Sparstolonin B

Sparstolonin B acts as a selective TLR2 and TLR4 antagonist and selectively blocks TLR2- and TLR4-mediated inflammatory signaling. Sparstolonin B has anti-HIV and anticancer activities[1][2].

Signaling Pathways >> Immunology/Inflammation >> Toll-like Receptor (TLR)

Research Areas >> Cancer

Signaling Pathways >> Anti-infection >> HIV

Research Areas >> Infection

Research Areas >> Inflammation/Immunology

TLR2

TLR4

HIV-1

Sparstolonin B (1-20 µM; 2-4 days) inhibits cell growth and viability of neuroblastoma cells[3]. Sparstolonin B inhibits TLR ligand-induced cytokine expression in mouse macrophages. Sparstolonin B inhibits MyD88 recruitment to TLR4 and TLR2[1]. Sparstolonin B generates reactive oxygen species (ROS) in neuroblastoma cells. Sparstolonin B reduces expression of N-myc in neuroblastoma cells[3]. Cell Viability Assay[3] Cell Line: SH-SY5Y, IMR-32, NGP, SKNF-1 and SK-N-BE(2) cells Concentration: 1 µM, 5 µM, 10 µM or 20 µM Incubation Time: 2-4 days Result: Effectively and dose-dependently inhibits the viability of all neuroblastoma cell lines after 2 days (SH-SY5Y and IMR-32), 3 days (NGP cells) or 4 days (SKNF-1 and SK-N-BE(2) cells) treatment.

Sparstolonin B (100 μg/mouse; i.p.) suppresses LPS-provoked inflammation in mice[1]. Animal Model: 5-6-week-old male C57Bl/6 mice (body weight 18-20 g)[1] Dosage: 100 μg/mouse Administration: I.p. Result: Significantly lower TNFα and IL-1β expression levels in LPS-induced sepsis mouse model.

[1]. Liang Q, et al. Characterization of sparstolonin B, a Chinese herb-derived compound, as a selective Toll-like receptor antagonist with potent anti-inflammatory properties. J Biol Chem. 2011;286(30):26470-26479.

[2]. Deng X, et al. The Chinese herb-derived Sparstolonin B suppresses HIV-1 transcription. Virol J. 2015;12:108. Published 2015 Jul 25.

[3]. Kumar A, et al. Sparstolonin B, a novel plant derived compound, arrests cell cycle and induces apoptosis in N-myc amplified and N-myc nonamplified neuroblastoma cells [published correction appears in PLoS One. 2016;11(7):e0159082]. PLoS One. 2014;9(5):e96343. Published 2014 May 1.