Inhibition of NF-κB activation is associated with anti-inflammatory and anti-apoptotic effects of Ginkgolide B in a mouse model of cerebral ischemia/reperfusion injury

Gu, Jin-Hua; Ge, Jingping; Li, Mei; Wu, Feng; Zhang, Wei; Qin, Zheng‐Hong

doi:10.1016/j.ejps.2012.07.016

Cited by 127 publications

(79 citation statements)

References 36 publications

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“…13,18 The dose of GB used in different cells varies from 25−1000 μΜ, and in our study, we demonstrated that GB exerted anti-inflammation and anti-apoptosis effects in chondrocytes at doses of 50−100 μΜ. 7,10,12 Previous studies have suggested that LPS markedly induces upregulation of genes and the generation of various matrix-degrading enzymes and proinflammatory cytokines, including IL-6, Cox-2, ADAMTS-5, ADAMTS-4, MMP-13 and MMP-3, in chondrocytes. 19 The expression of ADAMTSs and MMPs has been extensively detected in the process of OA.…”

Section: Discussionmentioning

confidence: 59%

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Ginkgolide B exerts anti-inflammatory and chondroprotective activity in LPS-induced chondrocytes

Hu¹,

Li²,

Xin³

et al. 2018

Adv Clin Exp Med

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Section: Discussionmentioning

confidence: 59%

“…33 Ginkolide B was proved to be an effective anti-inflammatory agent in different diseases. 10,11,34 MAPK is an important pathway that is involved in chondrocyte mechanical stress and inflammation. 35 The effect of inhibiting p38 in cartilage was tested in a previous study.…”

Section: Discussionmentioning

confidence: 99%

Ginkgolide B exerts anti-inflammatory and chondroprotective activity in LPS-induced chondrocytes

Hu¹,

Li²,

Xin³

et al. 2018

Adv Clin Exp Med

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“…When activated by various stimulants such as LPS, IκBα is phosphorylated by IκB kinase (IKK) and is separated from NF-κB. Free NF-κB then translocates from the cytoplasm into the nucleus, where it binds specifically to certain DNA sequences, promoting the expression of specific target genes (Corbetta et al, 2005;Gu et al, 2012). Previous studies reported that treatments of BV2 and THP1 cells with LPS greatly upregulated the phosphorylation level of NF-κB p65, indicating activation of the NF-κB signal pathway (Lim et al, 2012; …”

Section: Fig 5 Effect Of Punicalagin On Lps-induced Nf-κb Activationmentioning

confidence: 99%

Punicalagin protects bovine endometrial epithelial cells against lipopolysaccharide-induced inflammatory injury

Lyu

Chen

Wang

et al. 2017

J. Zhejiang Univ. Sci. B

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Abstract:Objective: Bovine endometritis is one of the most common reproductive disorders in cattle. The aim of this study was to investigate the anti-inflammation potential of punicalagin in lipopolysaccharide (LPS)-induced bovine endometrial epithelial cells (bEECs) and to uncover the underlying mechanisms. Methods: bEECs were stimulated with different concentrations (1, 10, 30, 50, and 100 μg/ml) of LPS for 3, 6, 9, 12, and 18 h. MTT assay was used to assess cell viability and to identify the conditions for inflammatory injury and effective concentrations of punicalagin. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to assess gene expression of pro-inflammatory cytokines. Western blotting was used to assess levels of inflammation-related proteins. Results: Treatment of bEECs with 30 µg/ml LPS for 12 h induced cell injury and reduced cell viability. Punicalagin (5, 10, or 20 µg/ml) pretreatment significantly decreased LPS-induced productions of interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor-α (TNF-α) in bEECs. Molecular research showed that punicalagin inhibited the activation of the upstream mediator nuclear factor-κB (NF-κB) by suppressing the production of inhibitor κBα (IκBα) and phosphorylation of p65. Results also indicated that punicalagin can suppress the phosphorylation of mitogen-activated protein kinases (MAPKs) including p38, c-Jun N-terminal kinase (JNK), and extracellular signal-regulated kinase (ERK). Conclusions: Punicalagin may attenuate LPS-induced inflammatory injury and provide a potential option for the treatment of dairy cows with Escherichia coli endometritis.

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“…NFκB is a multifunctional transcription factor and is an important target in controlling inflammation, as the transcription of numerous proinflammatory molecules depends on the activation of NFκB (32,33). Therefore, several anti-inflammatory therapies have aimed to inhibit NFκB activity in LPS models or inflammatory diseases (34). Caspase-3 is crucial in cell death and CNS inflammation (35).…”

Section: Discussionmentioning

confidence: 99%

Determining the neuroprotective effects of dextromethorphan in lipopolysaccharide-stimulated BV2 microglia

Cheng

Hou

et al. 2014

Molecular Medicine Reports

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Abstract. Microglial activation has been recognized as being vital in the pathogenesis of several neurodegenerative disorders. Therefore, the identification of therapeutic drugs to prevent microglial activation and thus protect against inflammation-mediated neuronal injury, is required. In the present study, dextromethorphan (DM), a compound widely used in antitussive remedies that has been demonstrated to possess neuroprotective effects, was shown to reduce proinflammatory mediator production in lipopolysaccharide (LPS)-stimulated BV2 mouse microglial cells. Western blot analysis revealed that DM markedly suppressed the activation of nuclear factor-κB (NFκB), caspase-3 signaling and the expression of another inflammation-inducing factor, heat shock protein 60 (HSP60) and heat shock factor-1, induced by LPS in BV2 cells. Results from ELISA assay demonstrated that DM reduced the release of HSP60, nitric oxide (NO), inducible NO synthase, tumor necrosis factor-α, interleukin (IL)-1β and IL-6 induced by LPS in BV2 microglia. These results were confirmed by immunofluorescence, suggesting that DM may exert a neuroprotective and anti-inflammatory effect by inhibiting microglial activation through the HSP60-NFκB signaling pathway. Therefore, DM may offer substantial therapeutic benefits in the treatment of neurodegenerative diseases that are accompanied by microglial activation.

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Inhibition of NF-κB activation is associated with anti-inflammatory and anti-apoptotic effects of Ginkgolide B in a mouse model of cerebral ischemia/reperfusion injury

Cited by 127 publications

References 36 publications

Ginkgolide B exerts anti-inflammatory and chondroprotective activity in LPS-induced chondrocytes

Ginkgolide B exerts anti-inflammatory and chondroprotective activity in LPS-induced chondrocytes

Punicalagin protects bovine endometrial epithelial cells against lipopolysaccharide-induced inflammatory injury

Determining the neuroprotective effects of dextromethorphan in lipopolysaccharide-stimulated BV2 microglia

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