Ferroptosis-centered Drug Response Information

General Information of the Drug (ID: ferrodrug0358)
Name
Cyanidin-3-glucoside
Synonyms
Cyanidin 3-glucoside; 7084-24-4; Cyanidin 3-O-glucoside; cyanidin-3-o-glucoside chloride; 2-[2-(3,4-dihydroxyphenyl)-5,7-dihydroxychromenylium-3-yl]oxy-6-(hydroxymethyl)oxane-3,4,5-triol;chloride; 27214-71-7; Chrysanthemin; (2S,3R,4S,5S,6R)-2-[2-(3,4-dihydroxyphenyl)-5,7-dihydroxychromenylium-3-yl]oxy-6-(hydroxymethyl)oxane-3,4,5-triol;chloride; C21-H21-O11.Cl; Chrysontemin;Cyanidin 3-O-glucoside chloride; Cyanidin galactoside; Cyanindin-3-Gal; Idaein; Ideain; Ideanin; CHEBI:189578; BCP28559; AKOS015968430; FT-0638681; Chrysontemin; Cyanidin 3-O-glucoside chloride; A818960; 2-[[2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-1-benzopyrylium-3-yl]oxy]-6-(hydroxymethyl)oxane-3,4,5-triol chloride; 2-[2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-chromenylium-3-yl]oxy-6-(hydroxymethyl)tetrahydropyran-3,4,5-triol chloride

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Structure
3D MOL
2D MOL
Formula
C21H21ClO11
IUPAC Name
2-[2-(3,4-dihydroxyphenyl)-5,7-dihydroxychromenylium-3-yl]oxy-6-(hydroxymethyl)oxane-3,4,5-triol;chloride
Canonical SMILES
C1=CC(=C(C=C1C2=[O+]C3=CC(=CC(=C3C=C2OC4C(C(C(C(O4)CO)O)O)O)O)O)O)O.[Cl-]
InChI
InChI=1S/C21H20O11.ClH/c22-7-16-17(27)18(28)19(29)21(32-16)31-15-6-10-12(25)4-9(23)5-14(10)30-20(15)8-1-2-11(24)13(26)3-8;/h1-6,16-19,21-22,27-29H,7H2,(H3-,23,24,25,26);1H
InChIKey
YTMNONATNXDQJF-UHFFFAOYSA-N
PubChem CID
12303220
Full List of Ferroptosis Target Related to This Drug
Transferrin receptor protein 1 (TFRC)
 Target Info 
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/Driver
Responsed Disease Ischemia/reperfusion injury ICD-11: DB98
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell proliferation
Cell autophagy
In Vitro Model CHO-S/H9C2 cells Normal Cricetulus griseus CVCL_A0TS
In Vivo Model
Adult male Sprague Dawley (SD) rats weighing 260-280 g were purchased from Qinglongshan Animal Farm (Nanjing, China). After a week of adaptation, the rats were randomly assigned into five groups (n = 8): (1) sham group, rats receiving saline gavage and sham surgery were used as control group; (2) I/R model group, rats receiving saline gavage and left anterior descending (LAD) ligation surgery were used as the model group; (3) C3G-10 group, I/R model plus intraperitoneal injection of 10 mg/kg C3G; (4) C3G-20 group, I/R model plus intraperitoneal injection of 20 mg/kg C3G; and (5) DIL group, I/R model plus oral administration of 20 mg/kg diltiazem. C3G and DIL were dissolved in DMSO and then diluted with saline so that the DMSO concentration was less than 0.1% (v/v).

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Response regulation The administration of Cyanidin-3-glucoside (C3G) reduced the infarction area, mitigated pathological alterations, inhibited ST segment elevation, and attenuated oxidative stress and ferroptosis-related protein expression. C3G also suppressed the expressions of USP19, Beclin1, NCOA4, and LC3II/LC3I. In addition, treatment with C3G relieved oxidative stress, downregulated LC3II/LC3I, reduced autophagosome number, downregulated TfR1 expression, and upregulated the expressions of FTH1 and GPX4 in OGD/R-induced H9c2 cells. Taken together, C3G could be a potential agent to protect myocardium from myocardial ischemia-reperfusion (IR) injury.
Nuclear receptor coactivator 4 (NCOA4)
 Target Info 
In total 1 item(s) under this Target
Experiment 1 Reporting the Ferroptosis-centered Drug Act on This Target [1]
Target for Ferroptosis Driver
Responsed Disease Ischemia/reperfusion injury ICD-11: DB98
 Disease Info 
Pathway Response Fatty acid metabolism hsa01212
Ferroptosis hsa04216
Autophagy hsa04140
Cell Process Cell ferroptosis
Cell proliferation
Cell autophagy
In Vitro Model CHO-S/H9C2 cells Normal Cricetulus griseus CVCL_A0TS
In Vivo Model
Adult male Sprague Dawley (SD) rats weighing 260-280 g were purchased from Qinglongshan Animal Farm (Nanjing, China). After a week of adaptation, the rats were randomly assigned into five groups (n = 8): (1) sham group, rats receiving saline gavage and sham surgery were used as control group; (2) I/R model group, rats receiving saline gavage and left anterior descending (LAD) ligation surgery were used as the model group; (3) C3G-10 group, I/R model plus intraperitoneal injection of 10 mg/kg C3G; (4) C3G-20 group, I/R model plus intraperitoneal injection of 20 mg/kg C3G; and (5) DIL group, I/R model plus oral administration of 20 mg/kg diltiazem. C3G and DIL were dissolved in DMSO and then diluted with saline so that the DMSO concentration was less than 0.1% (v/v).

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Response regulation The administration of Cyanidin-3-glucoside (C3G) reduced the infarction area, mitigated pathological alterations, inhibited ST segment elevation, and attenuated oxidative stress and ferroptosis-related protein expression. C3G also suppressed the expressions of USP19, Beclin1, NCOA4, and LC3II/LC3I. In addition, treatment with C3G relieved oxidative stress, downregulated LC3II/LC3I, reduced autophagosome number, downregulated TfR1 expression, and upregulated the expressions of FTH1 and GPX4 in OGD/R-induced H9c2 cells. Taken together, C3G could be a potential agent to protect myocardium from myocardial ischemia-reperfusion (IR) injury.
References
Ref 1 The Protective Effect of Cyanidin-3-Glucoside on Myocardial Ischemia-Reperfusion Injury through Ferroptosis. Oxid Med Cell Longev. 2021 Feb 6;2021:8880141. doi: 10.1155/2021/8880141. eCollection 2021.