Ginkgolide B reduces neuronal cell apoptosis in the hemorrhagic rat brain: Possible involvement of Toll-like receptor 4/nuclear factor-kappa B pathway

Hu, Yahong; Huang, Man; Dong, Xiao-Qiao; Xu, Qiuping; Yu, Wenhua; Zhang, Zu-Yong

doi:10.1016/j.jep.2011.08.034

Cited by 52 publications

(28 citation statements)

References 52 publications

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“…Accumulating evidence has shown that inflammation plays an important role in modulating cerebral injury and apoptosis caused by ischemia/reperfusion [20,21]; we thus examined the effects of ischemic postconditioning on the production of neurotoxic cytokine IL-1β. As Figure 4 shows, when compared with that in the sham group, either the expressional or the transcriptional level of IL-1β increased significantly in both the 2 hour ischemia group and the 4.5 hour ischemia group.…”

Section: Resultsmentioning

confidence: 99%

Protection of ischemic post conditioning against transient focal ischemia-induced brain damage is associated with inhibition of neuroinflammation via modulation of TLR2 and TLR4 pathways

Wang

Yang

et al. 2014

J Neuroinflammation

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Background and purposeIschemic postconditioning has been demonstrated to be a protective procedure to brain damage caused by transient focal ischemia/reperfusion. However, it is elusive whether the protection of postconditioning against brain damage and neuroinflammation is via regulating TLR2 and TLR4 pathways. In the present study, we examined the protection of ischemic postconditioning performed immediately prior to the recovery of cerebral blood supply on brain damage caused by various duration of ischemia and tested the hypothesis that its protection is via inhibition of neuroinflammation by modulating TLR2/TLR4 pathways.MethodsBrain damage in rats was induced by using the middle cerebral artery occlusion (MCAO) model. Ischemic postconditioning consisting of fivecycles of ten seconds of ischemia and reperfusion was performed immediately following theischemic episode Theduration of administration of ischemic postconditioning was examined by comparing its effects on infarction volume, cerebral edema and neurological function in 2, 3, 4, 4.5and 6 hour ischemia groups. The protective mechanism of ischemic postconditioning was investigated by comparing its effects on apoptosis, production of the neurotoxic cytokine IL-1β and the transcription and expression of TLR2, TLR4 and IRAK4 in the 2 and 4.5 hour ischemia groups.ResultsIschemic postconditioning significantly attenuated cerebral infarction, cerebral edema and neurological dysfunction in ischemia groups of up to 4 hours duration, but not in 4.5and 6 hour ischemia groups. It also inhibited apoptosis, production of IL-1β, abnormal transcription and expression of TLR2, TLR4 and IRAK4 in the 2 hour ischemia group, but not in the 4.5 hour ischemia group.ConclusionsIschemic postconditioning protected brain damage caused by 2, 3 and 4 hours of ischemia, but not by 4.5 and 6 hours of ischemia. The protection of ischemic postconditioning is associated with its inhibition of neuroinflammation via inhibition of TLR2 and TLR4 pathways.

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Section: Resultsmentioning

confidence: 99%

Protection of ischemic post conditioning against transient focal ischemia-induced brain damage is associated with inhibition of neuroinflammation via modulation of TLR2 and TLR4 pathways

Wang

Yang

et al. 2014

J Neuroinflammation

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“…For instance, quercetin decreases the phosphorylation of I κ B β , which decreased the activation of NF- κ B [152]. However, it has been reported that bilobalide blocks apoptosis of dopaminergic neurons through the suppression of the expression of p65 protein decreasing its nuclear translocation in rat substantia nigra [153] and that administration of ginkgolide B significantly suppresses gene expression of TLR-4 and NF- κ B, lessens concentrations of TNF α , IL-1 β , and IL-6, and reduces the number of apoptotic neuronal cells in hemorrhagic rat brain [154]. TLR4 stimulates the phosphorylation and degradation of I κ B, resulting in nuclear translocation of NF- κ B, which initiates transcription of genes associated with apoptosis and inflammation [155, 156].…”

Section: Molecular Targets Of Egb 761mentioning

confidence: 99%

Antiapoptotic Effects of EGb 761

Serrano-García

Pedraza‐Chaverrí

Mares-Sámano

et al. 2013

Evidence-Based Complementary and Alternative Medicine

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Ginkgo biloba extracts have long been used in Chinese traditional medicine for hundreds of years. The most significant extract obtained from Ginkgo biloba leaves has been EGb 761, a widely used phytopharmaceutical product in Europe. EGb 761 is a well-defined mixture of active compounds, which contains two main active substances: flavonoid glycosides (24–26%) and terpene lactones (6–8%). These compounds have shown antiapoptotic effects through the protection of mitochondrial membrane integrity, inhibition of mitochondrial cytochrome c release, enhancement of antiapoptotic protein transcription, and reduction of caspase transcription and DNA fragmentation. Other effects include the reduction of oxidative stress (which has been related to the occurrence of vascular, degenerative, and proliferative diseases), coupled to strong induction of phase II-detoxifying and cellular defense enzymes by Nrf2/ARE activation, in addition to the modulation of transcription factors, such as CREB, HIF-1α, NF-κB, AP-1, and p53, involved in the apoptosis process. This work reviews experimental results about the antiapoptotic effects induced by the standardized extract of Ginkgo biloba leaves (EGb 761).

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“…Activated NF-κB was identified in the cytoplasm and cell nucleus of neurons after 24 h of injury. During the acute inflammatory reaction process, NF-κB participates in the activation of macrophages and hemamoeba, and controls the genetic expression of proinflammatory factors (22). Controlling this process would lead to the amplification of inflammatory responses and tissue injuries (23).…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of berberine against learning and memory deficits in diffuse axonal injury

Wang

Chen

et al. 2017

Exp Ther Med

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Abstract. The aim of the present study was to assess the neuroprotective effect of berberine against learning and memory deficits in diffuse axonal injury (DAI). DAI rats were orally gavaged with berberine at a dose of 200 mg/kg of body weight for 4 weeks. Behavioral tests were used to analyze the neuroprotective effect of berberine against DAI-induced learning and memory deficits. In the present study, treatment with berberine significantly protected against DAI-induced inhibition of learning and memory in rats. Notably, berberine significantly suppressed the levels of tumor necrosis factor, interleukin-1β and monocyte chemoattractant protein-1, as well as reduced the protein expression levels of nuclear factor-κB, Bcl-2-associated X protein and cytochrome c in DAI rats. In addition, berberine significantly suppressed the protein expression of p38 mitogen-activated protein kinase, activating transcription factor 2 and vascular endothelial growth factor in DAI rats. These results suggested that berberine exhibited a neuroprotective effect against learning and memory deficits in severe DAI through the suppression of inflammation, angiogenesis and apoptosis in a rat model.

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Ginkgolide B reduces neuronal cell apoptosis in the hemorrhagic rat brain: Possible involvement of Toll-like receptor 4/nuclear factor-kappa B pathway

Cited by 52 publications

References 52 publications

Protection of ischemic post conditioning against transient focal ischemia-induced brain damage is associated with inhibition of neuroinflammation via modulation of TLR2 and TLR4 pathways

Protection of ischemic post conditioning against transient focal ischemia-induced brain damage is associated with inhibition of neuroinflammation via modulation of TLR2 and TLR4 pathways

Antiapoptotic Effects of EGb 761

Neuroprotective effect of berberine against learning and memory deficits in diffuse axonal injury

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