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Taurine Supplementation Improves Cardiac Ischemia/Reperfusion Injury by Inhibiting Intra‐Cardiac Renin‐Angiotensin System Overactivity in Adult Female Rats Perinatally Depleted of Taurine
Author(s) -
Kulthinee Supaporn,
Navar L. Gabriel,
Roysommuti Sanya
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.846.6
Subject(s) - taurine , medicine , endocrinology , cardiac function curve , renin–angiotensin system , angiotensin ii , weaning , heart failure , biology , blood pressure , amino acid , biochemistry
Perinatal taurine depletion particularly followed by a high sugar diet exacerbates cardiac injury, sympathoexcitation, and arterial pressure dysregulation after ischemia/reperfusion (IR) in adult male rats, while taurine treatment before and after cardiac IR prevents or reduces the adverse effects of IR. This study tested the hypothesis that in adult female rats perinatally depleted of taurine followed by a high sugar diet, taurine supplementation mitigates the cardiac IR injury by inhibiting intra‐cardiac renin‐angiotensin system overactivity. Female Sprague‐Dawley rats were fed normal rat chow with tap water alone (control, C) or tap water containing 3% beta‐alanine (taurine depletion, TD) from conception to weaning. Female offspring were fed the normal rat chow and drank 5% glucose in tap water (CG and TDG) or tap water alone (TDW and CW) throughout the study. One week before surgery, half of the rats in each treatment were supplemented with 3% taurine in tap water (CW+T, CG+T, TDW+T, and TDG+T). At 7–8 weeks of age, cardiac angiotensin II content and plasma cardiac injury markers were studied in anesthetized rats after cardiac IR induction and in untreated Sham control rats. Body, heart, and heart to body weight ratios were not significantly different among the nine groups. While plasma cardiac injury markers significantly increased in all IR groups compared to Sham control, the marked cardiac damage was observed in the TDG group (creatine kinase MB: Sham 211 ± 2 u/l, CW 300 ± 7 u/l, CW+T 245 ± 5 u/l, CG 313 ± 7 u/l, CG+T 251 ± 9 u/l, TDW 330 ± 6 u/l, TDW+T 318 ± 7 u/l, TDG 367 ± 3 u/l, TDG+T 334 ± 8 u/l; cardiac troponin C: TDG 0.9 ± 0.1 ng/ml, TDG+T 0.4 ± 0.1 ng/ml, other groups < 0.01 ng/ml; N‐terminal prohormone brain natriuretic peptide: TDG 8.8 ± 0.3 pg/ml, TDG+T 6.3 ± 0.2 pg/ml, other groups < 5.0 pg/ml). Further, cardiac angiotensin II levels significantly increased in CG, TDW, and TDG compared to Sham and CW groups (Sham 32.3 ± 1.5 pg/ml, CW 43.6 ± 3.0 pg/ml, CW+T 43.3 ± 2.6 pg/ml, CG 75.9 ± 8.41 pg/ml, CG+T 46.3 ± 2.5 pg/ml, TDW 80.3 ± 5.7 pg/ml, TDW+T 53.2 ± 2.4 pg/ml, TDG 139.0 ± 8.1 pg/ml, TDG+T 82.4 ± 3.7 pg/ml). The adverse effects of IR on cardiac injury and angiotensin II content were similarly attenuated, at least in part, by taurine supplementation. The present study demonstrates that perinatal taurine depletion particularly followed by a high sugar diet exacerbates cardiac IR injury via intra‐cardiac renin‐angiotensin system overactivity in adult female rats, and this adverse effect can be reduced by short‐term taurine supplementation. Support or Funding Information This work was supported by Khon Kaen University, Khon Kaen, Thailand.