Key result
Scutellarin attenuates diabetic cardiac injury, oxidative stress, and myocardial apoptosis in mice.
Why the study?
The study was conducted to investigate the potential protective effects and associated mechanisms of scutellarin on experimental type 2 diabetes-induced cardiac injury.
Does scutellarin reduce type 2 diabetes-induced cardiac injury and modulate related molecular pathways in a high-fat diet/streptozotocin mouse model?
Does scutellarin reduce type 2 diabetes-induced cardiac injury and modulate related molecular pathways in a high-fat diet/streptozotocin mouse model?
Scutellarin demonstrates promising cardioprotective effects in experimental diabetic cardiomyopathy by targeting Nrf2/Keap1 oxidative and TLR4/NF-κB inflammatory pathways.
Answers are grounded in this paper and cite their sources.
Scutellarin should not yet inform clinical practice in diabetic cardiomyopathy; hypothesis-generating in mice and requires human trials.
BACKGROUND: Diabetes is a serious global health concern which severely affected public health as well as socio-economic growth worldwide. Scutellarin (SCU), a bioactive flavonoid, is known for its efficacious action against a range of ailments including cardiovascular problems. The present study was conducted to find out possible protective effect and its associated mechanisms of SCU on experimental type 2 diabetes-induced cardiac injury. METHODS: Type 2 diabetes was induced by treating animals with high fat diet for 4 weeks and a single intraperitoneal dose (35 mg/kg body weight) of streptozotocin and diabetic animals received SCU (10 or 20 mg/kg/day) for 6 weeks. RESULTS: Scutellarin attenuated type 2 diabetes-induced hyperglycemia, bodyweight loss, hyperlipidaemia, cardiac functional damage with histopathological alterations and fibrosis. Scutellarin treatment to type 2 diabetic mice ameliorated oxidative stress, inflammatory status and apoptosis in heart. Furthermore, the underlying mechanisms for such mitigation of oxidative stress, inflammation and apoptosis in heart involved modulation of Nrf2/Keap1 pathway, TLR4/MyD88/NF-κB mediated inflammatory pathway and intrinsic (mitochondrial) apoptosis pathway, respectively. CONCLUSIONS: The current findings suggest that SCU is effective in protecting type 2 diabetes-induced cardiac injury by attenuating oxidative stress and inflammatory responses and apoptosis, and it is also worth considering the efficacious potential of SCU to treat diabetic cardiomyopathy patients.
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Huo et al. (2021) studied Type 2 diabetes-induced cardiac injury (experimental model) (n=40). Scutellarin vs. Vehicle (untreated diabetic control) was evaluated on Cardiac injury biomarkers (CK-MB, Troponin, BNP) and histopathological damage (p=<0.05). Scutellarin at 10 or 20 mg/kg/day significantly attenuated type 2 diabetes-induced cardiac functional damage, oxidative stress, inflammation, and apoptosis in mice.
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