Galloylpaeoniflorin

Galloylpaeoniflorin (6'-O-Galloyl paeoniflorin) is an orally active galloylated derivative of Paeoniflorin (HY-N0293) found in peony roots with various anti-inflammatory and antioxidant activities. Galloylpaeoniflorin suppresses RANKL-induced activation of ERK, JNK, c-Fos, c-Jun, and NFATc1, and reduces osteoclast-specific gene expression. Galloylpaeoniflorin activates Nrf2 and PI3K/Akt pathways, inhibits NF-κB activation, and scavenges ROS to reduce oxidative DNA, lipid, and protein damage. Galloylpaeoniflorin attenuates neuroinflammation, inhibits apoptosis, reduces Helicobacter pylori-induced gastric mucosa injury and UVB-induced cell damage. Galloylpaeoniflorin can be used for the research of osteoporosis, gastritis, ischemic stroke and skin diseases^{[1][2][3][4][5]}. In Vitro:Galloylpaeoniflorin (0-160 µM; 96 h) shows no significant cytotoxicity to primary murine bone marrow-derived macrophages/monocytes at concentrations up to 80 µM after 96 hours of incubation^[1].
Galloylpaeoniflorin (10-40 µM; 1-7 days) dose-dependently inhibits RANKL-induced osteoclastogenesis in primary murine bone marrow-derived macrophages/monocytes^[1].
Galloylpaeoniflorin (0-40 µM; 5 days) dose-dependently suppresses the expression of osteoclast-specific genes (c-Fos, NFATc1, Acp5) in primary murine bone marrow-derived macrophages/monocytes stimulated with RANKL^[1].
Galloylpaeoniflorin (10-40 µM) dose-dependently inhibits podosome belt formation, reduces cell size, and decreases multinucleation in primary murine bone marrow-derived macrophages/monocytes differentiated into osteoclasts with RANKL^[1].
Galloylpaeoniflorin (10-40 µM) dose-dependently inhibits the bone resorptive function of mature osteoclasts derived from primary murine bone marrow-derived macrophages/monocytes^[1].
Galloylpaeoniflorin (10-40 µM) dose-dependently scavenges RANKL-induced intracellular ROS in primary murine bone marrow-derived macrophages/monocytes^[1].
Galloylpaeoniflorin (40 µM; 2 h) suppresses RANKL-induced activation of ERK and JNK MAPK pathways, as well as downstream c-Fos and NFATc1 protein expression, in primary murine bone marrow-derived macrophages/monocytes, with no effect on p38 or NF-κB pathways^[1].
Galloylpaeoniflorin (20-100 μg/mL; 8-24 h) up to 60 μg/mL has no cytotoxic effect on uninfected GES-1 human gastric epithelial cells after 8, 16, or 24 h of treatment, while concentrations of 80 and 100 μg/mL induce concentration-dependent cytotoxicity^[2].
Galloylpaeoniflorin (60 μg/mL; 8-24 h) significantly increases the viability of H. pylori-infected GES-1 human gastric epithelial cells^[2].
Galloylpaeoniflorin (60 μg/mL; 24 h) significantly inhibits H. pylori-induced early and late apoptosis in GES-1 human gastric epithelial cells^[2].
Galloylpaeoniflorin (60 μg/mL; 24 h) significantly reduces ROS, MDA production and increases SOD activity in H. pylori-infected GES-1 human gastric epithelial cells^[2].
Galloylpaeoniflorin (60 μg/mL; 24 h) significantly reduces mRNA and protein expression of pro-inflammatory cytokines COX2, TNF-α, and IL-6, and significantly increases mRNA and protein expression of antioxidant genes HMOX1, NQO1 and MUC1 in H. pylori-infected GES-1 human gastric epithelial cells^[2].
Galloylpaeoniflorin (60 μg/mL; 24 h) significantly inhibits adhesion of H. pylori to GES-1 human gastric epithelial cells^[2].
Galloylpaeoniflorin (60 μg/mL; 24 h) significantly increases Nrf2 mRNA and protein expression in H. pylori-infected GES-1 human gastric epithelial cells^[2].
Galloylpaeoniflorin (20 μM; 1 h pre-incubation before UVB exposure, 24 h incubation after UVB exposure) significantly scavenges UVB-induced intracellular ROS in human HaCaT keratinocytes^[5].
Galloylpaeoniflorin (20 μM; 1 h pre-incubation before UVB exposure, 2 h incubation after UVB exposure) attenuates UVB-induced DNA strand breaks in human HaCaT keratinocytes^[5].
Galloylpaeoniflorin (20 μM; 1 h pre-incubation before UVB exposure, 24 h incubation after UVB exposure) attenuates UVB-induced lipid peroxidation and protein carbonylation in human HaCaT keratinocytes^[5].
Galloylpaeoniflorin (20 μM; 1 h pre-incubation before UVB exposure, 24 h incubation after UVB exposure) protects human HaCaT keratinocytes against UVB-induced cell death, increasing cell viability from 46% to 55%^[5].
Galloylpaeoniflorin (20 μM; 1 h pre-incubation before UVB exposure, 24 h incubation after UVB exposure) reduces UVB-induced apoptosis in human HaCaT keratinocytes^[5].
Galloylpaeoniflorin (20 μM; 1 h pre-incubation before UVB exposure, 24 h incubation after UVB exposure) reduces UVB-induced apoptotic sub-G1 hypodiploid cells in human HaCaT keratinocytes, lowering the sub-G1 population from 35% to 26%^[5].
Galloylpaeoniflorin (20 μM; 1 h pre-incubation before UVB exposure) inhibits the mitochondrial apoptotic pathway in UVB-exposed human HaCaT keratinocytes by reducing cleaved caspase 9, cleaved caspase 3, and cleaved PARP levels, and restoring Bcl-2/Bax protein balance^[5]. In Vivo:Galloylpaeoniflorin (10 mg/kg; i.p.; every 2 days; 6 weeks) prevents ovariectomy-induced osteoporosis in mice by increasing bone structural parameters and reducing osteoclast formation^[1].
Galloylpaeoniflorin (5 mg/kg; i.g.; once daily; 2 weeks pretreatment) attenuates H. pylori-induced chronic gastritis in male C57BL/6 mice by reducing gastric mucosal inflammation, enhancing antioxidant responses, and activating Nrf2 signaling^[2].
Galloylpaeoniflorin (2.5-10 mg/kg; i.p.; daily; 14 days) exerts dose-dependent neuroprotective effects against CIRI in male Wistar rats by reducing infarct volume, improving neurological function, mitigating oxidative stress, suppressing inflammation, and reducing neuronal apoptosis, via activation of the PI3K/Akt/Nrf2 pathway^[3].