Alpha-mangostin decreases high glucose-induced damage on human umbilical vein endothelial cells by increasing autophagic protein expression
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Farhad Eisvand1, Kasra Rezvani1, Hossein Hosseinzadeh1,2
1Department of Pharmacodynamics and Toxicology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran.
Objectives:
Diabetes is a chronic disorder that occurs as a result of impaired glucose metabolism. In hyperglycaemic states, the balance between oxidative stress and antioxidant enzymes is disrupted leading to oxidative damage and cell death. In addition, impaired autophagy leads to the storage of dysfunctional proteins and cellular organelles in the cell. Hence, the cytoprotective function of autophagy may be disrupted by high glucose conditions. Alpha-mangostin (A-MG) is an essential xanthone purified from the mangosteen fruit. The different pharmacological benefits of alpha-mangostin, including antioxidant, anti-obesity, and antidiabetic, were demonstrated.
Materials And Methods:
We evaluated the protective influence of A-MG on autophagic response impaired by high concentrations of glucose in human umbilical vein endothelial cells (HUVECs). The HUVECs were treated with various glucose concentrations (5-60 mM) and A-MG (1.25-10 μM) for three days. Then, HUVECs were treated with 60 mM of glucose+2.5 μM of A-MG to measure viability, ROS, and NO content. Finally, the levels of autophagic proteins including LC3, SIRT1, and beclin 1 were evaluated by western blot.
Results:
The results expressed that high glucose condition (60 mM) decreased viability and increased ROS and NO content in HUVECs. In addition, LC3, SIRT1, and beclin 1 protein levels declined when HUVECs were exposed to the high concentration of glucose. A-MG reversed these detrimental effects and elevated autophagic protein levels.
Conclusion:
Our data represent that A-MG protects HUVECs against high glucose conditions by decreasing ROS and NO generation as well as increasing the expression of autophagy proteins.
Insights
Alpha-mangostin protects against high glucose damage in cells by reducing oxidative stress and enhancing autophagy. This natural compound offers potential therapeutic benefits for diabetes complications.
Area of Science:
- Biochemistry
- Cell Biology
- Pharmacology
Background:
- Diabetes mellitus is a metabolic disorder characterized by impaired glucose metabolism and hyperglycemia.
- Hyperglycemia induces oxidative stress, disrupting the balance between reactive oxygen species (ROS) and antioxidant enzymes, leading to cellular damage.
- Autophagy, a cellular degradation process, is crucial for maintaining cellular health but can be impaired under high glucose conditions, leading to the accumulation of damaged components.
Purpose of the Study:
- To investigate the protective effects of alpha-mangostin (A-MG) on high glucose-induced autophagic dysfunction in human umbilical vein endothelial cells (HUVECs).
- To evaluate the impact of A-MG on cell viability, oxidative stress markers (ROS and NO), and key autophagy-related proteins (LC3, SIRT1, beclin 1) under hyperglycemic conditions.
Main Methods:
- HUVECs were exposed to varying concentrations of glucose (5-60 mM) and A-MG (1.25-10 μM) for three days.
- Cell viability, ROS, and nitric oxide (NO) content were measured in HUVECs treated with 60 mM glucose and 2.5 μM A-MG.
- Western blot analysis was employed to quantify the expression levels of autophagy proteins LC3, SIRT1, and beclin 1.
Main Results:
- High glucose (60 mM) significantly reduced HUVEC viability and increased ROS and NO levels.
- Exposure to high glucose led to decreased expression of autophagy proteins LC3, SIRT1, and beclin 1.
- A-MG treatment counteracted the detrimental effects of high glucose, restoring cell viability and increasing the levels of essential autophagy proteins.
Conclusions:
- Alpha-mangostin demonstrates significant cytoprotective effects against high glucose-induced damage in HUVECs.
- A-MG mitigates oxidative stress by reducing ROS and NO generation.
- A-MG enhances the autophagic pathway, as evidenced by increased expression of key autophagy-related proteins, suggesting its potential as a therapeutic agent for diabetic complications.
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