| 体外研究 |
Galloypaeoniflorin (0-160 µM; 96 h) showed no significant cytotoxicity towards primary mouse bone marrow-derived macrophages/monocytes at a concentration of up to 80 µM after 96 hours of incubation.
Galloypaeoniflorin (10-40 µM; 1-7 days) can dose dependently inhibit RANKL induced osteoclastogenesis of primary mouse bone marrow-derived macrophages/monocytes.
Galloylpaeoniflorin (0-40 µM; 5 days) can dose dependently inhibit the expression of osteoclast specific genes (c-Fos, NFATc1, Acp5) in primary mouse bone marrow-derived macrophages/monocytes stimulated by RANKL.
Galloypaeoniflorin (10-40 µM) can dose dependently inhibit podocyte band formation, reduce cell volume, and decrease multinucleation levels of primary mouse bone marrow-derived macrophages/monocytes induced to differentiate into osteoclasts by RANKL.
Galloypaeoniflorin (10-40 µM) dose dependently inhibits the bone resorption function of mature osteoclasts differentiated from primary mouse bone marrow-derived macrophages/monocytes.
Galloylpaeoniflorin (10-40 µM) can dose dependently clear reactive oxygen species in RANKL induced primary mouse bone marrow-derived macrophages/monocytes.
Galloypaeoniflorin (40 µM; 2 h) can inhibit RANKL induced activation of ERK and JNK MAPK pathways, as well as downstream expression of c-Fos and NFATc1 proteins, in primary mouse bone marrow-derived macrophages/monocytes, but has no effect on p38 or NF - κ B pathways .
Cell Viability Assay
| Cell Line: |
primary murine bone marrow-derived macrophages/monocytes |
| Concentration: |
| 5, 10, 20, 40, 80, 160 µM |
|
| Incubation Time: |
96 hours |
| Result: |
Showed no significant cytotoxicity at 5- 80 µM.
Slightly reduced cell viability at 160 µM. |
Western Blot Analysis
| Cell Line: |
primary murine bone marrow-derived macrophages/monocytes |
| Concentration: |
40 µM |
| Incubation Time: |
2 hours |
| Result: |
Reduced p-ERK, p-JNK expression.
Rduced c-Fos and NFATc1 protein expression.
Had no effect on p38 or NF-κB pathways. |
|
| 体内研究 |
Galloypaeoniflorin (10 mg/kg; intraperitoneal injection; Once every 2 days; Continuous treatment for 6 weeks can prevent osteoporosis induced by ovariectomy in mice by improving bone structure parameters and reducing osteoclast formation.
Galloypaeoniflorin (5 mg/kg; gavage; Once a day; Pre treatment for 2 weeks can alleviate H. pylori induced chronic gastritis in male C57BL/6 mice by reducing gastric mucosal inflammation, enhancing antioxidant response, and activating the Nrf2 signaling pathway.
Galloypaeoniflorin (2.5-10 mg/kg; intraperitoneal injection; Once daily for 14 consecutive days, activation of the PI3K/Akt/Nrf2 pathway can reduce infarct volume, improve neurological function, alleviate oxidative stress, inhibit inflammatory response, and reduce neuronal apoptosis, exerting a dose-dependent neuroprotective effect on cerebral ischemia-reperfusion injury (CIRI) in male Wistar rats.
| Animal Model: |
C57BL/6J (female, 11 weeks old, 19.5 g, bilateral ovariectomy-induced osteoporosis) |
| Dosage: |
10 mg/kg |
| Administration: |
i.p.; every 2 days; 6 weeks |
| Result: |
Increased bone volume/tissue volume (BV/TV), trabecular number (Tb.
N), trabecular thickness (Tb.
Th), connectivity density (Conn.
Dn), and bone surface (BS) compared to ovariectomized controls.
Decreased trabecular separation (Tb.
Sp) compared to ovariectomized controls.
Significantly reduced the number of TRAP-positive osteoclasts per bone surface compared to ovariectomized controls. |
| Animal Model: |
C57BL/6 with H. pylori infection (male, 6-8 weeks old) |
| Dosage: |
5 mg/kg |
| Administration: |
p.o.; once daily; 2 weeks pretreatment |
| Result: |
Alleviated H.
pylori-induced inflammatory cell infiltration in gastric mucosa and submucosa.
Reduced relative optical density of gastric tissue inflammatory markers COX2 and IL6.
Increased relative optical density of gastric tissue antioxidant markers HMOX1 and NQO1.
Repressed H.
pylori-induced upregulation of COX2, TNF-α, and IL6 mRNA expression in gastric mucosa.
Enhanced H.
pylori-induced upregulation of HMOX1 and NQO1 mRNA expression in gastric mucosa.
Repressed H.
pylori-induced upregulation of COX2, IL6, and TNF-α protein expression in gastric mucosa.
Enhanced H.
pylori-induced upregulation of HMOX1, NQO1, and Nrf2 protein expression in gastric mucosa.
Increased relative optical density of Nrf2 in gastric tissue. |
| Animal Model: |
Wistar with CIRI (male, 7-8 months old, 270 g) |
| Dosage: |
2.5 mg/kg; 5 mg/kg; 10 mg/kg |
| Administration: |
i.p.; daily; 14 days |
| Result: |
Reduced infarct volume by a statistically significant amount compared to untreated CIRI rats.
Reduced neurological score compared to untreated CIRI rats.
Decreased brain malondialdehyde (MDA) levels and increased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH) levels compared to untreated CIRI rats.
Reduced the percentage of Iba1-, p-p38 MAPK-, and p-JNK-positive cells, and reduced IL-1β and TNF-α mRNA expression compared to untreated CIRI rats.
Reduced the percentage of TUNEL-positive cells and caspase-3 activity compared to untreated CIRI rats.
Increased nuclear Nrf2 and heme oxygenase 1 (HO-1) protein expression compared to untreated CIRI rats.
Reduced infarct volume to a greater statistically significant extent compared to untreated CIRI rats.
Reduced neurological score to a greater extent compared to untreated CIRI rats.
Further decreased brain MDA levels and further increased SOD, GSH-Px, and GSH levels compared to untreated CIRI rats.
Further reduced the percentage of Iba1-, p-p38 MAPK-, and p-JNK-positive cells, and further reduced IL-1β and TNF-α mRNA expression compared to untreated CIRI rats.
Further reduced the percentage of TUNEL-positive cells and caspase-3 activity compared to untreated CIRI rats.
Further increased nuclear Nrf2 and HO-1 protein expression compared to untreated CIRI rats.
Reduced infarct volume to the greatest statistically significant extent compared to untreated CIRI rats.
Reduced neurological score to the greatest extent compared to untreated CIRI rats.
Achieved the greatest reduction in brain MDA levels and greatest increases in SOD, GSH-Px, and GSH levels compared to untreated CIRI rats.
Achieved the greatest reduction in the percentage of Iba1-, p-p38 MAPK-, and p-JNK-positive cells, and greatest reduction in IL-1β and TNF-α mRNA expression compared to untreated CIRI rats.
Achieved the greatest reduction in the percentage of TUNEL-positive cells and caspase-3 activity compared to untreated CIRI rats.
Achieved the greatest increases in nuclear Nrf2 and HO-1 protein expression compared to untreated CIRI rats.
Attenuated all protective effects when rats were pretreated with Ly294002. |
|
Data Sheet