Evidence map›Paper›PMID 39990819›Full record

ArticleSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition2024

[Protective Effect of Ginsenoside Rg3 on Lipopolysaccharide-Induced Neuronal-Galial Interaction Injury Model].

Xingyu Cai, Daofeng Yang, Xuerui Zhuo, Yiming Sun

Abstract readEnglish Abstract
In one paragraph

Article in Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Xingyu Cai( 233030) College of Clinical Medicine, Bengbu Medical University, Bengbu 233030, China.
Daofeng Yang( 233030) College of Clinical Medicine, Bengbu Medical University, Bengbu 233030, China.
Xuerui Zhuo( 233030) College of Clinical Medicine, Bengbu Medical University, Bengbu 233030, China.
Yiming Sun( 233030) College of Clinical Medicine, Bengbu Medical University, Bengbu 233030, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objective: To investigate the protective effect of ginsenoside Rg3 on lipopolysaccharide-induced galial-neuronal interaction injury model. Methods: Primary microglia cells and HT-22 cell lines were cultured, and the cells were divided into the control group (CON), the 100 ng/mL LPS group (LPS), the control inflammation model group (CM), the ginsenoside Rg3 group, and the inflammation model plus ginsenoside Rg3 treatment group (CM+Rg3). Ginsenoside Rg3 was administered in the ginsenoside Rg3 group and the CM+Rg3 group at the doses of 2.5, 5, 10, and 20 μmol/L. Galial-neuronal interaction modeling was performed in the CM group and the CM+Rg3 group. The purity of the primary microglia cells was assessed by immunofluorescence, the viability of the HT-22 cells in each group was assessed by CCK-8, and changes in the levels of inflammatory cytokines, including interleukin (IL)-1β, IL-6, tumor necrosis factor α (TNF-α), and IL-10, in the cell samples of each group were assessed with the ELISA kits. The level of cellular oxidative damage was measured with a ROS kit, and the expression of apoptosis-related proteins, including Bax and Bcl-2, was assessed by Western blot. The activity of Caspase-3 enzyme in each group was measured with a Caspase-3 enzyme activity kit. Results: The purity of the microglia cultured reached over 95% and was suitable for subsequent experiments. After ginsenoside Rg3 stimulation at different doses, the survival rate of HT-22 was not much different from that of the CON group. The survival rate of neurons after 100 ng/mL LPS stimulation was 98%, indicating that Rg3 and LPS had no effect on the survival of neurons. Compared with that of the CON group, the survival rate of HT-22 cells in the CM group was significantly decreased ( Conclusion: Ginsenoside Rg3 may play a role in the alleviation of neuronal apoptosis by regulating glial cell damage, reducing the secretion of inflammatory factors, and inhibiting neuronal apoptosis.

Indexed as

GinsenosidesLipopolysaccharidesMicrogliaNeuronsNeuroprotective AgentsAnimalsApoptosisCell LineCells, CulturedCell SurvivalMiceTumor Necrosis Factor-alphaginsenoside Rg3GinsenosidesLipopolysaccharidesNeuroprotective AgentsTumor Necrosis Factor-alphaApoptosisGinsenoside Rg3Glial-neuronal interaction injury modelLipopolysaccharide

Identifiers

PMID39990819
PMCPMC11839363

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.