairment, Aβ deposition, and pro-inflammatory microglial activation in APP/PS1 Tg mice, whereas it significantly enhanced PAF-AH and PPARγ expression. A preferential COX-2 inhibitor, meloxicam, did not affect the pharmacological activity by YY-1224, suggesting that the COX-2 gene is a critical mediator of the neuroprotective effects of YY-1224. The protective activity of YY-1224 appeared to be more efficacious than a standard G. biloba extract (Gb) against Aβ insult.ConclusionsOur results suggest that the protective effects of YY-1224 against Aβ toxicity may be associated with its PAF antagonistic- and PPARγ agonistic-potential as well as inhibition of the Aβ-mediated pro-inflammatory switch of microglia phenotypes through suppression of COX-2 expression.Electronic supplementary materialThe online version of this article (doi:10.1186/s12974-017-0866-x) contains supplementary material, which is available to authorized users.

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Protective potential of IL-6 against trimethyltin-induced neurotoxicity in vivo

Cited by 59 publications

References 50 publications

Analysis of Plasma Multiplex Cytokines for Children With Febrile Seizures and Severe Acute Encephalitis

Analysis of Plasma Multiplex Cytokines for Children With Febrile Seizures and Severe Acute Encephalitis

Soluble factors from stellate cells induce pancreatic cancer cell proliferation via Nrf2-activated metabolic reprogramming and ROS detoxification

YY-1224, a terpene trilactone-strengthened Ginkgo biloba, attenuates neurodegenerative changes induced by β-amyloid (1-42) or double transgenic overexpression of APP and PS1 via inhibition of cyclooxygenase-2

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