Abstract
At present, there are few reports concerning the relationship between miR-122 and diabetes. In addition, the effect of miR-122 on streptozotocin- (STZ-) induced oxidative damage in INS-1 cells remains unclear. The present study aimed to investigate the role and modulatory mechanisms involving miR-122 in diabetes. STZ was used to induce INS-1 cell damage. Reverse transcription-quantitative PCR was used to investigate the expression of miR-122. A TUNEL cell apoptosis detection kit was used to detect apoptosis. Intracellular ROS levels were determined using dichlorofluorescein-diacetate. The activities of insulin secretion, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-px) were measured using ELISA kits. Western blotting was used to measure the expression levels of Bax, Bcl-2, PI3K, p-PI3K, caspase-3 and caspase-9, cleaved-caspase-3 and cleaved-caspase-9, AKT, and p-AKT. Then, LY294002 (LY, PI3K inhibitor) was used to treat INS-1 cells, and oxidative stress and apoptosis were measured. The results showed that STZ-induced inhibitory effects on insulin secretion were mitigated by miR-122 inhibitor, and the activities of SOD, CAT, and GSH-px were also increased. Furthermore, miR-122 inhibitor inhibited apoptosis and oxidative stress in STZ-induced INS-1 cells. Finally, the addition of LY increased insulin levels; reduced the activities of SOD, CAT, and GSH-px; and promoted apoptosis in STZ-induced INS-1 cells. In conclusion, interference with miR-122 can inhibit oxidative stress and apoptosis in STZ-induced INS-1 cells, involving a mechanism of action related to the PI3K/AKT pathway.
Highlights
MicroRNAs are a type of noncoding singlestranded RNA comprising small molecules 18–25 nucleotides in length [1] that mainly promote the degradation of mRNA or inhibit target messenger RNAs through complementary base pairing with downstream target gene mRNA [2]. miRNAs are of diverse types and have complex functions that are widely involved in regulating the proliferation and differentiation of various cells [3], and dysregulation of expression can promote or inhibit tumor development. miR-122 is a type of miRNA with tumor suppressor properties [4]
Type 2 diabetes mellitus (T2DM) accounts for 90% of all diabetes cases. e International Diabetes Federation announced that 336 million people worldwide currently suffer from T2DM and that the disease is responsible for 4.6 million deaths each year, or one death every seven seconds [9]
Increased activity was identified in the STZ + miR-122 inhibitor group, indicating that miR-122 could enhance the activity of superoxide dismutase (SOD), CAT, and GSH-Px. erefore, our experiments have shown that miR-122 inhibitor can inhibit cellular oxidative stress
Summary
MicroRNAs (miRNAs) are a type of noncoding singlestranded RNA comprising small molecules 18–25 nucleotides in length [1] that mainly promote the degradation of mRNA or inhibit target messenger RNAs (mRNAs) through complementary base pairing with downstream target gene mRNA [2]. miRNAs are of diverse types and have complex functions that are widely involved in regulating the proliferation and differentiation of various cells [3], and dysregulation of expression can promote or inhibit tumor development. miR-122 is a type of miRNA with tumor suppressor properties [4]. MiRNAs are of diverse types and have complex functions that are widely involved in regulating the proliferation and differentiation of various cells [3], and dysregulation of expression can promote or inhibit tumor development. It has been confirmed that miR122 exhibits low expression in liver cancer [5] and breast malignancies [6], whereas there are a few studies concerning relationships involving miR-122 and pancreatic β cells. Diabetes mellitus (DM) is a chronic metabolic disease that currently affects > 400 million people worldwide [7]. E International Diabetes Federation announced that 336 million people worldwide currently suffer from T2DM and that the disease is responsible for 4.6 million deaths each year, or one death every seven seconds [9]. Pancreatic β-cells are responsible for insulin secretion and control of plasma glucose levels [10]
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