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Updated: Jan 28, 2026

Acute Myocardial Infarction in Rats
Published on: February 16, 2011
Dioscin Attenuates Myocardial Damages in Diabetic Rats maybe by Regulating NO-sGC-cGMP-PKG Pathway
Qian Wei1, Tonggang Zhu2, Xue Xiao1
1Department of Heart Disease, Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, Jilin, China.
Purpose:
The objective of this research was to explore the effect of dioscin on myocardium in streptozotocin (STZ)-induced diabetic rats and the underlying mechanisms.
Methods:
Diabetic rat model was established by a single intravenous injection of streptozocin (STZ). The rats were divided into 5 groups: control group, control+dioscin group, model group (diabetes), DDL group (diabetic rats treated with 100 μg/kg/day dioscin) and DDH group (diabetic rats treated with 200 μg/kg/day dioscin). Each group was continuously intervened for 6 weeks. Hemodynamic parameters were detected and pathological alterations of myocardium were observed by hematoxylin-eosin (HE) staining. Inflammatory response and related proteins in the NO-sGC-cGMP-PKG pathway were detected by western blot.
Results:
Dioscin treatment can increase ejection fraction (EF) and decrease left ventricular end-diastolic pressure (LVEDP) as well as time constant of left ventricular pressure decay (Tau) parameters in diabetic rats, suggesting the improvement of left ventricular function. By histopathology observation, we found that dioscin treatment can also improve myocardial histological lesions caused by diabetes. In addition, the levels of inflammatory cytokines TGF-β1, TNF-α and IL-1β of the model group were remarkably higher than those in the control group (p<0.01), while after being treated with dioscin these cytokines were obviously decreased (p<0.05). The levels of PDE-5, PKG and p-VASP in the diabetic rats were significantly declined after being treated by dioscin in a dose-dependent manner (p<0.05).
Conclusion:
Dioscin may prevent the myocardial injury in diabetic rats by up-regulating NO-sGC-cGMP-PKG pathway.
Insights
Dioscin improves cardiac function and reduces inflammation in diabetic rats by enhancing the NO-sGC-cGMP-PKG pathway, offering a potential treatment for diabetic cardiomyopathy.
Area of Science:
- Cardiovascular Research
- Diabetology
- Pharmacology
Background:
- Diabetic cardiomyopathy is a significant complication of diabetes mellitus.
- Streptozotocin (STZ)-induced diabetes in rats is a common model for studying diabetic complications.
- Understanding the mechanisms of myocardial injury in diabetes is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the protective effects of dioscin on the myocardium of STZ-induced diabetic rats.
- To elucidate the underlying molecular mechanisms, particularly focusing on the NO-sGC-cGMP-PKG pathway.
Main Methods:
- Establishment of a rat model of diabetes using streptozotocin (STZ).
- Administration of varying doses of dioscin (100 and 200 μg/kg/day) to diabetic rats for 6 weeks.
- Assessment of hemodynamic parameters, myocardial histology (HE staining), and protein expression (Western blot) related to inflammation and the NO-sGC-cGMP-PKG pathway.
Main Results:
- Dioscin treatment improved left ventricular function, evidenced by increased ejection fraction (EF) and decreased LVEDP and Tau.
- Histopathological examination revealed that dioscin ameliorated myocardial lesions in diabetic rats.
- Dioscin significantly reduced levels of inflammatory cytokines (TGF-β1, TNF-α, IL-1β) and modulated the NO-sGC-cGMP-PKG pathway by affecting PDE-5, PKG, and p-VASP levels.
Conclusions:
- Dioscin demonstrates cardioprotective effects in STZ-induced diabetic rats.
- The mechanism involves the upregulation of the nitric oxide-soluble guanylate cyclase-cyclic guanosine monophosphate-protein kinase G (NO-sGC-cGMP-PKG) pathway.
- Dioscin holds potential as a therapeutic agent for diabetic cardiomyopathy.
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