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Cardiac dysfunction is attenuated by ginkgolide B via reducing oxidative stress and fibrosis in diabetic rats
Yu-Xin Jiang1,2, Wei Li3, Jing Wang2
1School of Medicine, Jiaxing University, Jiaxing, P.R. China.
Insights
Ginkgolide B improves heart function in diabetic rats by reducing oxidative stress and cardiac fibrosis. This natural compound offers a potential therapeutic strategy for diabetic cardiomyopathy.
Area of Science:
- Biochemistry
- Cardiology
- Pharmacology
Background:
- Diabetic cardiomyopathy significantly increases morbidity and mortality in diabetic patients.
- Ginkgolide B has previously shown efficacy in alleviating endothelial dysfunction in diabetic rat models.
- Understanding ginkgolide B's mechanism in diabetic cardiac dysfunction is crucial for therapeutic development.
Purpose of the Study:
- To investigate the effects of ginkgolide B on cardiac dysfunction in streptozotocin-induced diabetic rats.
- To elucidate the underlying mechanisms, including oxidative stress, cardiac fibrosis, and inflammatory pathways.
Main Methods:
- Diabetes was induced using streptozotocin (STZ) in rats.
- Cardiac function was assessed via hemodynamic monitoring.
- Oxidative stress markers (MDA, SOD), cardiac fibrosis (Masson's trichrome, TGF-β1, α-SMA, p-Smad2/3), and signaling pathways (AMPK, PI3K/Akt, p38, JNK) were analyzed.
Main Results:
- Ginkgolide B treatment significantly improved cardiac hemodynamics in diabetic rats.
- It reduced oxidative stress, inflammation, and cardiac fibrosis markers.
- Ginkgolide B modulated key signaling pathways, including increasing SIRT1, HO-1, p-AMPK, p-PI3K, and p-Akt, while decreasing p-p38 and p-JNK.
Conclusions:
- Ginkgolide B effectively alleviates cardiac dysfunction in diabetic rats.
- The therapeutic effects are attributed to the reduction of oxidative stress and cardiac fibrosis.
- Ginkgolide B demonstrates potential as a treatment for diabetic cardiomyopathy.
Objectives:
Diabetic cardiomyopathy is a leading factor of high morbidity and mortality in diabetic patients. Our previous results revealed that ginkgolide B alleviates endothelial dysfunction in diabetic rats. This study aimed to investigate the effect of ginkgolide B on cardiac dysfunction and its mechanism in diabetic rats.
Materials And Methods:
Diabetes was induced in rats through the intraperitoneal injection of streptozotocin (STZ). Hemodynamics was monitored to assess cardiac function. Oxidative stress was examined by detecting levels of malondialdehyde (MDA) and superoxide dismutase (SOD) in serum, and expression of sirtuin (SIRT)1, heme oxygenase (HO)-1, and phosphorylated AMPK in the heart. Masson's trichrome staining and expression of transforming growth factor (TGF)-β1, smooth muscle actin (α-SMA), and phosphorylated (p-) Smad2 and Smad3 were used to evaluate cardiac fibrosis. Inflammatory cytokine in serum and levels of p-PI3K, p-Akt, p-p38, and p-JNK in the heart were determined.
Results:
Ginkgolide B significantly improved hemodynamics in diabetic rats. Compared with diabetic rats, treatment with ginkgolide B significantly decreased levels of inflammatory cytokines, improved oxidative stress via reducing MDA concentration, and elevating SOD activity in serum and increasing expression of SIRT1, HO-1, and p-AMPK. Further, ginkgolide B alleviated cardiac fibrosis by decreasing expression of TGF-β1, α-SMA, and p-Smad2 and p-Smad3. Meanwhile, ginkgolide B reduced Levels of p-P38, and p-JNK, and increased levels of p-PI3K and p-Akt.
Conclusion:
The results suggested that ginkgolide B alleviated cardiac dysfunction by reducing oxidative stress and cardiac fibrosis.
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