Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10482)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
MAOB
can regulate the following target(s), and cause disease/drug response(s). You can browse detail information of target(s) or disease/drug response(s).
Browse Target
Browse Disease
Browse Drug
Unspecific Target [Unspecific Target]
| In total 1 item(s) under this target | |||||
| Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
| Responsed Disease | Ischemia/reperfusion injury | ICD-11: DB98 | |||
| Responsed Drug | Apigenin | Investigative | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Cell Process | Cell ferroptosis | ||||
| Cell proliferation | |||||
In Vitro Model |
HUVECs (Human umbilical vein endothelial cells) | ||||
| In Vivo Model |
Mice were exposed to 12/12 h of light/darkness and given free access to food and water. All C57BL/6J mice were fasted for 12 h and anesthetized by intraperitoneal injection of 1% sodium pentobarbital before modeling. Later, the superior mesenteric artery (SMA) was subjected to 45 min of global no-flow ischemia, followed by 90 min of reperfusion to induce IIRI. The successful model could be revealed by the microcirculation detector. In order to investigate the effects of APG, mice were randomly divided into different groups: Sham group, IIRI group, APG groups (2 mg/kg, 4 mg/kg and 8 mg/kg), ZnPPIX group (Protoporphyrin Zinc(), Dalian Meilun Biotech Co., Ltd., China, 10mg/kg), Selegiline group (10 mg/kg, Shandong Topscience Biotech Co., Ltd., China) and the ZnPPIX + Selegiline group (10 mg/kg ZnPPIX and 10 mg/kg Selegiline). As mentioned above, drug was intraperitoneal injected after a 10-min-ischemia.
Click to Show/Hide
|
||||
| Response regulation | MST analysis suggested that Apigenin could specifically bind to heme oxygenase 1 (HO-1) and monoamine oxidase b (MAO-B). Simultaneously, APG could attenuate ROS generation and Fe2+ accumulation, maintain mitochondria function thus inhibit ferroptosis and alleviate intestinal ischemia-reperfusion injury. | ||||
Ischemia/reperfusion injury [ICD-11: DB98]
| In total 1 item(s) under this disease | |||||
| Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
| Target Regulator | Amine oxidase [flavin-containing] B (MAOB) | Protein coding | |||
| Responsed Drug | Apigenin | Investigative | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Cell Process | Cell ferroptosis | ||||
| Cell proliferation | |||||
In Vitro Model |
HUVECs (Human umbilical vein endothelial cells) | ||||
| In Vivo Model |
Mice were exposed to 12/12 h of light/darkness and given free access to food and water. All C57BL/6J mice were fasted for 12 h and anesthetized by intraperitoneal injection of 1% sodium pentobarbital before modeling. Later, the superior mesenteric artery (SMA) was subjected to 45 min of global no-flow ischemia, followed by 90 min of reperfusion to induce IIRI. The successful model could be revealed by the microcirculation detector. In order to investigate the effects of APG, mice were randomly divided into different groups: Sham group, IIRI group, APG groups (2 mg/kg, 4 mg/kg and 8 mg/kg), ZnPPIX group (Protoporphyrin Zinc(), Dalian Meilun Biotech Co., Ltd., China, 10mg/kg), Selegiline group (10 mg/kg, Shandong Topscience Biotech Co., Ltd., China) and the ZnPPIX + Selegiline group (10 mg/kg ZnPPIX and 10 mg/kg Selegiline). As mentioned above, drug was intraperitoneal injected after a 10-min-ischemia.
Click to Show/Hide
|
||||
| Response regulation | MST analysis suggested that Apigenin could specifically bind to heme oxygenase 1 (HO-1) and monoamine oxidase b (MAO-B). Simultaneously, APG could attenuate ROS generation and Fe2+ accumulation, maintain mitochondria function thus inhibit ferroptosis and alleviate intestinal ischemia-reperfusion injury. | ||||
Apigenin
[Investigative]
| In total 1 item(s) under this drug | |||||
| Experiment 1 Reporting the Ferroptosis-centered Drug Response | [1] | ||||
| Drug for Ferroptosis | Suppressor | ||||
| Response Target | Unspecific Target | ||||
| Responsed Disease | Ischemia/reperfusion injury | ICD-11: DB98 | |||
| Pathway Response | Fatty acid metabolism | hsa01212 | |||
| Cell Process | Cell ferroptosis | ||||
| Cell proliferation | |||||
In Vitro Model |
HUVECs (Human umbilical vein endothelial cells) | ||||
| In Vivo Model |
Mice were exposed to 12/12 h of light/darkness and given free access to food and water. All C57BL/6J mice were fasted for 12 h and anesthetized by intraperitoneal injection of 1% sodium pentobarbital before modeling. Later, the superior mesenteric artery (SMA) was subjected to 45 min of global no-flow ischemia, followed by 90 min of reperfusion to induce IIRI. The successful model could be revealed by the microcirculation detector. In order to investigate the effects of APG, mice were randomly divided into different groups: Sham group, IIRI group, APG groups (2 mg/kg, 4 mg/kg and 8 mg/kg), ZnPPIX group (Protoporphyrin Zinc(), Dalian Meilun Biotech Co., Ltd., China, 10mg/kg), Selegiline group (10 mg/kg, Shandong Topscience Biotech Co., Ltd., China) and the ZnPPIX + Selegiline group (10 mg/kg ZnPPIX and 10 mg/kg Selegiline). As mentioned above, drug was intraperitoneal injected after a 10-min-ischemia.
Click to Show/Hide
|
||||
| Response regulation | MST analysis suggested that Apigenin could specifically bind to heme oxygenase 1 (HO-1) and monoamine oxidase b (MAO-B). Simultaneously, APG could attenuate ROS generation and Fe2+ accumulation, maintain mitochondria function thus inhibit ferroptosis and alleviate intestinal ischemia-reperfusion injury. | ||||
References