Rifampicin inhibits microglial inflammation and improves neuron survival against inflammation

Bi, Wei; Zhu, Lihong; Wang, Chuanming; Liang, Yucheng; Li, Jun; Shi, Qi; Tao, Enxiang

doi:10.1016/j.brainres.2011.04.019

Cited by 80 publications

(81 citation statements)

References 49 publications

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“…It has been documented that MAPKs, such as p38, JNK, and ERK, are major modulators for iNOS expression induced by LPS in microglial cells (6,7). MAPKs modulate iNOS expression via up-regulating NF-κB activity (6,7). In our previous study, the increase of MAPKs was detected after 15 min of LPS stimulation, reached a maximum after 30 min, and then decreased.…”

Section: Discussionmentioning

confidence: 77%

“…Regulation of NO include two critical signal transduction molecules, MAPK and NF-κB (4,6,8). It has been documented that MAPKs, such as p38, JNK, and ERK, are major modulators for iNOS expression induced by LPS in microglial cells (6,7). MAPKs modulate iNOS expression via up-regulating NF-κB activity (6,7).…”

Section: Discussionmentioning

confidence: 99%

“…Activated NF-κB and MAPKs participate in production of NO and iNOS induced by LPS (4,7,24). MAPK regulated NO and iNOS production has been proved to require NF-κB activation in glial cells (24,25).…”

Section: Puerarin Represses Phosphorylation Of Some Of Mapks In N9 Cementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…Microglia cell inflammatory response to LPS is involved in speedy regulation of many signal transduction molecules. The regulation of a signal pathway, such as mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB), is implicated in major molecular mechanisms of LPS-induced NO and ROS production in microglial cells (4,(6)(7)(8).O-Linked O-GlcNAcylation of protein, a single monosaccharide N-acetylglucosamine (GlcNAc) attached to the hydroxyl groups of specific serine or threonine residues, is an important post-translational modification on nuclear and cytoplasmic proteins (9,10). More than 500 proteins have been identified to be O-GlcNAcylated, and these proteins are involved in regulation of cell processes including cell cycle, transcription, trafficking and signaling (11).…”

mentioning

confidence: 99%

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Puerarin suppresses production of nitric oxide and inducible nitric oxide synthase in lipopolysaccharide-induced N9 microglial cells through regulating MAPK phosphorylation, O-GlcNAcylation and NF-κB translocation

Zheng

Yu²,

Yang

2012

Int J Oncol

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Abstract. Microglial cells play a critical role in mediating central nervous system inflammatory processes. Activated microglial cells induced by proinflammatory factor, such as lipopolysaccharide (LPS), release many kinds of neurotoxic cytokines including reactive oxygen species (ROS) which contributes to the pathogenesis of neurodegenerative diseases. Puerarin, extracted from kudzu root, possesses the characteristic of neuroprotection, antioxidation and anticancer. In the present study, we observed that LPS induced over-production of nitric oxide (NO) and increased the level of intracellular ROS in N9 microglial cells, but it was inhibited by puerarin. Furthermore, treatment with puerarin on N9 cells suppressed the over-expression of inducible nitric oxide synthase (iNOS) induced by LPS which is implicated in intracellular O-linked β-N-acetylglucosamine (O-GlcNAc) level, phosphorylation of mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) signaling pathway. We also observed that the enhanced phosphorylation of p38, JNK and ERK1/2 in N9 cells induced by LPS were inhibited by puerarin, otherwise the down-regulation of O-GlcNAcylation level of protein in N9 cell induced by LPS was up-regulated by pretreatment with puerarin. These results indicate that puerarin effectively inhibits microglia activation induced by LPS through inhibiting expression of iNOS, production of NO and ROS which was mediated via regulating O-GlcNAcylation, phosphorylation of MAPK and NF-κB translocation. IntroductionMicroglial cells, macrophage-like cells in the central nervous system, participate in CNS immune response through releasing a variety of factors, including trophic factors and chemokines, to promote neuroprotection (1). Whereas under chronic inflammatory environment, excessive activation of microglia cells secrete cytotoxic substances and neurotoxic cytokines, such as reactive oxygen species (ROS) and nitric oxide (NO) which contribute to the pathogenesis of neurodegenerative diseases (2). Lipopolysaccharide (LPS), which consist in outer membrane of gram-negative bacteria as potent pro-inflammatory agents, induce microglial cell inflammatory injury through releasing proinflammatory mediators such as NO generated by inducible nitric oxide synthase (iNOS) (3,4). NO is considered as a main risk factor of progressive damage in neurodegenerative diseases (5,6). Microglia cell inflammatory response to LPS is involved in speedy regulation of many signal transduction molecules. The regulation of a signal pathway, such as mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB), is implicated in major molecular mechanisms of LPS-induced NO and ROS production in microglial cells (4,(6)(7)(8).O-Linked O-GlcNAcylation of protein, a single monosaccharide N-acetylglucosamine (GlcNAc) attached to the hydroxyl groups of specific serine or threonine residues, is an important post-translational modification on nuclear and cytoplasmic proteins (9,10). More than 500 proteins have been identified to be O-GlcNAcylated...

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Section: Discussionmentioning

confidence: 77%

Section: Discussionmentioning

confidence: 99%

Section: Puerarin Represses Phosphorylation Of Some Of Mapks In N9 Cementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Puerarin suppresses production of nitric oxide and inducible nitric oxide synthase in lipopolysaccharide-induced N9 microglial cells through regulating MAPK phosphorylation, O-GlcNAcylation and NF-κB translocation

Zheng

Yu²,

Yang

2012

Int J Oncol

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Targeted brain delivery of RVG29‐modified rifampicin‐loaded nanoparticles for Alzheimer's disease treatment and diagnosis

Zhou

Zhu

Zeng

et al. 2022

Bioengineering & Transla Med

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Alzheimer's disease (AD) is an aging-related neurodegenerative disease. The main pathological features of AD are β-amyloid protein (Aβ) deposition and tau protein hyperphosphorylation. Currently, there are no effective drugs for the etiological treatment of AD. Rifampicin (RIF) is a semi-synthetic broad-spectrum antibiotic with anti-β-amyloid deposition, anti-inflammatory, anti-apoptosis, and neuroprotective effects, but its application in AD treatment has been limited for its strong hydrophobicity, high toxicity, short half-life, low bioavailability, and blood-brain barrier hindrance. We designed a novel brain-targeted and MRI-characteristic nanomedicine via loading rabies virus protein 29 (RVG29), rifampicin, and Gd on poly (L-lactide) nanoparticles

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AGEs and chronic subclinical inflammation in diabetes: disorders of immune system

Jiang

Ren

et al. 2015

Diabetes Metabolism Res

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Chronic subclinical inflammation represents a risk factor of type 2 diabetes and several diabetes complications, including neuropathy and atherosclerosis including macro-vasculopathy and micro-vasculopathy. However, the inflammatory response in the diabetic wound was shown to be remarkably hypocellular, unregulated and ineffective. Advanced glycation end products (AGEs) and one of its receptors, RAGE, were involved in inducing chronic immune imbalance in diabetic patients. Such interactions attracts immune cell into diffused glycated tissue and activates these cells to induce inflammatory damage, but disturbs the normal immune rhythm in diabetic wound. Traditional measurements of AGEs are high-performance liquid chromatography and immunohistochemistry staining, but their application faces the limitations including complexity, cost and lack of reproducibility. A new noninvasive method emerged in 2004, using skin autofluorescence as indicator for AGEs accumulation. It had been reported to be informative in evaluating the chronic risk of diabetic patients. Studies have indicated therapeutic potentials of anti-AGE recipes. These recipes can reduce AGE absorption/de novo formation, block AGE-RAGE interaction and arrest downstream signaling after RAGE activation.

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Rifampicin inhibits microglial inflammation and improves neuron survival against inflammation

Cited by 80 publications

References 49 publications

Puerarin suppresses production of nitric oxide and inducible nitric oxide synthase in lipopolysaccharide-induced N9 microglial cells through regulating MAPK phosphorylation, O-GlcNAcylation and NF-κB translocation

Puerarin suppresses production of nitric oxide and inducible nitric oxide synthase in lipopolysaccharide-induced N9 microglial cells through regulating MAPK phosphorylation, O-GlcNAcylation and NF-κB translocation

Targeted brain delivery of RVG29‐modified rifampicin‐loaded nanoparticles for Alzheimer's disease treatment and diagnosis

AGEs and chronic subclinical inflammation in diabetes: disorders of immune system

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