Ferroptosis Regulator Information
General Information of the Ferroptosis Regulator (ID: REG10384)
Full List of the Ferroptosis Target of This Regulator and Corresponding Disease/Drug Response(s)
CNR2
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 | Ulcerative colitis | ICD-11: DD71 | |||
Responsed Drug | Caryophyllene | Phase 2 | |||
Pathway Response | Glutathione metabolism | hsa00480 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
RAW 264.7 cells | Leukemia | Mus musculus | CVCL_0493 | |
In Vivo Model |
After 10 days of acclimation, the mice were randomly assigned to five groups (n = 6 each): control, model (3% DSS), BCP (50 mg/kg body weight), AM630 (10 mg/kg body weight) and AM630 + BCP. All mice (except those in the control group) were provided with a solution of filtered water containing 3% (w/v) DSS ad libitum during the experiment period. The mice in the control group received only normal drinking water. For the treatment groups, BCP was dissolved in corn oil at doses of 50 mg/kg and administered orally once a day. The mice in the AM630 group were injected intraperitoneally with AM630 (10 mg/kg). The mice in the AM630 + BCP group received an intraperitoneal injection of AM630 (10 mg/kg) given 30 min before the BCP (50 mg/kg). During the study, symptomatic parameters including body weight, stool character and bleeding were recorded daily. The disease activity index (DAI) was calculated according to our previous study. After 8 days of treatment, all mice were anesthetized with pentobarbital sodium. The blood and colon samples were collected for subsequent analysis. The collected blood was left to coagulate for 20 min at room temperature and centrifuged for 15 min at 3000 g to obtain the serum.
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Response regulation | B-Caryophyllene (BCP) activated the type 2 cannabinoid receptor (CB2R) to inhibit macrophage ferroptosis and its induced inflammatory response both in vivo and in vitro. These results revealed that macrophage ferroptosis is a potential therapeutic target for ulcerative colitis and identified a novel mechanism of BCP in ameliorating experimental colitis. | ||||
Ulcerative colitis [ICD-11: DD71]
In total 1 item(s) under this disease | |||||
Experiment 1 Reporting the Ferroptosis-centered Disease Response | [1] | ||||
Target Regulator | Cannabinoid receptor 2 (CNR2) | Protein coding | |||
Responsed Drug | Caryophyllene | Phase 2 | |||
Pathway Response | Glutathione metabolism | hsa00480 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
RAW 264.7 cells | Leukemia | Mus musculus | CVCL_0493 | |
In Vivo Model |
After 10 days of acclimation, the mice were randomly assigned to five groups (n = 6 each): control, model (3% DSS), BCP (50 mg/kg body weight), AM630 (10 mg/kg body weight) and AM630 + BCP. All mice (except those in the control group) were provided with a solution of filtered water containing 3% (w/v) DSS ad libitum during the experiment period. The mice in the control group received only normal drinking water. For the treatment groups, BCP was dissolved in corn oil at doses of 50 mg/kg and administered orally once a day. The mice in the AM630 group were injected intraperitoneally with AM630 (10 mg/kg). The mice in the AM630 + BCP group received an intraperitoneal injection of AM630 (10 mg/kg) given 30 min before the BCP (50 mg/kg). During the study, symptomatic parameters including body weight, stool character and bleeding were recorded daily. The disease activity index (DAI) was calculated according to our previous study. After 8 days of treatment, all mice were anesthetized with pentobarbital sodium. The blood and colon samples were collected for subsequent analysis. The collected blood was left to coagulate for 20 min at room temperature and centrifuged for 15 min at 3000 g to obtain the serum.
Click to Show/Hide
|
||||
Response regulation | B-Caryophyllene (BCP) activated the type 2 cannabinoid receptor (CB2R) to inhibit macrophage ferroptosis and its induced inflammatory response both in vivo and in vitro. These results revealed that macrophage ferroptosis is a potential therapeutic target for ulcerative colitis and identified a novel mechanism of BCP in ameliorating experimental colitis. | ||||
Caryophyllene
[Phase 2]
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 | Ulcerative colitis | ICD-11: DD71 | |||
Pathway Response | Glutathione metabolism | hsa00480 | |||
Ferroptosis | hsa04216 | ||||
Cell Process | Cell ferroptosis | ||||
In Vitro Model |
RAW 264.7 cells | Leukemia | Mus musculus | CVCL_0493 | |
In Vivo Model |
After 10 days of acclimation, the mice were randomly assigned to five groups (n = 6 each): control, model (3% DSS), BCP (50 mg/kg body weight), AM630 (10 mg/kg body weight) and AM630 + BCP. All mice (except those in the control group) were provided with a solution of filtered water containing 3% (w/v) DSS ad libitum during the experiment period. The mice in the control group received only normal drinking water. For the treatment groups, BCP was dissolved in corn oil at doses of 50 mg/kg and administered orally once a day. The mice in the AM630 group were injected intraperitoneally with AM630 (10 mg/kg). The mice in the AM630 + BCP group received an intraperitoneal injection of AM630 (10 mg/kg) given 30 min before the BCP (50 mg/kg). During the study, symptomatic parameters including body weight, stool character and bleeding were recorded daily. The disease activity index (DAI) was calculated according to our previous study. After 8 days of treatment, all mice were anesthetized with pentobarbital sodium. The blood and colon samples were collected for subsequent analysis. The collected blood was left to coagulate for 20 min at room temperature and centrifuged for 15 min at 3000 g to obtain the serum.
Click to Show/Hide
|
||||
Response regulation | B-Caryophyllene (BCP) activated the type 2 cannabinoid receptor (CB2R) to inhibit macrophage ferroptosis and its induced inflammatory response both in vivo and in vitro. These results revealed that macrophage ferroptosis is a potential therapeutic target for ulcerative colitis and identified a novel mechanism of BCP in ameliorating experimental colitis. | ||||