PMID- 34054947
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210601
IS  - 1687-8337 (Print)
IS  - 1687-8345 (Electronic)
IS  - 1687-8337 (Linking)
VI  - 2021
DP  - 2021
TI  - MiR-122 Participates in Oxidative Stress and Apoptosis in STZ-Induced Pancreatic 
      beta Cells by Regulating PI3K/AKT Signaling Pathway.
PG  - 5525112
LID - 10.1155/2021/5525112 [doi]
LID - 5525112
AB  - 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.
CI  - Copyright (c) 2021 Jing Wang et al.
FAU - Wang, Jing
AU  - Wang J
AUID- ORCID: 0000-0001-7531-5056
AD  - Department of Endocrinology, Rheumatism and Immunology, Shengzhou People's 
      Hospital, The First Affiliated Hospital of Zhejiang University Shengzhou Branch, 
      Zhejiang, Shengzhou 312400, China.
FAU - Dong, Zhichun
AU  - Dong Z
AUID- ORCID: 0000-0001-7541-8741
AD  - Department of Endocrinology, Rheumatism and Immunology, Shengzhou People's 
      Hospital, The First Affiliated Hospital of Zhejiang University Shengzhou Branch, 
      Zhejiang, Shengzhou 312400, China.
FAU - Lou, Liyin
AU  - Lou L
AUID- ORCID: 0000-0001-5259-3117
AD  - Department of Endocrinology, Rheumatism and Immunology, Shengzhou People's 
      Hospital, The First Affiliated Hospital of Zhejiang University Shengzhou Branch, 
      Zhejiang, Shengzhou 312400, China.
FAU - Yang, Lijuan
AU  - Yang L
AUID- ORCID: 0000-0002-6000-6530
AD  - Department of Endocrine and Metabolic Diseases, The First Affiliated Hospital of 
      Wenzhou Medical University, Zhejiang, Shengzhou 312400, China.
FAU - Qiu, Jingying
AU  - Qiu J
AUID- ORCID: 0000-0002-6528-1355
AD  - Department of Endocrinology, Rheumatism and Immunology, Shengzhou People's 
      Hospital, The First Affiliated Hospital of Zhejiang University Shengzhou Branch, 
      Zhejiang, Shengzhou 312400, China.
LA  - eng
PT  - Journal Article
DEP - 20210512
PL  - Egypt
TA  - Int J Endocrinol
JT  - International journal of endocrinology
JID - 101516376
PMC - PMC8133841
COIS- The authors declare that there are no conflicts of interest regarding this paper.
EDAT- 2021/06/01 06:00
MHDA- 2021/06/01 06:01
PMCR- 2021/05/12
CRDT- 2021/05/31 06:09
PHST- 2021/01/18 00:00 [received]
PHST- 2021/04/29 00:00 [accepted]
PHST- 2021/05/31 06:09 [entrez]
PHST- 2021/06/01 06:00 [pubmed]
PHST- 2021/06/01 06:01 [medline]
PHST- 2021/05/12 00:00 [pmc-release]
AID - 10.1155/2021/5525112 [doi]
PST - epublish
SO  - Int J Endocrinol. 2021 May 12;2021:5525112. doi: 10.1155/2021/5525112. 
      eCollection 2021.