Evidence map›Paper›PMID 42762468›Full record

ArticlePharmacology research & perspectives2026

Ginsenosides Rb1 and Rg1 Suppress Lipopolysaccharide-Induced Inflammatory Gene Expression in Microglia and Astrocytes, Unlike Rb2.

Hanwoong Woo, Jeong-Im Choi, Sohee Kim, Jung Ki Min, Eunbi Lim, Sehyun Chae, Jieun Kim

Abstract readComparative Study
In one paragraph

Article in Pharmacology research & perspectives, 2026. 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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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Hanwoong WooMultidimensional Genomics Research Center, Kangwon National University, Chuncheon, Republic of Korea.
Jeong-Im ChoiDepartment of Bio-Health Convergence, Kangwon National University, Chuncheon, Republic of Korea.
Sohee KimDepartment of Bio-Health Convergence, Kangwon National University, Chuncheon, Republic of Korea.
Jung Ki MinMultidimensional Genomics Research Center, Kangwon National University, Chuncheon, Republic of Korea.
Eunbi LimMultidimensional Genomics Research Center, Kangwon National University, Chuncheon, Republic of Korea.
Sehyun ChaeMultidimensional Genomics Research Center, Kangwon National University, Chuncheon, Republic of Korea.
Jieun KimMultidimensional Genomics Research Center, Kangwon National University, Chuncheon, Republic of Korea.ORCID https://orcid.org/0009-0002-4489-6825

Funding

Ministry of Education, Republic of Korea RS-2023-00301850National Research Foundation of Korea (NRF) RS-2024-00351023National Research Foundation of Korea (NRF) RS-2026-25494803
6 · The paper itself

Abstract

Neuroinflammation, mediated by activated microglia and astrocytes, contributes to the progression of neurodegenerative diseases. Ginsenosides derived from Panax ginseng possess anti-inflammatory properties. However, the comparative efficacy of structurally distinct ginsenosides and their activity across multiple glial cell types remains incompletely understood. In this study, we systematically compared the effects of ginsenosides Rb1 (protopanaxadiol-type), Rb2 (protopanaxadiol-type), and Rg1 (protopanaxatriol-type) in lipopolysaccharide (LPS)-activated BV2 microglia and C8-D1A astrocytes. Following LPS stimulation, cells were treated with ginsenosides, and inflammatory responses were assessed by cell viability assay, real-time polymerase chain reaction, enzyme-linked immunosorbent assay (ELISA), and western blotting. None of the three ginsenosides up to 20 μM concentration reduced cell viability. Rb1 and Rg1 suppressed LPS-induced expression of proinflammatory genes, including Il-6, Il-1β, and Cox-2, across multiple concentrations, with inhibitory effects particularly notable at 5 and 10 μM. ELISA further confirmed that Rb1 and Rg1 reduced interleukin (IL)-6 and IL-1β secretion in both glial cell types. In contrast, Rb2 showed limited and inconsistent anti-inflammatory effects, despite being structurally similar to Rb1. Rb1 and Rg1 reduced LPS-induced phosphorylation of nuclear factor kappa B (NF-κB) in nuclei of both cell types, whereas Rb2 suppressed NF-κB phosphorylation only in BV2 microglia. Rb1 reduced AKT and p38 phosphorylation in C8-D1A astrocytes, indicating compound- and cell-type-specific regulation of inflammatory signaling. Notably, Rb2-mediated NF-κB suppression did not translate into broad inhibition of inflammatory gene or cytokine expression. These findings identify Rb1 and Rg1 as ginsenosides with broad anti-inflammatory activity in microglia and highlight glycosylation-dependent functional differences among structurally related ginsenosides.

Indexed as

Anti-Inflammatory AgentsAstrocytesGinsenosidesInflammationMicrogliaAnimalsCell LineCell SurvivalGene Expression RegulationLipopolysaccharidesMiceNF-kappa BPanaxSapogeninsAnti-Inflammatory Agentsginsenoside Rb1ginsenoside Rb2ginsenoside Rg1GinsenosidesLipopolysaccharidesNF-kappa BSapogeninsastrocytescomparative pharmacologyginsenosidesmicroglianeuroinflammationstructure–activity relationship

Identifiers

PMID42762468
PMCPMC13589614

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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.