Key result
Scutellarin significantly reduced high glucose-induced apoptosis and reactive oxygen species production in H9c2 cardiomyocytes in a dose-dependent manner.
Why the study?
Diabetic cardiomyopathy is an important cause of death in diabetes, and the mechanism by which scutellarin reduces high glucose-induced cardiomyocyte injury to prevent diabetic cardiomyopathy required investigation.
Does scutellarin reduce high glucose-induced cardiomyocyte injury in an in vitro model of diabetic cardiomyopathy?
Does scutellarin reduce high glucose-induced cardiomyocyte injury in an in vitro model of diabetic cardiomyopathy?
Scutellarin alleviates high glucose-induced myocardial injury in vitro by inhibiting oxidative stress and apoptosis, suggesting potential therapeutic value for diabetic cardiomyopathy.
Answers are grounded in this paper and cite their sources.
Scutellarin effects in high-glucose H9c2 cells remain preclinical; leaves open any role in diabetic cardiomyopathy prevention.
Diabetic cardiomyopathy (DCM) is an important cause of death in patients with diabetes. DCM can be simulated by cardiomyocyte injury induced by high glucose (HG) in vitro. Scutellarin (Scu) is a flavonoid extracted from Erigeron breviscapus. The H9c2 cell line was used as an in vitro model in the present study to investigate the mechanism by which Scu reduces HG‑induced cardiomyocyte injury. Moreover, the present study aimed to provide scientific evidence on the mechanism by which Scu prevents DCM. The following groups were used: Control, model, Scu (50/100/200/400 µM) and curcumin. Following H9c2 cell adherence, the control and model groups were treated with normal medium; the Scu group cells were treated with different concentrations of Scu, whereas the curcumin group cells were treated with 4 µM curcumin for 4 h. Subsequently, the normal group was cultured in normal medium, and the other groups were treated with medium containing 100 mM HG for 48 h. The results indicated that Scu improved the morphology of H9c2 cells treated by HG, enhanced cell proliferative activity, reduced the production of reactive oxygen species and the induction of apoptosis. Moreover, Scu promoted the expression of Bcl‑2 and inhibited the expression levels of caspase‑3, cleaved caspase‑3, caspase‑9, cleaved caspase‑9, caspase‑12, Bax, NADPH oxidase (Nox)2 and Nox4. The findings indicated that Scu could inhibit oxidative stress and reduce the induction of apoptosis in cardiomyocytes, thereby alleviating HG‑induced myocardial injury.
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Wei et al. (2025) studied Diabetic cardiomyopathy (in vitro model). Scutellarin vs. High glucose (100 mM) model group was evaluated on Apoptosis rate and ROS production (p=<0.01). Scutellarin significantly reduced high glucose-induced apoptosis and reactive oxygen species production in H9c2 cardiomyocytes in a dose-dependent manner.
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