Hesperidin regresses cardiac hypertrophy by virtue of PPAR‐γ agonistic, anti‐inflammatory, antiapoptotic, and antioxidant properties
Hesperidin (HES), a flavanone glycoside, predominant in citrus fruits, has an agonistic activity on peroxisome proliferator‐activated receptor gamma (PPAR‐γ). PPAR‐γ is an inhibitor of cardiac hypertrophy (CH) signaling pathways. In this study, we investigated the cardioprotective effect of HES in i...
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Published in: | Journal of biochemical and molecular toxicology Vol. 33; no. 5; pp. e22283 - n/a |
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Abstract | Hesperidin (HES), a flavanone glycoside, predominant in citrus fruits, has an agonistic activity on peroxisome proliferator‐activated receptor gamma (PPAR‐γ). PPAR‐γ is an inhibitor of cardiac hypertrophy (CH) signaling pathways. In this study, we investigated the cardioprotective effect of HES in isoproterenol (ISO)‐induced CH through PPAR‐γ agonistic activity. For this, male albino Wistar rats were divided into six groups (n = 6), that is, normal, ISO‐control, HES treatment group (200 mg kg−1; p.o.), HES per se (200 mg kg−1; p.o.), enalapril treatment group (30 mg kg−1; p.o.), and combination group (HES 200 mg kg−1; p.o.+enalapril 30 mg kg−1; p.o.). ISO (3 mg kg−1; s.c.) was administered to all groups except normal and per se to induce CH. HES or enalapril treatment of 28 days significantly attenuated pathological changes, improved cardiac hemodynamics, suppressed oxidative stress, and apoptosis along with an increased PPAR‐γ expression. The combination of enalapril with HES exhibited an effect similar to that of HES or enalapril alone on all the aforementioned parameters. Therefore, HES may be further evaluated as a promising molecule for the alleviation of CH. |
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AbstractList | Hesperidin (HES), a flavanone glycoside, predominant in citrus fruits, has an agonistic activity on peroxisome proliferator‐activated receptor gamma (PPAR‐γ). PPAR‐γ is an inhibitor of cardiac hypertrophy (CH) signaling pathways. In this study, we investigated the cardioprotective effect of HES in isoproterenol (ISO)‐induced CH through PPAR‐γ agonistic activity. For this, male albino Wistar rats were divided into six groups (n = 6), that is, normal, ISO‐control, HES treatment group (200 mg kg −1 ; p.o.), HES per se (200 mg kg −1 ; p.o.), enalapril treatment group (30 mg kg −1 ; p.o.), and combination group (HES 200 mg kg −1 ; p.o.+enalapril 30 mg kg −1 ; p.o.). ISO (3 mg kg −1 ; s.c.) was administered to all groups except normal and per se to induce CH. HES or enalapril treatment of 28 days significantly attenuated pathological changes, improved cardiac hemodynamics, suppressed oxidative stress, and apoptosis along with an increased PPAR‐γ expression. The combination of enalapril with HES exhibited an effect similar to that of HES or enalapril alone on all the aforementioned parameters. Therefore, HES may be further evaluated as a promising molecule for the alleviation of CH. Hesperidin (HES), a flavanone glycoside, predominant in citrus fruits, has an agonistic activity on peroxisome proliferator‐activated receptor gamma (PPAR‐γ). PPAR‐γ is an inhibitor of cardiac hypertrophy (CH) signaling pathways. In this study, we investigated the cardioprotective effect of HES in isoproterenol (ISO)‐induced CH through PPAR‐γ agonistic activity. For this, male albino Wistar rats were divided into six groups (n = 6), that is, normal, ISO‐control, HES treatment group (200 mg kg−1; p.o.), HES per se (200 mg kg−1; p.o.), enalapril treatment group (30 mg kg−1; p.o.), and combination group (HES 200 mg kg−1; p.o.+enalapril 30 mg kg−1; p.o.). ISO (3 mg kg−1; s.c.) was administered to all groups except normal and per se to induce CH. HES or enalapril treatment of 28 days significantly attenuated pathological changes, improved cardiac hemodynamics, suppressed oxidative stress, and apoptosis along with an increased PPAR‐γ expression. The combination of enalapril with HES exhibited an effect similar to that of HES or enalapril alone on all the aforementioned parameters. Therefore, HES may be further evaluated as a promising molecule for the alleviation of CH. Hesperidin (HES), a flavanone glycoside, predominant in citrus fruits, has an agonistic activity on peroxisome proliferator-activated receptor gamma (PPAR-γ). PPAR-γ is an inhibitor of cardiac hypertrophy (CH) signaling pathways. In this study, we investigated the cardioprotective effect of HES in isoproterenol (ISO)-induced CH through PPAR-γ agonistic activity. For this, male albino Wistar rats were divided into six groups (n = 6), that is, normal, ISO-control, HES treatment group (200 mg kg ; p.o.), HES per se (200 mg kg ; p.o.), enalapril treatment group (30 mg kg ; p.o.), and combination group (HES 200 mg kg ; p.o.+enalapril 30 mg kg ; p.o.). ISO (3 mg kg ; s.c.) was administered to all groups except normal and per se to induce CH. HES or enalapril treatment of 28 days significantly attenuated pathological changes, improved cardiac hemodynamics, suppressed oxidative stress, and apoptosis along with an increased PPAR-γ expression. The combination of enalapril with HES exhibited an effect similar to that of HES or enalapril alone on all the aforementioned parameters. Therefore, HES may be further evaluated as a promising molecule for the alleviation of CH. Hesperidin (HES), a flavanone glycoside, predominant in citrus fruits, has an agonistic activity on peroxisome proliferator-activated receptor gamma (PPAR-γ). PPAR-γ is an inhibitor of cardiac hypertrophy (CH) signaling pathways. In this study, we investigated the cardioprotective effect of HES in isoproterenol (ISO)-induced CH through PPAR-γ agonistic activity. For this, male albino Wistar rats were divided into six groups (n = 6), that is, normal, ISO-control, HES treatment group (200 mg kg-1 ; p.o.), HES per se (200 mg kg-1 ; p.o.), enalapril treatment group (30 mg kg-1 ; p.o.), and combination group (HES 200 mg kg-1 ; p.o.+enalapril 30 mg kg-1 ; p.o.). ISO (3 mg kg-1 ; s.c.) was administered to all groups except normal and per se to induce CH. HES or enalapril treatment of 28 days significantly attenuated pathological changes, improved cardiac hemodynamics, suppressed oxidative stress, and apoptosis along with an increased PPAR-γ expression. The combination of enalapril with HES exhibited an effect similar to that of HES or enalapril alone on all the aforementioned parameters. Therefore, HES may be further evaluated as a promising molecule for the alleviation of CH. |
Author | Verma, Vipin Kumar Malik, Salma Bhatia, Jagriti Bhargava, Poorva Arya, Dharamvir Singh Khan, Sana Irfan |
Author_xml | – sequence: 1 givenname: Poorva surname: Bhargava fullname: Bhargava, Poorva organization: Cardiovascular Research Laboratory, All India Institute of Medical Sciences – sequence: 2 givenname: Vipin Kumar surname: Verma fullname: Verma, Vipin Kumar organization: Cardiovascular Research Laboratory, All India Institute of Medical Sciences – sequence: 3 givenname: Salma surname: Malik fullname: Malik, Salma organization: Cardiovascular Research Laboratory, All India Institute of Medical Sciences – sequence: 4 givenname: Sana Irfan surname: Khan fullname: Khan, Sana Irfan organization: Cardiovascular Research Laboratory, All India Institute of Medical Sciences – sequence: 5 givenname: Jagriti surname: Bhatia fullname: Bhatia, Jagriti organization: Cardiovascular Research Laboratory, All India Institute of Medical Sciences – sequence: 6 givenname: Dharamvir Singh orcidid: 0000-0002-3062-0775 surname: Arya fullname: Arya, Dharamvir Singh email: dsarya16@gmail.com organization: Cardiovascular Research Laboratory, All India Institute of Medical Sciences |
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Cites_doi | 10.1016/j.biopha.2016.12.028 10.1016/j.lfs.2003.03.004 10.1016/0003-2697(79)90738-3 10.1155/2014/249031 10.1021/jf501373a 10.1371/journal.pone.0015909 10.1161/HYPERTENSIONAHA.115.06254 10.3109/13880209.2010.509734 10.2174/1381612822666161021160524 10.4103/2231-4040.90879 10.1016/j.mam.2005.07.008 10.1179/135100010X12826446921509 10.1007/s00011-010-0295-0 10.1161/01.RES.0000179226.34112.6d 10.1056/NEJMcp0909392 10.56499/jppres14.032_2.5.129 10.1211/jpp.60.2.0011 10.1016/j.ijcard.2007.02.004 10.1002/ptr.5256 10.1186/1471-2210-5-2 10.1080/01635580701419030 10.1371/journal.pone.0103628 10.1371/journal.pone.0111212 10.1016/0304-4165(79)90289-7 10.1002/glia.21101 10.1155/2016/9174190 10.1159/000447884 10.1016/B978-0-12-091302-2.50032-3 10.4103/0022-3859.153104 10.1002/ajmg.1398 10.1161/hc1002.105225 10.1016/j.yjmcc.2014.11.009 10.1038/nrd3431 10.1039/C3FO60575B 10.2165/00129784-200202010-00001 10.1111/j.1432-1033.1974.tb03714.x 10.1111/j.1747-0285.2007.00606.x 10.1007/s13402-015-0222-z 10.1016/j.cbi.2014.06.010 10.1007/s001090050176 10.1016/S0008-6363(98)00166-7 10.1161/HYPERTENSIONAHA.113.02313 10.1016/j.lfs.2007.01.052 10.1139/cjpp-2014-0204 |
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Keywords | hesperidin (HES) inflammation peroxisome proliferator-activated receptor gamma (PPAR-γ) isoproterenol (ISO) oxidative stress cardiac hypertrophy (CH) |
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References | e_1_2_8_1_36_1 e_1_2_8_1_13_1 e_1_2_8_1_34_1 e_1_2_8_1_32_1 e_1_2_8_1_30_1 e_1_2_8_1_9_1 e_1_2_8_1_27_1 e_1_2_8_1_29_1 e_1_2_8_1_48_1 e_1_2_8_1_47_1 e_1_2_8_1_24_1 e_1_2_8_1_45_1 e_1_2_8_1_43_1 e_1_2_8_1_20_1 e_1_2_8_1_41_1 Linck B. (e_1_2_8_1_39_1) 1998; 286 McMurray J. J. (e_1_2_8_1_11_1); 14 e_1_2_8_1_3_1 e_1_2_8_1_7_1 e_1_2_8_1_5_1 e_1_2_8_1_19_1 e_1_2_8_1_15_1 e_1_2_8_1_17_1 e_1_2_8_1_38_1 e_1_2_8_1_12_1 e_1_2_8_1_35_1 e_1_2_8_1_14_1 e_1_2_8_1_33_1 e_1_2_8_1_10_1 e_1_2_8_1_50_1 Tejada S. (e_1_2_8_1_22_1) 2017 e_1_2_8_1_8_1 e_1_2_8_1_26_1 e_1_2_8_1_28_1 e_1_2_8_1_49_1 e_1_2_8_1_46_1 e_1_2_8_1_25_1 e_1_2_8_1_44_1 e_1_2_8_1_42_1 e_1_2_8_1_21_1 e_1_2_8_1_40_1 Ding Z. (e_1_2_8_1_23_1) 2018 e_1_2_8_1_2_1 e_1_2_8_1_6_1 e_1_2_8_1_4_1 Abdel‐Raheem I. T. (e_1_2_8_1_31_1) 2009; 21 Hitlera D. (e_1_2_8_1_16_1) 2014; 2 e_1_2_8_1_18_1 e_1_2_8_1_37_1 |
References_xml | – volume: 286 start-page: 531 year: 1998 ident: e_1_2_8_1_39_1 publication-title: J. Pharmacol. Exp. Ther. contributor: fullname: Linck B. – ident: e_1_2_8_1_18_1 doi: 10.1016/j.biopha.2016.12.028 – ident: e_1_2_8_1_42_1 doi: 10.1016/j.lfs.2003.03.004 – ident: e_1_2_8_1_34_1 doi: 10.1016/0003-2697(79)90738-3 – ident: e_1_2_8_1_44_1 doi: 10.1155/2014/249031 – ident: e_1_2_8_1_50_1 doi: 10.1021/jf501373a – ident: e_1_2_8_1_26_1 doi: 10.1371/journal.pone.0015909 – ident: e_1_2_8_1_3_1 doi: 10.1161/HYPERTENSIONAHA.115.06254 – ident: e_1_2_8_1_19_1 doi: 10.3109/13880209.2010.509734 – ident: e_1_2_8_1_17_1 doi: 10.2174/1381612822666161021160524 – ident: e_1_2_8_1_7_1 doi: 10.4103/2231-4040.90879 – ident: e_1_2_8_1_15_1 doi: 10.1016/j.mam.2005.07.008 – year: 2018 ident: e_1_2_8_1_23_1 publication-title: Antivir. Ther. contributor: fullname: Ding Z. – ident: e_1_2_8_1_32_1 doi: 10.1179/135100010X12826446921509 – ident: e_1_2_8_1_21_1 doi: 10.1007/s00011-010-0295-0 – ident: e_1_2_8_1_9_1 doi: 10.1161/01.RES.0000179226.34112.6d – ident: e_1_2_8_1_12_1 doi: 10.1056/NEJMcp0909392 – volume: 2 start-page: 129 year: 2014 ident: e_1_2_8_1_16_1 publication-title: J. Pharm. Pharmacogn. Res doi: 10.56499/jppres14.032_2.5.129 contributor: fullname: Hitlera D. – ident: e_1_2_8_1_48_1 doi: 10.1211/jpp.60.2.0011 – ident: e_1_2_8_1_6_1 doi: 10.1016/j.ijcard.2007.02.004 – ident: e_1_2_8_1_20_1 doi: 10.1002/ptr.5256 – ident: e_1_2_8_1_43_1 doi: 10.1186/1471-2210-5-2 – ident: e_1_2_8_1_24_1 doi: 10.1080/01635580701419030 – ident: e_1_2_8_1_46_1 doi: 10.1371/journal.pone.0103628 – ident: e_1_2_8_1_30_1 doi: 10.1371/journal.pone.0111212 – ident: e_1_2_8_1_35_1 doi: 10.1016/0304-4165(79)90289-7 – volume: 14 start-page: 803 ident: e_1_2_8_1_11_1 publication-title: Eur. J. Heart Fail. 2012 contributor: fullname: McMurray J. J. – ident: e_1_2_8_1_27_1 doi: 10.1002/glia.21101 – ident: e_1_2_8_1_8_1 doi: 10.1155/2016/9174190 – ident: e_1_2_8_1_33_1 doi: 10.1159/000447884 – ident: e_1_2_8_1_37_1 doi: 10.1016/B978-0-12-091302-2.50032-3 – ident: e_1_2_8_1_14_1 doi: 10.4103/0022-3859.153104 – ident: e_1_2_8_1_45_1 doi: 10.1002/ajmg.1398 – ident: e_1_2_8_1_10_1 doi: 10.1161/hc1002.105225 – ident: e_1_2_8_1_2_1 doi: 10.1016/j.yjmcc.2014.11.009 – ident: e_1_2_8_1_13_1 doi: 10.1038/nrd3431 – ident: e_1_2_8_1_49_1 doi: 10.1039/C3FO60575B – ident: e_1_2_8_1_5_1 doi: 10.2165/00129784-200202010-00001 – ident: e_1_2_8_1_36_1 doi: 10.1111/j.1432-1033.1974.tb03714.x – ident: e_1_2_8_1_28_1 doi: 10.1111/j.1747-0285.2007.00606.x – ident: e_1_2_8_1_25_1 doi: 10.1007/s13402-015-0222-z – ident: e_1_2_8_1_41_1 doi: 10.1016/j.cbi.2014.06.010 – year: 2017 ident: e_1_2_8_1_22_1 publication-title: Curr. Med. Chem. contributor: fullname: Tejada S. – ident: e_1_2_8_1_38_1 doi: 10.1007/s001090050176 – volume: 21 start-page: 175 year: 2009 ident: e_1_2_8_1_31_1 publication-title: J. Egypt. Natl. Canc. Inst. contributor: fullname: Abdel‐Raheem I. T. – ident: e_1_2_8_1_40_1 doi: 10.1016/S0008-6363(98)00166-7 – ident: e_1_2_8_1_4_1 doi: 10.1161/HYPERTENSIONAHA.113.02313 – ident: e_1_2_8_1_47_1 doi: 10.1016/j.lfs.2007.01.052 – ident: e_1_2_8_1_29_1 doi: 10.1139/cjpp-2014-0204 |
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Snippet | Hesperidin (HES), a flavanone glycoside, predominant in citrus fruits, has an agonistic activity on peroxisome proliferator‐activated receptor gamma (PPAR‐γ).... Hesperidin (HES), a flavanone glycoside, predominant in citrus fruits, has an agonistic activity on peroxisome proliferator-activated receptor gamma (PPAR-γ).... |
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SubjectTerms | Animals Anti-Inflammatory Agents - pharmacology Antioxidants Antioxidants - pharmacology Apoptosis Apoptosis - drug effects cardiac hypertrophy (CH) Cardiomegaly - chemically induced Cardiomegaly - metabolism Cardiomegaly - prevention & control Cardiotonic Agents - pharmacology Citrus fruits Gene Expression Regulation - drug effects Heart Hemodynamics Hesperidin hesperidin (HES) Hesperidin - pharmacology Hypertrophy Inflammation Isoproterenol isoproterenol (ISO) Isoproterenol - adverse effects Isoproterenol - pharmacology Male Oxidative stress Oxidative Stress - drug effects Peroxisome proliferator-activated receptors peroxisome proliferator‐activated receptor gamma (PPAR‐γ) PPAR gamma - agonists PPAR gamma - biosynthesis Rats Rats, Wistar Rodents |
Title | Hesperidin regresses cardiac hypertrophy by virtue of PPAR‐γ agonistic, anti‐inflammatory, antiapoptotic, and antioxidant properties |
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