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Breviscapine ameliorates hypertrophy of cardiomyocytes induced by high glucose in diabetic rats via the PKC signaling pathway

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 inhibior Ro-31-8220;... Full description

Journal Title: Acta pharmacologica Sinica 2009, Vol.30 (8), p.1081-1091
Main Author: Wang, Min
Other Authors: Zhang, Wen-bin , Zhu, Jun-hui , Fu, Guo-sheng , Zhou, Bin-quan
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: United States: Nature Publishing Group
ID: ISSN: 1671-4083
Link: https://www.ncbi.nlm.nih.gov/pubmed/19597526
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title: Breviscapine ameliorates hypertrophy of cardiomyocytes induced by high glucose in diabetic rats via the PKC signaling pathway
format: Article
creator:
  • Wang, Min
  • Zhang, Wen-bin
  • Zhu, Jun-hui
  • Fu, Guo-sheng
  • Zhou, Bin-quan
subjects:
  • Animals
  • breviscapine
  • cardiomegaly
  • Cell Size - drug effects
  • Cells, Cultured
  • Diabetes Mellitus, Experimental - drug therapy
  • diabetic cardiomyopathy
  • Down-Regulation
  • Flavonoids - therapeutic use
  • Glucose - metabolism
  • Heart - drug effects
  • Hypertrophy - drug therapy
  • Male
  • Myocardium - pathology
  • Myocytes, Cardiac - drug effects
  • Myocytes, Cardiac - pathology
  • NF-kappa B - genetics
  • NF-kappa B - metabolism
  • Original
  • Original Article
  • protein kinase C
  • Protein Kinase C - genetics
  • Protein Kinase C - metabolism
  • Protein Kinase C beta
  • Protein Kinase C-alpha - genetics
  • Protein Kinase C-alpha - metabolism
  • Proto-Oncogene Proteins c-fos - genetics
  • Proto-Oncogene Proteins c-fos - metabolism
  • Rats
  • Rats, Sprague-Dawley
  • Tumor Necrosis Factor-alpha - genetics
  • Tumor Necrosis Factor-alpha - metabolism
  • 信号通路
  • 心肌细胞肥大
  • 灯盏花
  • 糖尿病大鼠
  • 蛋白激酶C
ispartof: Acta pharmacologica Sinica, 2009, Vol.30 (8), p.1081-1091
description: 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 inhibior Ro-31-8220; iv) high glucose+breviscapine; or v) high glucose+NF-KB inhibitor BAY11-7082. Cellular contraction frequency and volumes were measured; the expression of protein kinase C (PKC), NF-KB, 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^-l.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-KB, 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-kB, TNF-α, and c-los compared with the control group. Breviscapine could partly prevent these changes. Diabetic rats showed relative cardiac hypertrophy and a higher expression of PKC, NF-KB, 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-kB/c-fos signal transduction pathway.
language: eng
source:
identifier: ISSN: 1671-4083
fulltext: no_fulltext
issn:
  • 1671-4083
  • 1745-7254
url: Link


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titleBreviscapine ameliorates hypertrophy of cardiomyocytes induced by high glucose in diabetic rats via the PKC signaling pathway
creatorWang, Min ; Zhang, Wen-bin ; Zhu, Jun-hui ; Fu, Guo-sheng ; Zhou, Bin-quan
creatorcontribWang, Min ; Zhang, Wen-bin ; Zhu, Jun-hui ; Fu, Guo-sheng ; Zhou, Bin-quan
descriptionAim: 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 inhibior Ro-31-8220; iv) high glucose+breviscapine; or v) high glucose+NF-KB inhibitor BAY11-7082. Cellular contraction frequency and volumes were measured; the expression of protein kinase C (PKC), NF-KB, 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^-l.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-KB, 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-kB, TNF-α, and c-los compared with the control group. Breviscapine could partly prevent these changes. Diabetic rats showed relative cardiac hypertrophy and a higher expression of PKC, NF-KB, 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-kB/c-fos signal transduction pathway.
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languageeng
publisherUnited States: Nature Publishing Group
subjectAnimals ; breviscapine ; cardiomegaly ; Cell Size - drug effects ; Cells, Cultured ; Diabetes Mellitus, Experimental - drug therapy ; diabetic cardiomyopathy ; Down-Regulation ; Flavonoids - therapeutic use ; Glucose - metabolism ; Heart - drug effects ; Hypertrophy - drug therapy ; Male ; Myocardium - pathology ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - pathology ; NF-kappa B - genetics ; NF-kappa B - metabolism ; Original ; Original Article ; protein kinase C ; Protein Kinase C - genetics ; Protein Kinase C - metabolism ; Protein Kinase C beta ; Protein Kinase C-alpha - genetics ; Protein Kinase C-alpha - metabolism ; Proto-Oncogene Proteins c-fos - genetics ; Proto-Oncogene Proteins c-fos - metabolism ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; 信号通路 ; 心肌细胞肥大 ; 灯盏花 ; 糖尿病大鼠 ; 蛋白激酶C
ispartofActa pharmacologica Sinica, 2009, Vol.30 (8), p.1081-1091
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1Zhang, Wen-bin
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0Breviscapine ameliorates hypertrophy of cardiomyocytes induced by high glucose in diabetic rats via the PKC signaling pathway
1Acta pharmacologica Sinica
addtitleActa Pharmacologica Sinica
descriptionAim: 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 inhibior Ro-31-8220; iv) high glucose+breviscapine; or v) high glucose+NF-KB inhibitor BAY11-7082. Cellular contraction frequency and volumes were measured; the expression of protein kinase C (PKC), NF-KB, 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^-l.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-KB, 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-kB, TNF-α, and c-los compared with the control group. Breviscapine could partly prevent these changes. Diabetic rats showed relative cardiac hypertrophy and a higher expression of PKC, NF-KB, 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-kB/c-fos signal transduction pathway.
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0Animals
1breviscapine
2cardiomegaly
3Cell Size - drug effects
4Cells, Cultured
5Diabetes Mellitus, Experimental - drug therapy
6diabetic cardiomyopathy
7Down-Regulation
8Flavonoids - therapeutic use
9Glucose - metabolism
10Heart - drug effects
11Hypertrophy - drug therapy
12Male
13Myocardium - pathology
14Myocytes, Cardiac - drug effects
15Myocytes, Cardiac - pathology
16NF-kappa B - genetics
17NF-kappa B - metabolism
18Original
19Original Article
20protein kinase C
21Protein Kinase C - genetics
22Protein Kinase C - metabolism
23Protein Kinase C beta
24Protein Kinase C-alpha - genetics
25Protein Kinase C-alpha - metabolism
26Proto-Oncogene Proteins c-fos - genetics
27Proto-Oncogene Proteins c-fos - metabolism
28Rats
29Rats, Sprague-Dawley
30Tumor Necrosis Factor-alpha - genetics
31Tumor Necrosis Factor-alpha - metabolism
32信号通路
33心肌细胞肥大
34灯盏花
35糖尿病大鼠
36蛋白激酶C
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titleBreviscapine ameliorates hypertrophy of cardiomyocytes induced by high glucose in diabetic rats via the PKC signaling pathway
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2cardiomegaly
3Cell Size - drug effects
4Cells, Cultured
5Diabetes Mellitus, Experimental - drug therapy
6diabetic cardiomyopathy
7Down-Regulation
8Flavonoids - therapeutic use
9Glucose - metabolism
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11Hypertrophy - drug therapy
12Male
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14Myocytes, Cardiac - drug effects
15Myocytes, Cardiac - pathology
16NF-kappa B - genetics
17NF-kappa B - metabolism
18Original
19Original Article
20protein kinase C
21Protein Kinase C - genetics
22Protein Kinase C - metabolism
23Protein Kinase C beta
24Protein Kinase C-alpha - genetics
25Protein Kinase C-alpha - metabolism
26Proto-Oncogene Proteins c-fos - genetics
27Proto-Oncogene Proteins c-fos - metabolism
28Rats
29Rats, Sprague-Dawley
30Tumor Necrosis Factor-alpha - genetics
31Tumor Necrosis Factor-alpha - metabolism
32信号通路
33心肌细胞肥大
34灯盏花
35糖尿病大鼠
36蛋白激酶C
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atitleBreviscapine ameliorates hypertrophy of cardiomyocytes induced by high glucose in diabetic rats via the PKC signaling pathway
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4cardiomegaly
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abstractAim: 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 inhibior Ro-31-8220; iv) high glucose+breviscapine; or v) high glucose+NF-KB inhibitor BAY11-7082. Cellular contraction frequency and volumes were measured; the expression of protein kinase C (PKC), NF-KB, 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^-l.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-KB, 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-kB, TNF-α, and c-los compared with the control group. Breviscapine could partly prevent these changes. Diabetic rats showed relative cardiac hypertrophy and a higher expression of PKC, NF-KB, 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-kB/c-fos signal transduction pathway.
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pmid19597526
doi10.1038/aps.2009.95
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