@article{APS6621,
author = {Min Wang and Wen-bin Zhang and Jun-hui Zhu and Guo-sheng Fu and Bin-quan Zhou},
title = {Breviscapine ameliorates hypertrophy of cardiomyocytes induced by high glucose in diabetic rats via the PKC signaling pathway},
journal = {Acta Pharmacologica Sinica},
volume = {30},
number = {8},
year = {2016},
keywords = {},
abstract = {Aim: To investigate the influence of breviscapine on high glucose-induced hypertrophy of cardiomyocytes and the relevant mechanism in vitro and in vivo.
Methods: Cultured neonatal cardiomyocytes were divided into i) control; ii) high glucose concentrations; iii) high glucose+PKC inhibitor Ro-31-8220; iv) high glucose+breviscapine; or v) high glucose+NF-κB inhibitor BAY11–7082. Cellular contraction frequency and volumes were measured; the expression of protein kinase C (PKC), NF-κB, TNF-α, and c-fos were assessed by Western blot or reverse transcription-polymerase chain reaction (RT-PCR). Diabetic rats were induced by a single intraperitoneal injection of streptozotocin, and randomly divided into i) control rats; ii) diabetic rats; or iii) diabetic rats administered with breviscapine (10 or 25 mg·kg−1·d−1). After treatment with breviscapine for six weeks, the echocardiographic parameters were measured. All rats were then sacrificed and heart tissue was obtained for microscopy. The expression patterns of PKC, NF-κB, TNF-α, and c-fos were measured by Western blot or RT-PCR.
Results: Cardiomyocytes cultured in a high concentration of glucose showed an increased pulsatile frequency and cellular volume, as well as a higher expression of PKC, NF-κB, TNF-α, and c-fos compared with the control group. Breviscapine could partly prevent these changes. Diabetic rats showed relative cardiac hypertrophy and a higher expression of PKC, NF-κB, TNF-α, and c-fos; treatment with breviscapine could ameliorate these changes in diabetic cardiomyopathy.
Conclusion: Breviscapine prevented cardiac hypertrophy in diabetic rats by inhibiting the expression of PKC, which may have a protective effect in the pathogenesis of diabetic cardiomyopathy via the PKC/NF-κB/c-fos signal transduction pathway},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/6621}
}