PMID- 28042873
OWN - NLM
STAT- MEDLINE
DCOM- 20170321
LR  - 20181113
IS  - 1745-7254 (Electronic)
IS  - 1671-4083 (Print)
IS  - 1671-4083 (Linking)
VI  - 38
IP  - 3
DP  - 2017 Mar
TI  - A mini-network balance model for evaluating the progression of cardiovascular 
      complications in Goto-Kakizaki rats.
PG  - 362-370
LID - 10.1038/aps.2016.129 [doi]
AB  - Cardiovascular complications represent a leading cause of mortality in patients 
      with type 2 diabetes mellitus (T2DM). During such complicated progression, subtle 
      variations in the cardiovascular risk (CVR)-related biomarkers have been used to 
      identify cardiovascular disease at the incipient stage. In this study we attempt 
      to integrally characterize the progression of cardiovascular complications and to 
      assess the beneficial effects of metformin combined with salvianolic acid A (Sal 
      A), in Goto-Kakizaki (GK) rats with spontaneous T2DM. The rats were treated with 
      metformin (200 mg.kg(-1).d(-1), ig) alone or in combination with Sal A (1 
      mg.kg(-1).d(-1), ip) at ages from 8 to 22 weeks. During the treatment, the levels 
      of asymmetric dimethylarginine, L-arginine, superoxide dismutase, 
      malondialdehyde, glucose, high density lipoprotein and low density lipoprotein 
      were assessed. Based on alterations in these biomarkers, a mini-network balance 
      model was established using matrixes and vectors. Radar charts were created to 
      visually depict the disruption of CVR-related modules (endothelial function, 
      oxidative stress, glycation and lipid profiles). The description for the 
      progression of cardiovascular disorder was quantitatively represented by u, the 
      dynamic parameter of the model. The modeling results suggested that untreated GK 
      rats tended to have more severe cardiovascular complications than the treatment 
      groups. Metformin monotherapy retarded disease deterioration, whereas the 
      combination treatment ameliorated the disease progression via restoring the 
      balance. The current study, which focused on the balance of the mini-network and 
      interactions among CVR-related modules, proposes a novel method for evaluating 
      the progression of cardiovascular complications in T2DM as well as a more 
      beneficial intervention strategy.
FAU - Jiang, Hao
AU  - Jiang H
AD  - Center of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, 
      Nanjing 210009, China.
FAU - Wang, Yu-Hao
AU  - Wang YH
AD  - Center of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, 
      Nanjing 210009, China.
FAU - Wei, Chun-Xiang
AU  - Wei CX
AD  - Center of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, 
      Nanjing 210009, China.
FAU - Zhang, Xue
AU  - Zhang X
AD  - Center of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, 
      Nanjing 210009, China.
FAU - Liu, Hao-Chen
AU  - Liu HC
AD  - Center of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, 
      Nanjing 210009, China.
FAU - Liu, Xiao-Quan
AU  - Liu XQ
AD  - Center of Drug Metabolism and Pharmacokinetics, China Pharmaceutical University, 
      Nanjing 210009, China.
LA  - eng
PT  - Journal Article
DEP - 20170102
PL  - United States
TA  - Acta Pharmacol Sin
JT  - Acta pharmacologica Sinica
JID - 100956087
RN  - 0 (Alkenes)
RN  - 0 (Hypoglycemic Agents)
RN  - 0 (Polyphenols)
RN  - 0 (salvianolic acid)
RN  - 9100L32L2N (Metformin)
SB  - IM
MH  - Alkenes/therapeutic use
MH  - Animals
MH  - Cardiovascular Diseases/etiology/*physiopathology/prevention & control
MH  - Diabetes Complications/*physiopathology/prevention & control
MH  - Diabetes Mellitus, Type 2/complications/drug therapy/*physiopathology
MH  - Disease Progression
MH  - Drug Therapy, Combination
MH  - Hypoglycemic Agents/therapeutic use
MH  - Metformin/therapeutic use
MH  - *Models, Biological
MH  - Polyphenols/therapeutic use
MH  - Rats, Wistar
PMC - PMC5342663
EDAT- 2017/01/04 06:00
MHDA- 2017/03/23 06:00
PMCR- 2018/03/01
CRDT- 2017/01/03 06:00
PHST- 2016/06/27 00:00 [received]
PHST- 2016/10/12 00:00 [accepted]
PHST- 2017/01/04 06:00 [pubmed]
PHST- 2017/03/23 06:00 [medline]
PHST- 2017/01/03 06:00 [entrez]
PHST- 2018/03/01 00:00 [pmc-release]
AID - aps2016129 [pii]
AID - 10.1038/aps.2016.129 [doi]
PST - ppublish
SO  - Acta Pharmacol Sin. 2017 Mar;38(3):362-370. doi: 10.1038/aps.2016.129. Epub 2017 
      Jan 2.