Abstract

Type 2 diabetes mellitus is a complex multifactorial disease characterized by insulin resistance and dysfunction of pancreatic β-cells. Rice husk silica liquid (RHSL) is derived from rice husks and has not been explored in diabetes mellitus until now. Previous studies showed that rice husk is enriched with silica, and its silica nanoparticles are higher more biocompatible. To investigate the potential protective role of RHSL on pancreatic β cells, we utilized RIN-m5F pancreatic β cells and explored RHSL effect after streptozotocin (STZ)-stimulation. The recovery effects of RHSL were evaluated using flow cytometry, Western blotting, and immunofluorescence analysis. Results of our study showed that RHSL reversed the cell viability, insulin secretion, reactive oxygen species (ROS) production, and the change of mitochondria membrane potential (ΔΨm) in STZ-treated RIN-m5F cells. Moreover, the expression of phospho-receptor-interacting protein 3 (p-RIP3) and cleaved-poly (ADP-ribose) polymerase (PARP), phospho-mammalian target of rapamycin (p-mTOR), and sequestosome-1 (p62/SQSTM1) were significantly decreased, while the transition of light chain (LC)3-I to LC3-II was markedly increased after RHSL treatment in STZ-induced RIN-m5F cells. Interestingly, using autophagy inhibitors such as 3-methyladenine (3-MA) and chloroquine (CQ) both showed an increase in cleaved-PARP protein level, indicating apoptosis induction. Taken together, this study demonstrated that RHSL induced autophagy and alleviated STZ-induced ROS-mediated apoptosis in RIN-m5F cells.

Highlights

  • Introduction distributed under the terms andType 2 diabetes mellitus (T2DM) is a chronic metabolic disorder that has become a global concern [1]

  • These results suggest that Rice husk silica liquid (RHSL)-induced autophagy may attenuate apoptosis

  • The current study provides new insights regarding the potential utility of rice husk silica (RHSL)

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Summary

Introduction

Introduction distributed under the terms andType 2 diabetes mellitus (T2DM) is a chronic metabolic disorder that has become a global concern [1]. The major pathogenesis involves the loss or destruction of pancreatic β cells, which in turn induces the state of imbalance between insulin secretion and blood sugar control in the body [2]. Antioxidants 2021, 10, 1080 compound and widely used as a broad-spectrum antibiotic and cytotoxic chemical [3]. Due to its structural similarity to 2-deoxy-D-glucose, it can enter pancreatic β cells through the GLUT2 glucose transporter and efficiently accumulates intracellularly. Diabetes induced by STZ is the most similar to the structural, functional and biochemical changes observed in human diabetes, so it is often used to simulate diabetes models in animal experiments [4,5] as well as to verify the mechanism of pancreatic β-cells in in vitro experiments [6], which involve mitochondrial dysfunction, ROS production, necrosis, and apoptosis

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