Deoxyelephantopin ameliorates lipopolysaccharides (LPS)-induced memory impairments in rats: Evidence for its anti-neuroinflammatory properties

Andy, Shathiswaran N.; Pandy, Vijayapandi; Alias, Zazali; Kadir, Habsah Abdul

doi:10.1016/j.lfs.2018.05.035

Cited by 19 publications

(10 citation statements)

References 92 publications

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“…Consistently, we observed marked deposition of Aβ in LPS-induced group versus control groups. Activation of glial cells and astrocytes enhance BACE-1 activity, therefore increase the conversion of APP and Aβ [93,94]. BACE-1 enzyme is an important enzyme which plays a key role in converting APP to Aβ.…”

Section: Plos Onementioning

confidence: 99%

Ipriflavone and Ipriflavone loaded albumin nanoparticles reverse lipopolysaccharide induced neuroinflammation in rats

et al. 2020

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Background Neuroinflammation causes neurodegenerative conditions like Alzheimer's disease (AD). Ipriflavone (IP), therapeutic compound to postmenopausal osteoporosis, has limited estrogenic activity and is accounted as AChE inhibitor. The developing of drug delivery systems to enable drug targeting to specific sites increases the drug therapeutic effect. Objective The aim of the present study was to formulate and evaluate ipriflavone loaded albumin nanoparticles (IP-Np) along with free ipriflavone against lipopolysaccharide (LPS) induced neuroinflammation in rats. Methods Neuroinflammation was induced by intra-peritoneal (i.p) injection of LPS (250 μg/kg rat body weight) then treatments were conducted with (1) ipriflavone at two doses 50 mg/kg and 5 mg/kg, (2) IP-Np (5 mg ipriflavone/kg) or (3) IP-Np coated with polysorbate 80 (IP-Np-T80) (5 mg ipriflavone/kg). The alteration of the inflammatory response in male adult Wistar rats' brain hippocampus was investigated by examining associated indices using biochemical and molecular analyses. Results A significant upsurge in inflammatory mediators and decline in antioxidant status were observed in LPS-induced rats. In one hand, ipriflavone (50 mg/kg), IP-Np and IP-Np-T80 ameliorated LPS induced brain hippocampal inflammation where they depreciated the level

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Section: Plos Onementioning

confidence: 99%

Ipriflavone and Ipriflavone loaded albumin nanoparticles reverse lipopolysaccharide induced neuroinflammation in rats

et al. 2020

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“…Among them, NR1, NR2A, and NR2B are subunits of NMDA receptors, which contribute to long‐term potentiation in HPC 59 . Moreover, PSD‐95, which is involved in synaptic development, stability, and plasticity, 60 serves as an excitatory postsynaptic marker that has been directly related to various behavioral and cognitive functions 61 . These results revealed that PSO also plays an active role in improving synaptic dysfunction in PS cDKO mice.…”

Section: Discussionmentioning

confidence: 91%

Peony seed oil ameliorates neuroinflammation-mediated cognitive deficits by suppressing microglial activation through inhibition of NF-κB pathway in presenilin 1/2 conditional double knockout mice

Gao

Wang

Zhao

et al. 2021

Journal of Leukocyte Biology

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Chronic neuroinflammation has been shown to exert adverse influences on the pathology of Alzheimer's disease (AD), associated with the release of abundant proinflammatory mediators by excessively activated microglia, causing synaptic dysfunction, neuronal degeneration, and memory deficits. Thus, the prevention of microglial activation‐associated neuroinflammation is important target for deterring neurodegenerative disorders. Peony seed oil (PSO) is a new food resource, rich in α‐linolenic acid, the precursor of long chain omega‐3 polyunsaturated fatty acids, including docosahexaenoic acid and eicosapentaenoic acid, which exhibit anti‐inflammatory properties by altering cell membrane phospholipid fatty acid compositions, disrupting lipid rafts, and inhibiting the activation of the proinflammatory transcription factor NF‐κB. However, few studies have examined the anti‐neuroinflammatory effects of PSO in AD, and the relevant molecular mechanisms remain unclear. Presenilin1/2 conditional double knockout (PS cDKO) mice display obvious AD‐like phenotypes, such as neuroinflammatory responses, synaptic dysfunction, and cognitive deficits. Here, we assessed the potential neuroprotective effects of PSO against neuroinflammation‐mediated cognitive deficits in PS cDKO using behavioral tests and molecular biologic analyses. Our study demonstrated that PSO suppressed microglial activation and neuroinflammation through the down‐regulation of proinflammatory mediators, such as inducible NOS, COX‐2, IL‐1β, and TNF‐α, in the prefrontal cortex and hippocampus of PS cDKO mice. Further, PSO significantly lessened memory impairment by reversing hyperphosphorylated tau and synaptic proteins deficits in PS cDKO mice. Importantly, PSO's therapeutic effects on cognitive deficits were due to inhibiting neuroinflammatory responses mediated by NF‐κB signaling pathway. Taken together, PSO may represent an effective dietary supplementation to restrain the neurodegenerative processes of AD.

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“…Experimental exposure of rodents to viral mimetics or bacterial active ingredients, such as lipopolysaccharide (LPS), can enhance anxiety-and depression-like behaviors possibly through the reprogramming of the hypothalamicpituitary-adrenal axis [8]. In addition, neuroinflammation caused by a single intraperitoneal injection of LPS is known to significantly increase the levels of neuroinflammatory factors, such as cytokines [9]. LPS injection stimulates inflammatory cytokine through the Toll-like receptor 4 (TLR4), which leads to the activation of many inflammatory factors, such as IL-6, IL-1β, and the nuclear factor-kappaB (NF-κB) system [10].…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Quercetin on Anxiety‐Like Symptoms and Neuroinflammation Induced by Lipopolysaccharide in Rats

Lee

Yeom

Shim

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Recently, neuroinflammation is thought to be one of the important causes of many neuropsychiatric diseases. Quercetin (QUER) is a natural flavonoid, and it is well known that QUER has antioxidative, anti-inflammatory, and neuroprotective effects. In our study, lipopolysaccharide (LPS) was injected into the lateral ventricle of rats to induce anxiety-like behaviors and neuroinflammation, and it was confirmed that chronic administration of QUER could improve anxiety-like symptoms. We also investigated the effects of QUER on inflammatory markers and its major mechanisms associated with inflammation in the hippocampus. Daily administration of QUER (10, 50, and 100 mg/kg) daily for 21 days significantly improved anxiety-like behaviors in the elevated plus-maze test and open field test. QUER administration significantly reduced inflammatory markers such as interleukin-6, interleukin-1β, cyclooxygenase-2, and nuclear factor-kappaB levels in the brain. In addition, QUER significantly increased the brain-derived neurotrophic factor (BDNF) mRNA level and decreased the nitric oxide synthase (iNOS) mRNA level. Therefore, our results have shown that QUER can improve anxiety-like behaviors caused by chronic neuroinflammation. This anxiolytic effect of QUER has been shown to be due to its anti-inflammatory effects and appropriate regulation of BDNF and iNOS expression. Thus, QUER provides the potential as a therapeutic agent to inhibit anxiety-like symptoms in neuropsychiatric diseases, such as anxiety.

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Deoxyelephantopin ameliorates lipopolysaccharides (LPS)-induced memory impairments in rats: Evidence for its anti-neuroinflammatory properties

Cited by 19 publications

References 92 publications

Ipriflavone and Ipriflavone loaded albumin nanoparticles reverse lipopolysaccharide induced neuroinflammation in rats

Ipriflavone and Ipriflavone loaded albumin nanoparticles reverse lipopolysaccharide induced neuroinflammation in rats

Peony seed oil ameliorates neuroinflammation-mediated cognitive deficits by suppressing microglial activation through inhibition of NF-κB pathway in presenilin 1/2 conditional double knockout mice

Protective Effects of Quercetin on Anxiety‐Like Symptoms and Neuroinflammation Induced by Lipopolysaccharide in Rats

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