The neurotoxicity of β-amyloid peptide toward rat brain is associated with enhanced oxidative stress, inflammation and apoptosis, all of which can be attenuated by scutellarin

Guo, Lili; Guan, Zhi‐Zhong; Huang, Yong; Wang, Yonglin; Shi, Jing‐Shan

doi:10.1016/j.etp.2012.05.003

Cited by 72 publications

(31 citation statements)

References 39 publications

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“…Previous studies showed that SC had obvious anti-cancer effect in vivo and in vitro (Chan et al, 2009;Li et al, 2013aLi et al, , 2013b. Meanwhile, there are various reports which demonstrate that SC exerts well protection against oxidative damage and inflammatory injury (Liu et al, 2003;Tan et al, 2010;Chen et al, 2013;Guo et al, 2013). In addition, SC was reported to attenuate concanavalin A-, selenium-, and brain ischemia/reperfusion-induced liver injury Eltayeb et al, 2004;Tan et al, 2007).…”

Section: Introductionmentioning

confidence: 90%

Scutellarin protects against the liver injury induced by diosbulbin B in mice and its mechanism

Niu

Sheng

Yang

et al. 2015

Journal of Ethnopharmacology

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Section: Introductionmentioning

confidence: 90%

Scutellarin protects against the liver injury induced by diosbulbin B in mice and its mechanism

Niu

Sheng

Yang

et al. 2015

Journal of Ethnopharmacology

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“…These cells begin to proliferate, migrate and differentiate, release cytotoxins and inflammatory mediators, secrete cytokines, and upregulate immune expression. A series of previous studies showed that activated microglia in vitro released a large number of free radicals and inflammatory cytokines, which activated or aggravated neuronal damage; conversely, neuronal damage activated microglial cells, thus leading to a pathological cascade and aggravating the damage induced by ischemia[313233343536373839]. …”

Section: Discussionmentioning

confidence: 99%

“…Preliminary studies from our research group demonstrated that hypoxia damages rat cerebral cortical neurons, and induces apoptosis[45], indicating that neuronal damage is an important pathological contributor to hypoxic-ischemic encephalopathy.…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rb1 attenuates activated microglia-induced neuronal damage

Guo

et al. 2014

Neural Regen Res

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The microglia-mediated inflammatory reaction promotes neuronal damage under cerebral ischemia/hypoxia conditions. We therefore speculated that inhibition of hypoxia-induced microglial activation may alleviate neuronal damage. To test this hypothesis, we co-cultured ginsenoside Rb1, an active component of ginseng, and cortical neurons. Ginsenoside Rb1 protected neuronal morphology and structure in a single hypoxic culture system and in a hypoxic co-culture system with microglia, and reduced neuronal apoptosis and caspase-3 production. The protective effect was observable prior to placing in co-culture. Additionally, ginsenoside Rb1 inhibited levels of tumor necrosis factor-α in a co-culture system containing activated N9 microglial cells. Ginsenoside Rb1 also significantly decreased nitric oxide and superoxide production induced by N9 microglia. Our findings indicate that ginsenoside Rb1 attenuates damage to cerebral cortex neurons by downregulation of nitric oxide, superoxide, and tumor necrosis factor-α expression in hypoxia-activated microglia.

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“…Scutellarin isolated from Scutellaria barbata and Scutellaria lateriflora attenuated neurotoxicity of A␤ [397,398].…”

Section: Natural Productsmentioning

confidence: 97%

“…Immunization of P301L mutant mice with a twelve amino acid peptide of the human tau sequence (aa [395][396][397][398][399][400][401][402][403][404][405][406] together with CFA impeded the progression of neurofibrillary histopathology [789].…”

Section: Vaccines Against Tau and α-Synucleinmentioning

confidence: 99%

Cognitive Enhancers (Nootropics). Part 3: Drugs Interacting with Targets other than Receptors or Enzymes. Disease-Modifying Drugs. Update 2014

Froestl

Pfeifer

Muhs

2014

JAD

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Scientists working in the field of Alzheimer's disease and, in particular, cognitive enhancers, are very productive. The review "Drugs interacting with Targets other than Receptors or Enzymes. Disease-modifying Drugs" was accepted in October 2012. In the last 20 months, new targets for the potential treatment of Alzheimer's disease were identified. Enormous progress was realized in the pharmacological characterization of natural products with cognitive enhancing properties. This review covers the evolution of research in this field through May 2014.

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The neurotoxicity of β-amyloid peptide toward rat brain is associated with enhanced oxidative stress, inflammation and apoptosis, all of which can be attenuated by scutellarin

Cited by 72 publications

References 39 publications

Scutellarin protects against the liver injury induced by diosbulbin B in mice and its mechanism

Scutellarin protects against the liver injury induced by diosbulbin B in mice and its mechanism

Ginsenoside Rb1 attenuates activated microglia-induced neuronal damage

Cognitive Enhancers (Nootropics). Part 3: Drugs Interacting with Targets other than Receptors or Enzymes. Disease-Modifying Drugs. Update 2014

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