Resveratrol alleviates lipopolysaccharide-induced inflammation in PC-12 cells and in rat model

Zhang, Guiqi; Liu, Yi; Xu, Lichen; Sha, Chunhe; Zhang, Haibin; Xu, Weibing

doi:10.1186/s12896-019-0502-1

Cited by 33 publications

(22 citation statements)

References 37 publications

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“…Therefore, this particular bacterial cell outer membrane compound is widely used to induce inflammation in neuronal cells in in vitro models of spinal cord injury (SCI) or various neurodegenerative diseases, including AD [16,17]. It has been proved in many experiments that PC12 cells treated with LPS showed increased production of proinflammatory cytokines such as Il-1β, Il-6, and TNF-α, as confirmed by mRNA expression measurements [18][19][20][21][22]. It is generally recognized that the amount of microglia and amyloid is dependent on each other based on feedback.…”

Section: Introductionmentioning

confidence: 90%

Protective Activity of Aβ on Cell Cultures (PC12 and THP-1 after Differentiation) Preincubated with Lipopolysaccharide (LPS)

Wiatrak

Balon

2020

Mol Neurobiol

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Amyloid-β (Aβ), the influence of which is considered the pathomechanism of Alzheimer’s disease, is also present in healthy people. The microbiome’s impact is also taken into account, where bacterial lipopolysaccharide (LPS) activates inflammatory processes and stimulates microglia via TLRs. Molecules of bacterial origin can co-create senile plaques with Aβ. This study evaluated the activity of physiological Aβ concentrations on neuronal and microglial cells after preincubation with LPS. Two cell lines were used in the study: PC12 cells differentiated with NGF and THP-1 cells differentiated with phorbol 12-myristate 13-acetate (PMA). Cells were incubated with LPS at concentrations of 1–100 μM for 24 h and then with Aβ25–35 at a concentration of 0.001 μM or 1.0 μM for another 24 h. The viability of the culture and free oxygen radicals and the number of DNA strand breaks in both cell lines were evaluated. Additionally, for PC12 cells, neural features were assessed. Stimulation of repair processes in the presence of Aβ was observed for both studied cell lines. There was a decrease in free radical level and DNA damage number compared to control cultures (cells treated with LPS and without Aβ). The neurotrophic activity of Aβ was observed—the effect on neurites’ growth even after the preincubation of PC12 cells with LPS. At the lowest concentration of LPS used, the increase in neurite length was about 50% greater than in the negative control. At low concentrations, Aβ has a protective effect on neuron-like PC12 cells pretreated with LPS.

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Section: Introductionmentioning

confidence: 90%

Protective Activity of Aβ on Cell Cultures (PC12 and THP-1 after Differentiation) Preincubated with Lipopolysaccharide (LPS)

Wiatrak

Balon

2020

Mol Neurobiol

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“…The miR-132 is involved in multiple physiological and pathological mechanisms, such as neuronal cell development (56), synaptic plasticity (57,58) and inflammation (59,60). Recent studies indicate that miR-132 participates in the regulation of inflammation and is a negative regulator of the inflammatory response in PC12 (61). Interestingly, resveratrol treatment could ameliorate inflammatory response in PC-12 cells via up-regulating miR-132.…”

Section: The Modulation Role Of Neuroinflammation In Admentioning

confidence: 99%

The Regulation of microRNAs in Alzheimer's Disease

Kou

Chen

2020

Front. Neurol.

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MicroRNAs are small non-coding nucleic acids that are responsible for regulating the gene expression by binding to the coding region and 3' and 5' un-translated region of target messenger RNA. Approximately 70% of known microRNAs are expressed in the brain and increasing evidences demonstrate the possible involvement of microRNAs in Alzheimer's disease (AD) according to the statistics. The characteristic symptoms of AD are the progressive loss of memory and cognitive functions due to the deposition of amyloid β (Aβ) peptide, intracellular aggregation of hyperphosphorylated Tau protein, the loss of synapses, and neuroinflammation, as well as dysfunctional autophagy. Therefore, microRNA-mediated regulation for above-mentioned changes may be the potential therapeutic strategies for AD. In this review, the role of specific microRNAs involved in AD and corresponding applications are systematically discussed, including positive effects associated with the reduction of Aβ or Tau protein, the protection of synapses, the inhibition of neuroinflammation, the mitigation of aging, and the induction of autophagy in AD. It will be beneficial to develop effective targets for establishing a cross link between pharmacological intervention and AD in the near future.

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“…All mice were housed in the SPF condiction and provided with enough food and water. After a week of acclimatization, they were subcutaneously inoculated with HTC116 cells (1×10 6 ) and randomly divided in four groups: Control group (without resveratrol and 3-MA treatment), (30 mg/kg) group, 3-MA (1 mg/kg) group, resveratrol +3-MA group (30 mg/kg +1 mg/kg 3-MA treatment). Resveratrol or 3-MA treatments were performed once per 3 days for 18 consecutive days.…”

Section: Xenograft Modelsmentioning

confidence: 99%

“…For instance, resveratrol can act as a scavenger of reactive oxygen species such as hydroxyl-and superoxide-radicals to exert its anti-oxidative activity [4,5] . Resveratrol can also exert anti-inflammatory function via blocking NF-κB and p38MAPK pathways [6] . As well, the anti-aging effect of resveratrol has been found in lower organisms, such as zebrafish and yeast [7,8] .…”

Section: Introductionmentioning

confidence: 99%

Resveratrol induces apoptosis, autophagy and endoplasmic reticulum stress in colon cancer cells

Jia¹,

Wu²,

Li³

et al. 2019

CSRC

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Objective: Resveratrol exerts various biologic effects. This study was designed to investigate its anti-cancer effect and its impact on cell apoptosis, autophagy, and endoplasmic reticulum stress (ER-stress) in colon cancer. Methods: Colon cancer cells were treated with resveratrol. Cell viability, apoptosis, and autophagy were assessed by MTT, flow cytometry, and green fluorescence protein (GFP)-tagged LC3B analysis, respectively. Gene expression was detected by qRT-PCR and western blot. Xenograft model was subjected to verify the effects of resveratrol on tumorigenesis of colon cancer cells in vivo. Results: The viability of colon cancer cells was reduced by resveratrol. The cell apoptosis and the protein levels of apoptotic markers (cleaved-PARP and cleaved-Caspase3) were increased by resveratrol. The protein level of autophagic marker (MAP1LC3B) and the LC3B dots accumulation were elevated by resveratrol. Autophagy inhibitor (3-MA) partially reversed the effect of resveratrol on cell apoptosis. The protein and mRNA levels of ER-stress markers (IRE-1 and ATF6) and pro-apoptotic signals (GRP-78, GADD153) were up-regulated by resveratrol. The tumor growth of colon cancer cells was suppressed by resveratrol in vivo. Conclusion: Resveratrol exerts anti-cancer function of colon cancer, which is associated with its induction effect of cell apoptosis, autophagy and ER-stress.

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Resveratrol alleviates lipopolysaccharide-induced inflammation in PC-12 cells and in rat model

Cited by 33 publications

References 37 publications

Protective Activity of Aβ on Cell Cultures (PC12 and THP-1 after Differentiation) Preincubated with Lipopolysaccharide (LPS)

Protective Activity of Aβ on Cell Cultures (PC12 and THP-1 after Differentiation) Preincubated with Lipopolysaccharide (LPS)

The Regulation of microRNAs in Alzheimer's Disease

Resveratrol induces apoptosis, autophagy and endoplasmic reticulum stress in colon cancer cells

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