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Fucoidan derived from Sargassum pallidum alleviates metabolism disorders associated with improvement of cardiac injury and oxidative stress in diabetic mice. | LitMetric

AI Article Synopsis

  • Type 2 diabetes mellitus (T2DM) is a growing global health issue, with cardiovascular complications being a leading cause of death in diabetic patients.
  • This study aimed to examine the effects of fucoidan from Sargassum pallidum (Sp-Fuc) on diabetic symptoms and heart injury in db/db mice over 8 weeks.
  • Results showed that Sp-Fuc significantly improved metabolic disorders, reduced cardiac dysfunction and inflammation, and enhanced antioxidant activity by activating specific signaling pathways.

Article Abstract

Type 2 diabetes mellitus (T2DM) and its complications have become a serious global health epidemic. Cardiovascular complications have considered as a major cause of high mortality in diabetic patients. Fucoidans from brown algae have diverse medicinal activities, however, few studies reported pharmacological activity of Sargassum. pallidum fucoidan (Sp-Fuc). Therefore, the aim of this study was to investigate the effects of Sp-Fuc on diabetic symptoms and cardiac injury in spontaneous diabetic db/db mice. SP-Fuc at 200 mg/(kg/d) was administered intragastrically to db/db mice for 8 weeks, the effects on hyperlipidemia, hyperglycemia, insulin resistance, and cardiac damage, as well as oxidative stress, inflammation, Nrf2/ARE, and NF-κB signaling pathways, were investigated. Our data demonstrated that Sp-Fuc significantly (p < 0.05) decreased body weights, hyperlipidemia, and hyperglycemia in db/db mice, along with improved insulin sensitivity. Additionally, Sp-Fuc significantly (p < 0.05) alleviated cardiac dysfunction and pathological morphology of cardiac tissue. Sp-Fuc also significantly (p < 0.05) decreased lipid peroxidation, increased antioxidant function, as well as reduced cardiac inflammation, possibly through Nrf2/ARE and NF-κB signaling. Sp-Fuc can ameliorate the metabolism disorders of glucose and lipid in diabetic mice by activating Nrf2/ARE antioxidant signaling, simultaneously reducing cardiac redox imbalance and inflammatory damage. The present findings provide a perspective on the therapy strategy for T2DM and its complications.

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Source
http://dx.doi.org/10.1002/ptr.7901DOI Listing

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