Araliasaponin II isolated from leaves of Acanthopanax henryi (Oliv.) Harms inhibits inflammation by modulating the expression of inflammatory markers in murine macrophages

Abstract

Araliasaponin II (AS II) is a bioactive compound isolated from Acanthopanax henryi (Oliv.) Harms, a plant widely used in traditional oriental medicine. The present study investigated the anti‑inflammatory effects of AS II using murine macrophages. The effects of AS II on inflammatory mediator and cytokine production in lipopolysaccharide (LPS)‑stimulated RAW 264.7 cells was evaluated. Nitric oxide (NO) and cytokine production were determined using the Griess reagent and an ELISA kit. The expression levels of cytokines, inducible NO synthase (iNOS) and cyclooxygenase‑2 (COX‑2) mRNA were examined by reverse transcription‑quantitative polymerase chain reaction. The expression levels of iNOS, COX‑2 and toll‑like receptor (TLR)‑4 protein were examined by western blotting. Translocation of nuclear factor‑κB (NF‑κB) and TLR‑4 expression were visualized by immunofluorescence staining. AS II markedly inhibited the production of NO and prostaglandin E2, and reduced iNOS and COX‑2 expression at the transcriptional and translational levels. AS II downregulated the expression of interleukin‑6 and tumor necrosis factor‑α at the protein and mRNA levels. Furthermore, pre‑treatment with AS II significantly suppressed the TLR‑4‑NF‑κB signaling pathway; this effect may be cause by AS II competing with LPS for binding to TLR‑4 and subsequently inhibiting translocation of the NF‑κB/p65 protein to the nucleus. The results suggested that the anti‑inflammatory properties of AS II may result from inhibiting pro‑inflammatory mediators by suppressing the initiation of the inflammatory response and inhibiting TLR-4-NF-κB signaling pathways.

Codonopsis lanceolata attenuates allergic lung inflammation by inhibiting Th2 cell activation and augmenting mitochondrial ROS dismutase (SOD2) expression

“…The cells were cultured in a humidified incubator with 5% CO 2 atmosphere at 37 °C. The effects of CLE against macrophages were evaluated as described previously 60 . Briefly, to stimulate the cells, the medium was replaced with fresh RPMI 1640 medium followed by the addition of LPS in the presence or absence of CLE for 24 h. The MTS assay was used to determine the viability.…”

Discrimination and quality evaluation of fifteen components in Stauntonia hexaphylla leaves from different harvest time by HPLC–PDA–ESI–MS/MS and ELSD coupled with multivariate statistical analysis and anti-inflammatory activity evaluation

“…According to our previous experimental data and previous literature, peak 5 was tentatively identified as anhuienside C [11,12]. Peaks 13,14, and 15 are attributed to the same aglycone ions as that of peak 5; they were tentatively assigned as araliasaponin II, hexaphyloside A, and ciwujianoside C3, respectively, by comparison with known compounds isolated from S. hexaphylla and their families [13][14][15][16][17] Figure S4). The fragmentation of parent ion produced daughter ions at m/z 928.5, 752.5, and 603.2 attributed to the loss of Ara-Glc, Rha, and Glc.…”

“…Of note, these specific triterpenoid saponins exhibit various biological activities. For example, akebia saponin D can suppress both Alzheimer's disease-related neuro inflammation and memory system dysfunction [26,27]; cussonoside A exhibits a pronounced sedative effect [25]; araliasaponin II has strong anti-inflammatory activity [17]. This means that if SHL was chosen to treat Alzheimer's disease, inflammation, insomnia, and other diseases, SHL that was older than three years could be used.…”

Acanthopanax henryi: Review of Botany, Phytochemistry and Pharmacology

“…Some studies have reported that triterpenoid saponins isolated from the leaves of AH had a significant anti-inflammatory effect [11,20,21,[31][32][33]. For instance, Ciwujianoside C3 (29) exhibited no cytotoxicity at the measured concentrations in RAW264.7 macrophages.…”

“…Also, it downregulated the expression of interleukin-6 and tumor necrosis factor-α at the protein and mRNA levels. Furthermore, pre-treatment with Araliasaponin II significantly suppressed the TLR-4-NF-κB signaling pathway; this effect may be caused by Araliasaponin II competing with LPS for binding to TLR-4 and subsequently inhibiting translocation of the NF-κB/p65 protein to the nucleus [32].…”