Key result
25-OH-PPD significantly reduced markers of cardiac hypertrophy, fibrosis, and inflammation in a rat model of diabetic cardiomyopathy (P<0.05).
Why the study?
The study investigated the inhibitory effects and mechanism of 25-OH-PPD on cardiac hypertrophy, fibrosis, and inflammation in diabetic cardiomyopathy.
Does 25-OH-PPD improve cardiac hypertrophy, fibrosis, and inflammation in a rat model of diabetic cardiomyopathy?
Does 25-OH-PPD improve cardiac hypertrophy, fibrosis, and inflammation in a rat model of diabetic cardiomyopathy?
25-OH-PPD attenuates cardiac hypertrophy and fibrosis in a rat model of diabetic cardiomyopathy, likely via the PI3K/Akt/GSK-3β signaling pathway.
Answers are grounded in this paper and cite their sources.
May support 25-OH-PPD development for diabetic cardiomyopathy; hypothesis-generating and requires human validation.
The present study investigated the inhibitory effects and the associated mechanism of the compound 25-OH-PPD (PPD) on cardiac hypertrophy, fibrosis and inflammation. The signaling pathways associated with diabetic mellitus cardiomyopathy (DMCM) were investigated using a rat model. DMCM Sprague-Dawley rats were induced by injection of streptozotocin. The animals were divided into 5 groups as follows: Normal group (NG group), diabetic group, PPD treatment group, PPD/LY294002 group (inhibitor of PI3K/Akt) and PPD/LiCl group [inhibitor of glycogen synthase kinase (GSK) 3β]. The studies were carried out during the 12 weeks following induction of diabetes and the levels of plasma brain natriuretic peptide (BNP), creatine phosphokinase isoenzyme (CK-MB) were measured. In addition, the volume of myocardial collagen fraction (CVF) was tested. The expression levels of the inflammatory cytokines, including transforming growth factor beta 1 (TGF-β1), connective tissue growth factor (CTGF), cell adhesion molecules α-smooth muscle actin (α-SMA) and vascular adhesion molecule 1 (VCAM-1) and associated signaling proteins (Akt, GSK-3β) were measured by biochemical analyses. The levels of BNP and CK-MB, the volume of CVF, the expression levels of TGF-β1, CTGF, α-SMA and VCAM-1 in the diabetic group were higher compared with those of the normal control group (P<0.05). Conversely, the levels of these molecules were significantly decreased in the PPD treatment groups (P<0.05). The aforementioned effects were partially eliminated in the PPD/LY294002 and PPD/LiCl groups. In addition, PPD treatment significantly increased the expression levels of p-Akt and decreased the levels of phosphorylated GSK-3β compared with those of the DMCM group (P<0.05). The data demonstrated that the protective effects of 25-OH-PPD against DMCM may be attributed to the PI3k/Akt/GSK-3β signaling pathway, via the suppression of the α-SMA/VCAM axis and the downregulation of TGF-β1 and CTGF expression.
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Liu et al. (2020) studied Diabetic cardiomyopathy (n=50). 25-OH-PPD vs. Normal saline was evaluated on Levels of BNP, CK-MB, CVF, and inflammatory cytokines (p=<0.05). 25-OH-PPD significantly reduced markers of cardiac hypertrophy, fibrosis, and inflammation in a rat model of diabetic cardiomyopathy (P<0.05).
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