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Alogliptin Reduces Oxidative Stress in Cardiomyocytes and Ameliorates Diabetic Cardiomyopathy via the AURKB/NLGN2
Li-Jing Jiao1, Jing Zhou1, Jing Wang1
1Department of Endocrinology, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, People's Republic of China.
Abstract:
Diabetic cardiomyopathy (DCM) is a common complication of diabetes mellitus. This study investigated the effects of alogliptin on DCM and its underlying mechanisms. A DCM model was constructed and treated with alogliptin. Downstream targets of alogliptin were screened using bioinformatics analysis. An in vitro DCM model was constructed using mouse cardiomyocytes with a high concentration of glucose. Echocardiography was performed to measure the heart function parameters. Myocardial damage, collagenous fibrosis, and apoptosis of cardiomyocytes in mouse heart tissues were assessed using cardiac histological staining. AURKB and NLGN2 levels, ROS levels, MDA levels, SOD activity, and cardiomyocyte viability were determined. Alogliptin ameliorated DCM in mice. Bioinformatics analysis revealed that the target of alogliptin was AURKB, and the downstream target of AURKB was NLGN2. AURKB and NLGN2 levels were reduced in the heart tissues of streptozotocin-induced mice. Combined knockdown of AURKB and NLGN2 inhibited the therapeutic effect of alogliptin in DCM mice. Alogliptin attenuated oxidative stress, increased viability, and decreased apoptosis in cardiomyocytes treated with high glucose, which were reversed by combined knockdown of AURKB and NLGN2. Overall, alogliptin ameliorated oxidative stress in cardiomyocytes and DCM in mice by promoting AURKB expression to transcriptionally activate NLGN2.
Insights
Alogliptin effectively treats diabetic cardiomyopathy (DCM) by reducing oxidative stress. It works by increasing AURKB expression, which activates NLGN2, improving heart function in diabetic mice.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Diabetic cardiomyopathy (DCM) is a significant complication of diabetes mellitus, characterized by cardiac dysfunction.
- Understanding the molecular mechanisms underlying DCM is crucial for developing effective therapeutic strategies.
Purpose of the Study:
- To investigate the therapeutic effects of alogliptin on diabetic cardiomyopathy.
- To elucidate the underlying molecular mechanisms, including the roles of AURKB and NLGN2, in alogliptin's action.
Main Methods:
- A mouse model of diabetic cardiomyopathy was established and treated with alogliptin.
- Bioinformatics analysis was used to identify alogliptin's targets (AURKB) and downstream effectors (NLGN2).
- In vitro studies using high-glucose-treated cardiomyocytes assessed oxidative stress, apoptosis, and viability.
Main Results:
- Alogliptin treatment ameliorated cardiac dysfunction and fibrosis in DCM mice.
- Bioinformatics identified AURKB as a direct target and NLGN2 as a downstream target of alogliptin.
- Alogliptin attenuated high-glucose-induced oxidative stress and apoptosis in cardiomyocytes by upregulating AURKB and NLGN2.
Conclusions:
- Alogliptin demonstrates therapeutic potential for diabetic cardiomyopathy.
- The mechanism involves alogliptin promoting AURKB expression, which transcriptionally activates NLGN2, thereby mitigating oxidative stress and improving cardiac function.
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