PMID- 23573121
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20130704
LR  - 20220316
IS  - 1741-427X (Print)
IS  - 1741-4288 (Electronic)
IS  - 1741-427X (Linking)
VI  - 2013
DP  - 2013
TI  - Effect of Berberine on PPAR alpha /NO Activation in High Glucose- and Insulin-Induced 
      Cardiomyocyte Hypertrophy.
PG  - 285489
LID - 10.1155/2013/285489 [doi]
LID - 285489
AB  - Rhizoma coptidis, the root of Coptis chinensis Franch, has been used in China as 
      a folk medicine in the treatment of diabetes for thousands of years. Berberine, 
      one of the active ingredients of Rhizoma coptidis, has been reported to improve 
      symptoms of diabetes and to treat experimental cardiac hypertrophy, respectively. 
      The objective of this study was to evaluate the potential effect of berberine on 
      cardiomyocyte hypertrophy in diabetes and its possible influence on peroxisome 
      proliferator-activated receptor- alpha (PPAR alpha )/nitric oxide (NO) signaling pathway. 
      The cardiomyocyte hypertrophy induced by high glucose (25.5 mmol/L) and insulin 
      (0.1  mu mol/L) (HGI) was characterized in rat primary cardiomyocyte by measuring 
      the cell surface area, protein content, and atrial natriuretic factor mRNA 
      expression level. Protein and mRNA expression were measured by western blot and 
      real-time RT-PCR, respectively. The enzymatic activity of NO synthase (NOS) was 
      measured using a spectrophotometric assay, and NO concentration was measured 
      using the Griess assay. HGI significantly induced cardiomyocyte hypertrophy and 
      decreased the expression of PPAR alpha and endothelial NOS at the mRNA and protein 
      levels, which occurred in parallel with declining NOS activity and NO 
      concentration. The effect of HGI was inhibited by berberine (0.1 to 100  mu 
      mol/L), fenofibrate (0.3  mu mol/L), or L-arginine (100  mu mol/L). MK886 (0.3  mu 
      mol/L), a selective PPAR alpha antagonist, could abolish the effects of berberine and 
      fenofibrate. N (G) -nitro-L-arginine-methyl ester (100  mu mol/L), a NOS 
      inhibitor, could block the effects of L-arginine, but only partially blocked the 
      effects of berberine. These results suggest that berberine can blunt HGI-induced 
      cardiomyocyte hypertrophy in vitro, through the activation of the PPAR alpha /NO 
      signaling pathway.
FAU - Wang, Mingfeng
AU  - Wang M
AD  - Department of Pharmacology, Chongqing Key Laboratory of Biochemistry and 
      Molecular Pharmacology, Chongqing Medical University, Chongqing 400016, China.
FAU - Wang, Jia
AU  - Wang J
FAU - Tan, Rui
AU  - Tan R
FAU - Wu, Qin
AU  - Wu Q
FAU - Qiu, Hongmei
AU  - Qiu H
FAU - Yang, Junqing
AU  - Yang J
FAU - Jiang, Qingsong
AU  - Jiang Q
LA  - eng
PT  - Journal Article
DEP - 20130320
PL  - United States
TA  - Evid Based Complement Alternat Med
JT  - Evidence-based complementary and alternative medicine : eCAM
JID - 101215021
PMC - PMC3616349
EDAT- 2013/04/11 06:00
MHDA- 2013/04/11 06:01
PMCR- 2013/03/20
CRDT- 2013/04/11 06:00
PHST- 2012/10/14 00:00 [received]
PHST- 2013/02/22 00:00 [accepted]
PHST- 2013/04/11 06:00 [entrez]
PHST- 2013/04/11 06:00 [pubmed]
PHST- 2013/04/11 06:01 [medline]
PHST- 2013/03/20 00:00 [pmc-release]
AID - 10.1155/2013/285489 [doi]
PST - ppublish
SO  - Evid Based Complement Alternat Med. 2013;2013:285489. doi: 10.1155/2013/285489. 
      Epub 2013 Mar 20.