Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10186)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
RPL8
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).
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Unspecific Target [Unspecific Target]
In total 1 item(s) under this target | |||||
Experiment 1 Reporting the Ferroptosis Target of This Regulator | [1] | ||||
Responsed Disease | Intracerebral hemorrhage | ICD-11: 8B00 | |||
Responsed Drug | Rotenone | Approved | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
hBCs (Brain cells) | ||||
In Vivo Model |
Six-to-eight week old male ICR mice were purchased from the Experimental Animal Center of the Chinese Academy of Sciences (Shanghai, China). All animal procedures have been approved by the Institutional Animal Care and Use Committee of Ruijin hospital, Shanghai Jiao Tong University (Shanghai, China). Efforts were made as much as possible to reduce the number of mice used and to minimize suffering. Herein, a total of 51 mice were randomly divided into 3 groups: (i) sham group (n = 15), (ii) ICH group (n = 18), and (iii) ICH + Rot group (n = 18). To be specific, the current study was divided into two parts of the experimental design. Part 1: to observe the effects of Rot on the mitochondria-related genes, iron levels, MDA levels, SOD activity, hematoma volume, brain edema, and ultrastructural changes of mitochondria, animals were randomly divided into the sham group (n = 9), ICH group (n = 12), and ICH + Rot group (n = 12). All mice were euthanized at 3 d after operation and brain samples were harvested, as per our previously described reports. Part 2: to observe the effect of Rot on neurological deficits following ICH, 18 mice were randomly divided into additional 3 groups (sham group, ICH group, and ICH + Rot group). We evaluated mNSS scores at 1, 3, 7, and 14 days after ICH. We also assessed the memory function with the MWM test at 14 days after ICH.
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Response regulation | Intracerebral hemorrhage induced significant mitochondrial dysfunction and that mitochondrial inhibitor rotenone can trigger and enhance neuronal ferroptosis. The ferroptosis protein markers ACSL4, COX-2, xCT, RPL8, and GPX4 were significantly upregulated in the hemin group. Rot treatment further enhanced hemin-induced upregulation of ACSL4, COX-2, xCT, RPL8, and GPX4 levels. | ||||
Intracerebral hemorrhage [ICD-11: 8B00]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | 60S ribosomal protein L8 (RPL8) | Protein coding | |||
Responsed Drug | Rotenone | Approved | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
hBCs (Brain cells) | ||||
In Vivo Model |
Six-to-eight week old male ICR mice were purchased from the Experimental Animal Center of the Chinese Academy of Sciences (Shanghai, China). All animal procedures have been approved by the Institutional Animal Care and Use Committee of Ruijin hospital, Shanghai Jiao Tong University (Shanghai, China). Efforts were made as much as possible to reduce the number of mice used and to minimize suffering. Herein, a total of 51 mice were randomly divided into 3 groups: (i) sham group (n = 15), (ii) ICH group (n = 18), and (iii) ICH + Rot group (n = 18). To be specific, the current study was divided into two parts of the experimental design. Part 1: to observe the effects of Rot on the mitochondria-related genes, iron levels, MDA levels, SOD activity, hematoma volume, brain edema, and ultrastructural changes of mitochondria, animals were randomly divided into the sham group (n = 9), ICH group (n = 12), and ICH + Rot group (n = 12). All mice were euthanized at 3 d after operation and brain samples were harvested, as per our previously described reports. Part 2: to observe the effect of Rot on neurological deficits following ICH, 18 mice were randomly divided into additional 3 groups (sham group, ICH group, and ICH + Rot group). We evaluated mNSS scores at 1, 3, 7, and 14 days after ICH. We also assessed the memory function with the MWM test at 14 days after ICH.
Click to Show/Hide
|
||||
Response regulation | Intracerebral hemorrhage induced significant mitochondrial dysfunction and that mitochondrial inhibitor rotenone can trigger and enhance neuronal ferroptosis. The ferroptosis protein markers ACSL4, COX-2, xCT, RPL8, and GPX4 were significantly upregulated in the hemin group. Rot treatment further enhanced hemin-induced upregulation of ACSL4, COX-2, xCT, RPL8, and GPX4 levels. | ||||
Rotenone
[Approved]
In total 1 item(s) under this drug | |||||
Experiment 1 Reporting the Ferroptosis-centered Drug Response | [1] | ||||
Drug for Ferroptosis | Inducer | ||||
Response Target | Unspecific Target | ||||
Responsed Disease | Intracerebral hemorrhage | ICD-11: 8B00 | |||
Pathway Response | Fatty acid metabolism | hsa01212 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
hBCs (Brain cells) | ||||
In Vivo Model |
Six-to-eight week old male ICR mice were purchased from the Experimental Animal Center of the Chinese Academy of Sciences (Shanghai, China). All animal procedures have been approved by the Institutional Animal Care and Use Committee of Ruijin hospital, Shanghai Jiao Tong University (Shanghai, China). Efforts were made as much as possible to reduce the number of mice used and to minimize suffering. Herein, a total of 51 mice were randomly divided into 3 groups: (i) sham group (n = 15), (ii) ICH group (n = 18), and (iii) ICH + Rot group (n = 18). To be specific, the current study was divided into two parts of the experimental design. Part 1: to observe the effects of Rot on the mitochondria-related genes, iron levels, MDA levels, SOD activity, hematoma volume, brain edema, and ultrastructural changes of mitochondria, animals were randomly divided into the sham group (n = 9), ICH group (n = 12), and ICH + Rot group (n = 12). All mice were euthanized at 3 d after operation and brain samples were harvested, as per our previously described reports. Part 2: to observe the effect of Rot on neurological deficits following ICH, 18 mice were randomly divided into additional 3 groups (sham group, ICH group, and ICH + Rot group). We evaluated mNSS scores at 1, 3, 7, and 14 days after ICH. We also assessed the memory function with the MWM test at 14 days after ICH.
Click to Show/Hide
|
||||
Response regulation | Intracerebral hemorrhage induced significant mitochondrial dysfunction and that mitochondrial inhibitor rotenone can trigger and enhance neuronal ferroptosis. The ferroptosis protein markers ACSL4, COX-2, xCT, RPL8, and GPX4 were significantly upregulated in the hemin group. Rot treatment further enhanced hemin-induced upregulation of ACSL4, COX-2, xCT, RPL8, and GPX4 levels. | ||||