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2016 ; 20
(6
): 613-619
Nephropedia Template TP
gab.com Text
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English Wikipedia
Insulin-like growth factor-1 improves diabetic cardiomyopathy through
antioxidative and anti-inflammatory processes along with modulation of Akt/GSK-3?
signaling in rats
#MMPMID27847438
Wang CY
; Li XD
; Hao ZH
; Xu D
Korean J Physiol Pharmacol
2016[Nov]; 20
(6
): 613-619
PMID27847438
show ga
Diabetic cardiomyopathy (DCM), a serious complication of diabetes mellitus, is
associated with changes in myocardial structure and function. This study sought
to explore the ability of insulin-like growth factor-1 (IGF-1) to modulate DCM
and its related mechanisms. Twenty-four male Wistar rats were injected with
streptozotocin (STZ, 60 mg/kg) to mimic diabetes mellitus. Myocardial fibrosis
and apoptosis were evaluated by histopathologic analyses, and relevant proteins
were analyzed by Western blotting. Inflammatory factors were assessed by ELISA.
Markers of oxidative stress were tested by colorimetric analysis. Rats with DCM
displayed decreased body weight, metabolic abnormalities, elevated apoptosis (as
assessed by the bcl-2/bax ratio and TUNEL assays), increased fibrosis, increased
markers of oxidative stress (MDA and SOD) and inflammatory factors (TNF-? and
IL-1?), and decreased phosphorylation of Akt and glycogen synthase kinase
(GSK-3?). IGF-1 treatment, however, attenuated the metabolic abnormalities and
myocardial apoptosis, interstitial fibrosis, oxidative stress and inflammation
seen in diabetic rats, while also increasing the phosphorylation levels of Akt
and GSK-3?. These findings suggest that IGF-1 ameliorates the pathophysiological
progress of DCM along with an activation of the Akt/GSK-3? signaling pathway. Our
findings suggest that IGF-1 could be a potential therapeutic choice for
controlling DCM.