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2017 ; 38
(3
): 362-370
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A mini-network balance model for evaluating the progression of cardiovascular
complications in Goto-Kakizaki rats
#MMPMID28042873
Jiang H
; Wang YH
; Wei CX
; Zhang X
; Liu HC
; Liu XQ
Acta Pharmacol Sin
2017[Mar]; 38
(3
): 362-370
PMID28042873
show ga
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.
|*Models, Biological
[MESH]
|Alkenes/therapeutic use
[MESH]
|Animals
[MESH]
|Cardiovascular Diseases/etiology/*physiopathology/prevention & control
[MESH]
|Diabetes Complications/*physiopathology/prevention & control
[MESH]
|Diabetes Mellitus, Type 2/complications/drug therapy/*physiopathology
[MESH]