Ferroptosis-centered Drug Response Information
General Information of the Drug (ID: ferrodrug0393)
Name |
Panax notoginseng saponins
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Drug Type |
Traditional Chinese Medicin
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Full List of Ferroptosis Target Related to This Drug
Nuclear factor erythroid 2-related factor 2 (NFE2L2)
In total 1 item(s) under this Target | |||||
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target | [1] | ||||
Target for Ferroptosis | Marker/Suppressor | ||||
Responsed Disease | Cerebral ischemia | ICD-11: 8B10 | |||
Pathway Response | Glutathione metabolism | hsa00480 | |||
Fatty acid metabolism | hsa01212 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model | hBCs (Brain cells) | ||||
In Vivo Model |
Rats were randomly assigned to six groups: (1) the sham group, (2) the middle cerebral artery ischaemia-occlusion-reperfusion (MCAO/R) group, (3) the AST IV group, (4) the PNS group, (5) the combination group and (6) the combination + brusatol group. One hundred rats were used in the experiment, of which 9 died during surgery, 10 died of intracranial haemorrhage and brain injury and 63 rats were successfully modelled, for a final success rate of 76.8%. Each group included 9 rats. Behavioural testing was performed on 5 animals in each group. After behavioural testing, 3 rats were used for TTC staining and 6 were used for kit detection and western blot analysis. Existing studies have revealed the toxicological effects of the compatibility of astragalus and P. notoginseng. The dosage and method of AST IV (28 mg/kg) and PNS (80 mg/kg) alone or in combination have been previously determined and were administered intragastrically for three consecutive days (10 ml/kg each time), and the optimal administration times were 50, 26 and 2 h before model establishment.Brusatol (1 mg/kg) was administered intraperitoneally for 1 h prior to modelling. The sham group and the MCAO/R group were given the same amount of saline.
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Response regulation | Combining Astragaloside IV and Panax notoginseng saponins attenuates cerebral ischemia-reperfusion injury by activating Nrf2 to inhibit ferroptosis and inflammatory responses. | ||||