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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:
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
Publisher: United States: Nature Publishing Group
ID: ISSN: 1671-4083
Link: https://www.ncbi.nlm.nih.gov/pubmed/19597526
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recordid: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4006682
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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1EISSN: 1745-7254
2DOI: 10.1038/aps.2009.95
3PMID: 19597526
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
rights
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0Wang, Min
1Zhang, Wen-bin
2Zhu, Jun-hui
3Fu, Guo-sheng
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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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1Zhang, Wen-bin
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titleBreviscapine ameliorates hypertrophy of cardiomyocytes induced by high glucose in diabetic rats via the PKC signaling pathway
authorWang, Min ; Zhang, Wen-bin ; Zhu, Jun-hui ; Fu, Guo-sheng ; Zhou, Bin-quan
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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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atitleBreviscapine ameliorates hypertrophy of cardiomyocytes induced by high glucose in diabetic rats via the PKC signaling pathway
jtitleActa pharmacologica Sinica
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issn1671-4083
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0Q463
1diabetic cardiomyopathy; protein kinase C; cardiomegaly; breviscapine
2breviscapine
3diabetic cardiomyopathy
4cardiomegaly
5T-332
6protein kinase C
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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.
copUnited States
pubNature Publishing Group
pmid19597526
doi10.1038/aps.2009.95
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