Benzoylpaeoniflorin

Benzoylpaeoniflorin is an orally active monoterpene glycoside compound. Benzoylpaeoniflorin exerts anti-inflammatory, anti-allergic, psoriasis-improving and sepsis-improving effects by inhibiting signaling pathways such as TNF/NF-κB and MAPK, as well as regulating immune homeostasis. Benzoylpaeoniflorin can be used in research related to immune, allergic and inflammatory diseases^[1][2][3]. In Vitro:Benzoylpaeoniflorin (0-800 μM; 24-72 h) shows no cytotoxicity against human HaCaT keratinocytes at concentrations up to 200 μM and exposure durations up to 72 h, while higher concentrations induce dose- and time-dependent cytotoxicity^[1].
Benzoylpaeoniflorin (200 μM; 0-14 d) inhibits TNF-α-induced proliferation of human HaCaT keratinocytes by arresting cell cycle progression, and a sustained antiproliferative effect is observable within 14 d^[1].
Benzoylpaeoniflorin (200 μM) inhibits TNF-α-induced activation of the NF-κB pathway in human HaCaT keratinocytes, reduces the nuclear translocation of p-p65, and decreases the secretion of downstream proinflammatory cytokines IL-1β, IL-6 and CXCL10^[1].
Benzoylpaeoniflorin (0-10 μM; 9-30 h) inhibits LPS (HY-D1056)-induced mRNA and protein expression of IL-6 and TNF-α in HUVECs and THP-1 macrophages in a time- and dose-dependent manner^[2].
Benzoylpaeoniflorin (0-50 μM; 48 h) exhibits no cytotoxicity towards human umbilical vein endothelial cells (HUVECs) and THP-1 macrophages^[2].
Benzoylpaeoniflorin (2-10 μM; 9-30 h) inhibits LPS-induced iNOS mRNA and protein expression in a time- and dose-dependent manner, as well as NO production in human umbilical vein endothelial cells (HUVECs) induced by LPS + IFN-γ^[2].
Benzoylpaeoniflorin (2-10 μM; 7 h) inhibits the phosphorylation of NF-κB (p65) and mitogen-activated protein kinases (MAPKs, including p38, JNK, ERK) induced by LPS in human umbilical vein endothelial cells (HUVECs) and THP-1 macrophages in a time- and dose-dependent manner^[2].
Benzoylpaeoniflorin (5-100 μM; 24 h) inhibits HDC activity in *Klebsiella pneumoniae* cultures, and incubation at 100 μM for 24 h reduces histamine production by up to 50%^[3].
Benzoylpaeoniflorin (25 h) potently inhibits IgE-mediated mast cell degranulation in DNP-BSA-stimulated RBL-2H3 cells: it exhibits an EC₅₀ of 6.34 μM for inhibiting β-HEX and an EC₅₀ of 18.06 μM for inhibiting HIS, and shows no cytotoxicity at concentrations up to 100 μM^[3].
Benzoylpaeoniflorin (5-100 μM; 25 h) downregulates the production of proinflammatory cytokines IL-3, IL-4, IL-5 and IL-13 in DNP-BSA-stimulated RBL-2H3 cells^[3].
Benzoylpaeoniflorin inhibits the activation of the MAPK signaling pathway in DNP-BSA-stimulated RBL-2H3 cells by reducing the phosphorylation levels of p38, ERK1/2 and JNK proteins^[3]. In Vivo:Benzoylpaeoniflorin (0.3-0.6% cream; topical administration; once daily; for 7 consecutive days) significantly alleviates imiquimod (HY-B0180)-induced psoriasiform inflammation in female SKH-1 mice by restoring immune homeostasis, reducing keratinocyte proliferation, and inhibiting the TNF-α/NF-κB signaling pathway^[1].
Benzoylpaeoniflorin (0.09-0.44 mg/kg; intravenous injection; single administration concurrent with LPS treatment) dose-dependently reduces the production of inflammatory cytokines in serum and peritoneal fluid of LPS-induced mice, alleviates lung tissue injury in mice with non-lethal sepsis, and improves the survival rate of mice^[2].
Benzoylpaeoniflorin (45-180 mg/kg; p.o.; single administration) dose-dependently inhibits IgE-mediated passive cutaneous anaphylaxis in BALB/c mice^[3].