MiR-122 Participates in Oxidative Stress and Apoptosis in STZ-Induced Pancreatic β Cells by Regulating PI3K/AKT Signaling Pathway
Autor: | Zhichun Dong, Jingying Qiu, Liyin Lou, Lijuan Yang, Jing Wang |
---|---|
Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
Article Subject Endocrinology Diabetes and Metabolism Pharmacology medicine.disease_cause Diseases of the endocrine glands. Clinical endocrinology Superoxide dismutase 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Endocrinology medicine LY294002 Cell damage Protein kinase B PI3K/AKT/mTOR pathway biology Endocrine and Autonomic Systems business.industry RC648-665 medicine.disease Streptozotocin 030104 developmental biology chemistry Apoptosis biology.protein business 030217 neurology & neurosurgery Oxidative stress medicine.drug Research Article |
Zdroj: | International Journal of Endocrinology International Journal of Endocrinology, Vol 2021 (2021) |
ISSN: | 1687-8345 1687-8337 |
Popis: | 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. |
Databáze: | OpenAIRE |
Externí odkaz: |