Abstract
Oxidative stress is highly associated with the development of diabetes mellitus (DM), especially pancreatic beta-cell injury. Flavonoids derived from plants have caused important attention in the prevention or treatment of DM. Lotus seedpod belongs to a traditional Chinese herbal medicine and has been indicated to possess antioxidant, anti-age, anti-glycative, and hepatoprotective activities. The purpose of this study was to demonstrate the pancreatic beta-cell protective effects of lotus seedpod aqueous extracts (LSE) against oxidative injury. According to HPLC/ESI-MS-MS method, LSE was confirmed to have flavonoids derivatives, especially quercetin-3-glucuronide (Q3G). In vitro, LSE dose-dependently improved the survival and function of rat pancreatic beta-cells (RIN-m5F) from hydrogen peroxide (H2O2)-mediated loss of cell viability, impairment of insulin secretion, and promotion of oxidative stress. LSE showed potential in decreasing the H2O2-induced occurrence of apoptosis. In addition, H2O2-triggered acidic vesicular organelle formation and microtubule-associated protein light chain 3 (LC3)-II upregulation, markers of autophagy, were increased by LSE. Molecular data explored that antiapoptotic and autophagic effects of LSE, comparable to that of Q3G, might receptively be mediated via phospho-Bcl-2-associated death promoter (p-Bad)/B-cell lymphoma 2 (Bcl-2) and class III phosphatidylinositol-3 kinase (PI3K)/LC3-II signal pathway. In vivo, LSE improved the DM symptoms and pancreatic cell injury better than metformin, a drug that is routinely prescribed to treat DM. These data implied that LSE induces the autophagic signaling, leading to protect beta-cells from oxidative stress-related apoptosis and injury.
Highlights
Diabetes mellitus (DM) is a chronic and complex illness characterized mainly by hyperglycemia and other metabolic disorders with several symptoms, including polyphagia, polydipsia, polyuria, and pancreatic β-cell mass loss [1,2]
There were fewer islets areas, but these were rounder shaped than those of lotus seedpod aqueous extracts (LSE) groups (Figure 6c,d). These results demonstrated that metformin could repair the cell injury incurred by the pancreatic islets due to induction in high-fat diet (HFD)/STZ, whereas the groups orally treated with LSE showed better protective effects than metformin in terms of the recovery of HFD/STZ-caused impairment and apoptosis of pancreatic islets (Figure 6d)
In vivo results found that LSE functioned as a potential anti-diabetic agent to protect the pancreas from increasing cell injury, apoptosis, and even diabetes mellitus (DM) development. The findings of this present study provided evidence suggesting that LSE could protect beta-cells from oxidative injury through the downregulation of apoptosis and upregulation of autophagy (Figure 6h)
Summary
Diabetes mellitus (DM) is a chronic and complex illness characterized mainly by hyperglycemia and other metabolic disorders with several symptoms, including polyphagia, polydipsia, polyuria, and pancreatic β-cell (beta-cell) mass loss [1,2]. Insulin resistance, cell inflammation, and excess of lipids and other metabolic fuels, containing fatty acid and glucose, trigger beta-cell dysfunction over time [1,3]. It has been further indicated that hyperglycemia-induced reactive oxygen species (ROS) generation causes beta-cell dysfunction, playing a critical role in the DM progression [4]. Preventing apoptosis of beta-cells could be a valuable strategy to manage or treat DM, reversing and inhibiting this illness to an advanced degree instead of just lowering blood glucose
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