TY - JOUR
T1 - Zingerone alleviates the delayed ventricular repolarization and AV conduction in diabetes
T2 - Effect on cardiac fibrosis and inflammation
AU - El-bassossy, Hany M
AU - Al-Thubiani, Wafaa S.
AU - Elberry, Ahmed A
AU - Mujallid, Mohammad I.
AU - Ghareib, Salah A
AU - Azhar, Ahmad S.
AU - Banjar, Zainy M.
AU - Watson, Malcolm L.
PY - 2017/12/1
Y1 - 2017/12/1
N2 - Background: The study aims to analyse the action of zingerone in diabetes-related cardiac arrhythmias. Methods: Diabetes was induced by streptozocin while treatment groups received 20 mg/kg zingerone daily. Following extra seven weeks, electrocardiography, extraction of blood, urine and heart for biochemical analysis, histopathology and immunofluorescence were undertaken. Results: The suppression of QT and QTc prolongation in diabetic rats was indicative of prolonged cardiac repolarisation that was greatly reduced by zingerone treatment. In addition, the reduction in PR interval attested that zingerone improved AV delay in diabetic rats. The fibrogenic transforming growth factor β1 upregulation in diabetic hearts was suppressed by zingerone. The marked glycogen deposition and muscle degeneration seen in diabetic heart sections were also alleviated by zingerone. Furthermore, zingerone prevented the decrease in of the serum anti-inflammatory cytokine adiponectin in diabetics. The heightened levels of oxidative stress markers 8-isoprostane and uric acid in diabetic rats were suppressed. In the diabetic heart, the reduced catalase activity was improved and the excessive expression of angiotensin receptor 1 was inhibited by zingerone. Conclusion: Cardiac delayed repolarisation and AV conduction in rats with diabetes were halted by zingerone. It appears that inhibition of cardiac fibrosis and associated inflammation-oxidative stress signalling underpins the zingerone effect.
AB - Background: The study aims to analyse the action of zingerone in diabetes-related cardiac arrhythmias. Methods: Diabetes was induced by streptozocin while treatment groups received 20 mg/kg zingerone daily. Following extra seven weeks, electrocardiography, extraction of blood, urine and heart for biochemical analysis, histopathology and immunofluorescence were undertaken. Results: The suppression of QT and QTc prolongation in diabetic rats was indicative of prolonged cardiac repolarisation that was greatly reduced by zingerone treatment. In addition, the reduction in PR interval attested that zingerone improved AV delay in diabetic rats. The fibrogenic transforming growth factor β1 upregulation in diabetic hearts was suppressed by zingerone. The marked glycogen deposition and muscle degeneration seen in diabetic heart sections were also alleviated by zingerone. Furthermore, zingerone prevented the decrease in of the serum anti-inflammatory cytokine adiponectin in diabetics. The heightened levels of oxidative stress markers 8-isoprostane and uric acid in diabetic rats were suppressed. In the diabetic heart, the reduced catalase activity was improved and the excessive expression of angiotensin receptor 1 was inhibited by zingerone. Conclusion: Cardiac delayed repolarisation and AV conduction in rats with diabetes were halted by zingerone. It appears that inhibition of cardiac fibrosis and associated inflammation-oxidative stress signalling underpins the zingerone effect.
UR - http://www.scopus.com/inward/record.url?scp=85036638476&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0189074
DO - 10.1371/journal.pone.0189074
M3 - Article
AN - SCOPUS:85036638476
SN - 1932-6203
VL - 12
JO - PLoS ONE
JF - PLoS ONE
IS - 12
M1 - e0189074
ER -