Magnesium Lithospermate B Protects Neurons Against Amyloid β (1–42)-Induced Neurotoxicity Through the NF-κB Pathway

Jiang, Feng; Mao, Yiqi; Liu, Huixiang; Xu, Ping; Zhang, Li; Qian, Xiaohong; Sun, Xiaofeng

doi:10.1007/s11064-015-1691-1

Cited by 9 publications

(5 citation statements)

References 36 publications

(45 reference statements)

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“…Our study found that SH-SY5Y cells exposed to Aβ displayed higher concentration and expression of IL-1β, TNF-α and IL-6 than that of the control groups. In agreement with our results, Jiang et al [25] revealed that Aβ could induce release of pro-inflammatory cytokines IL-1β, IL-10, and TNF-α. Previous studies confirmed that PGE2 played pivotal functions in inflammation and was elevated together with the expression of COX-2, a rate-limiting enzyme catalyzing PGE2 production, in the brain of AD patients [22, 23].…”

Section: Discussionsupporting

confidence: 94%

Tanshinone IIA attenuates Aβ-induced neurotoxicity by down-regulating COX-2 expression and PGE2 synthesis via inactivation of NF-κB pathway in SH-SY5Y cells

Geng

Liu

Chen

2019

J of Biol Res-Thessaloniki

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Amyloid-β (Aβ)-induced neurotoxicity is a major pathological mechanism of Alzheimer’s disease (AD). Tanshinone IIA (Tan IIA), extracted from traditional Chinese herb Radix salvia miltiorrhiza, possesses anti-oxidant and anti-inflammatory actions, as well as neuroprotective effects. The present study aims to explore the possible mechanism by which Tan IIA attenuated Aβ-induced neurotoxicity. Exposure of SH-SY5Y cells to different concentrations of Aβ led to neurotoxicity by reducing cell viability, inducing cell apoptosis and increasing neuroinflammation in a dose-dependent manner. Moreover, Aβ treatment promoted cyclooxygenase-2 (COX-2) expression and Prostaglandin E2 (PGE2) secretion, and activated nuclear transcription factor kappa (NF-κB) pathway in SH-SY5Y cells. However, pretreatment of SH-SY5Y cells with Tan IIA prior to Aβ prevented these Aβ-induced cellular events noticeably. These data suggested that Tan IIA exerted its neuroprotective action by alleviating Aβ-induced increase in COX-2 expression and PGE2 secretion via inactivation of NF-κB pathway.

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Section: Discussionsupporting

confidence: 94%

Tanshinone IIA attenuates Aβ-induced neurotoxicity by down-regulating COX-2 expression and PGE2 synthesis via inactivation of NF-κB pathway in SH-SY5Y cells

Geng

Liu

Chen

2019

J of Biol Res-Thessaloniki

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“…The NF-κB pathway is well known to promote the expression of genes related to neuronal inflammation [18][19][20]. Our cumulative results demonstrated the anti-inflammatory effects of ISO.…”

Section: Iso Inhibits Aβ 25-35 -Mediated Nf-κb Signaling Pathwaysupporting

confidence: 59%

“…The NF-κB pathway is well known to promote the expression of genes related to neuronal inflammation [18][19][20]. Our cumulative results demonstrated the anti-inflamma- Accumulation and aggregation of Aβ peptides generally lead to activation of neuroglia cells, which eventually initiates neuronal oxygen response and release of inflammatory cytokines such as interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) [16,17].…”

Section: Iso Inhibits Aβ25-35-mediated Nf-κb Signaling Pathwaymentioning

confidence: 96%

Isoorientin Inhibits Amyloid β25–35-Induced Neuronal Inflammation in BV2 Cells by Blocking the NF-κB Signaling Pathway

2021

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Alzheimer’s disease (AD) is a severe neurodegenerative disorder. AD is pathologically characterized by the formation of intracellular neurofibrillary tangles, and extracellular amyloid plaques which were comprised of amyloid-beta (Aβ) peptides. Aβ induces neurodegeneration by activating microglia, which triggers neurotoxicity by releasing various inflammatory mediators and reactive oxygen species (ROS). Nuclear factor-kappa B (NF-κB) is expressed in human tissues including the brain and plays an important role in Aβ-mediated neuronal inflammation. Thus, the identification of molecules that inhibit the NF-κB pathway is considered an attractive strategy for the treatment and prevention of AD. Isoorientin (3′,4′,5,7-Tetrahydroxy-6-C-glucopyranosyl flavone; ISO), which can be extracted from several plant species, such as Philostachys and Patrinia is known to have various pharmacological activities such as anticancer, antioxidant, and antibacterial activity. However, the effect of ISO on Aβ-mediated inflammation and apoptosis in the brain has yet to be elucidated. In the present study, we investigated whether ISO regulated Aβ-induced neuroinflammation in microglial cells and further explored the underlying mechanisms. Our results showed that ISO inhibited the expression of iNOS and COX-2 induced by Aβ25–35. And, it inhibited the secretion of pro-inflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). In addition, ISO reduced the ROS production in Aβ25–35-induced BV2 cells and inhibited NF-κB activation. Furthermore, ISO blocked Aβ25–35-induced apoptosis of BV2 cells. Based on these findings, we suggest that ISO represents a promising therapeutic drug candidate for the treatment and prevention of AD.

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“…The NF κ B pathway has been shown to be involved in the pathological effects of A β [ 42 – 44 ]. It has also been reported that the anti-inflammatory effects of statins work at least in part through inhibition of the NF κ B pathway [ 45 – 47 ].…”

Section: Resultsmentioning

confidence: 99%

Statins Inhibit Fibrillary β-Amyloid Induced Inflammation in a Model of the Human Blood Brain Barrier

et al. 2016

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BackgroundAstrocytes and cerebral endothelial cells are important components of the blood-brain barrier (BBB). Disruption to this barrier through inflammation is a major contributor to Alzheimer’s disease (AD) pathology. The amyloid beta (Aβ) protein is known to exist in several forms and is a key modulator of AD that is known to cause inflammation and changes to BBB function. While one of these forms, fibrillary Aβ (fAβ), is known to cause endothelial cell death at the BBB, no studies have looked specifically at its role on inflammation in a model of the human BBB.AimsTo determine if fAβ is inflammatory to the human BBB. As statins have been shown to be anti-inflammatory and protective in AD, we also tested if these could inhibit the inflammatory effect of fAβ.MethodsUsing cultured cerebral endothelial cells and astrocytes we determined changes in cytokine release, cell toxicity and barrier function in response to fibrillary β-amyloid1–42 (fAβ1–42) alone and in combination with statins.ResultsfAβ1–42 induced inflammatory cytokine release from endothelial cells in the absence of cell toxicity. It also induced astrocyte cytokine release and cell death and caused a loss of barrier integrity. Statin treatment inhibited all of these effects.ConclusionsWe conclude that fAβ1–42 has both inflammatory and cytotoxic effects on the BBB and the protective effect of statins in AD may in part be through inhibiting these effects.

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Magnesium Lithospermate B Protects Neurons Against Amyloid β (1–42)-Induced Neurotoxicity Through the NF-κB Pathway

Cited by 9 publications

References 36 publications

Tanshinone IIA attenuates Aβ-induced neurotoxicity by down-regulating COX-2 expression and PGE2 synthesis via inactivation of NF-κB pathway in SH-SY5Y cells

Tanshinone IIA attenuates Aβ-induced neurotoxicity by down-regulating COX-2 expression and PGE2 synthesis via inactivation of NF-κB pathway in SH-SY5Y cells

Isoorientin Inhibits Amyloid β25–35-Induced Neuronal Inflammation in BV2 Cells by Blocking the NF-κB Signaling Pathway

Statins Inhibit Fibrillary β-Amyloid Induced Inflammation in a Model of the Human Blood Brain Barrier

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