AIM: To evaluate the protective effects of allicin on Ang II-induced cardiac hypertrophy. METHODS: Sprague-Dawley male rats were randomized into 3 groups:1)sham group (saline)(n = 12), 2) Ang II group(n = 9), 3) allicin group (Ang II + allicin)(n = 9). They received infusions of either saline or Ang II (250 ng/kg body weight per min) through mini-osmotic pumps implanted subcutaneously for 2 weeks and given a diet containing 180 mg/kg/day of allicin for 8 consecutive weeks. Hemodynamic, morphological, histological, and biochemical changes were evaluated at corresponding time points. RESULTS: Ang II infusion increased blood pressure, heart rate and heart weight to body weight ratio, and resulted in anatomical and functional changes, such as increased LV mass, posterior wall thickness and LV end-diastolic diameter, and decreased fractional shortening and EF compared with sham rats. Nrf2 and HO-1 in the hearts of rats in the Ang II group were moderately elevated at both mRNA and protein levels compared to sham group mice, but NQO1 andγ-GCS were significantly lower. GPx activities, levels of GSH and T-AOC in the hearts of the rats in the Ang II group were also significantly lower, and the levels of TBARS, reactive oxygen species and protein carbonyl were significant increased. Allicin attenuated LV mass, posterior wall thickness and LV end-diastolic diameter (1.10 ± 0.04 vs. 1.37 ± 0.05, 2.26 ± 0.08 vs. 2.96 ± 0.12, 7.27 ± 0.36 vs. 8.56 ± 0.41, respectively; all P < 0.05), and increased fractional shortening and EF (28.30 ± 3.21 vs. 25.40 ± 2.57, 60.27 ± 5.63 vs. 51.30 ± 4.78, respectively; both P < 0.05) in the Ang II-induced hypertrophic rats compared to the untreated Ang II rats. Furthermore, allicin treatment attenuated the accumulation of interstitial collagen and collagen I/III (P < 0.01 vs. the untreated Ang II group), decreased the levels of reactive oxygen species, protein carbonyl and TBARS and increased GPx activities. Moreover, allicin significantly increased mRNA expression and protein levels of Nrf2, NQO1, and γ-GCS ( P < 0.01, P < 0.05 vs. the untreated Ang II group). CONCLUSION: Allicin could prevent the development of cardiac remodeling and the progression of cardiac hypertrophy to cardiac dysfunction caused by enhancing the Nrf2 antioxidant signaling pathways.
AIM: To evaluate the protective effects of allicin on Ang II-induced cardiac hypertrophy. METHODS: Sprague-Dawley male rats were randomized into 3 groups:1)sham group (saline)(n = 12), 2) Ang II group(n = 9), 3) allicin group (Ang II + allicin)(n = 9). They received infusions of either saline or Ang II (250 ng/kg body weight per min) through mini-osmotic pumps implanted subcutaneously for 2 weeks and given a diet containing 180 mg/kg/day of allicin for 8 consecutive weeks. Hemodynamic, morphological, histological, and biochemical changes were evaluated at corresponding time points. RESULTS:Ang II infusion increased blood pressure, heart rate and heart weight to body weight ratio, and resulted in anatomical and functional changes, such as increased LV mass, posterior wall thickness and LV end-diastolic diameter, and decreased fractional shortening and EF compared with sham rats. Nrf2 and HO-1 in the hearts of rats in the Ang II group were moderately elevated at both mRNA and protein levels compared to sham group mice, but NQO1 andγ-GCS were significantly lower. GPx activities, levels of GSH and T-AOC in the hearts of the rats in the Ang II group were also significantly lower, and the levels of TBARS, reactive oxygen species and protein carbonyl were significant increased. Allicin attenuated LV mass, posterior wall thickness and LV end-diastolic diameter (1.10 ± 0.04 vs. 1.37 ± 0.05, 2.26 ± 0.08 vs. 2.96 ± 0.12, 7.27 ± 0.36 vs. 8.56 ± 0.41, respectively; all P < 0.05), and increased fractional shortening and EF (28.30 ± 3.21 vs. 25.40 ± 2.57, 60.27 ± 5.63 vs. 51.30 ± 4.78, respectively; both P < 0.05) in the Ang II-induced hypertrophicrats compared to the untreated Ang II rats. Furthermore, allicin treatment attenuated the accumulation of interstitial collagen and collagen I/III (P < 0.01 vs. the untreated Ang II group), decreased the levels of reactive oxygen species, protein carbonyl and TBARS and increased GPx activities. Moreover, allicin significantly increased mRNA expression and protein levels of Nrf2, NQO1, and γ-GCS ( P < 0.01, P < 0.05 vs. the untreated Ang II group). CONCLUSION:Allicin could prevent the development of cardiac remodeling and the progression of cardiac hypertrophy to cardiac dysfunction caused by enhancing the Nrf2 antioxidant signaling pathways.
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