PMID- 35873704
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220726
IS  - 2090-8083 (Print)
IS  - 2042-0080 (Electronic)
IS  - 2042-0080 (Linking)
VI  - 2022
DP  - 2022
TI  - Semaglutide Protects against 6-OHDA Toxicity by Enhancing Autophagy and 
      Inhibiting Oxidative Stress.
PG  - 6813017
LID - 10.1155/2022/6813017 [doi]
LID - 6813017
AB  - Parkinson's disease (PD) is the second most prevalent neurodegenerative disorder 
      for which no effective treatment is available. Studies have demonstrated that 
      improving insulin resistance in type 2 diabetes mellitus (T2DM) can benefit 
      patients with PD. In addition, a neuroprotective effect of glucagon-like 
      peptide-1 (GLP-1) receptor agonists was demonstrated in experimental models of 
      PD. In addition, there are some clinical trials to study the neuroprotective 
      effect of GLP-1 analog on PD patients. Semaglutide is a long-acting, once-a-week 
      injection treatment and the only available oral form of GLP-1 analog. In the 
      present study, we treated the human neuroblastoma SH-SY5Y cell line with 
      6-hydroxydopamine (6-OHDA) as a PD in vitro model to explore the neuroprotective 
      effects and potential mechanisms of semaglutide to protect against PD. Moreover, 
      we compared the effect of semaglutide with liraglutide given at the same dose. We 
      demonstrated that both semaglutide and liraglutide protect against 6-OHDA 
      cytotoxicity by increasing autophagy flux and decreasing oxidative stress as well 
      as mitochondrial dysfunction in SH-SY5Y cells. Moreover, by comparing the 
      neuroprotective effects of semaglutide and liraglutide on PD cell models at the 
      same dose, we found that semaglutide was superior to liraglutide for most 
      parameters measured. Our results indicate that semaglutide, the new long-acting 
      and only oral GLP-1 analog, may be represent a promising treatment for PD.
CI  - Copyright (c) 2022 Dong-xing Liu et al.
FAU - Liu, Dong-Xing
AU  - Liu DX
AUID- ORCID: 0000-0002-7269-8888
AD  - Department of Neurology, Shanxi Cardiovascular Hospital, Taiyuan, Shanxi, China.
FAU - Zhao, Chen-Sheng
AU  - Zhao CS
AUID- ORCID: 0000-0003-3113-4987
AD  - Department of Neurology, Shanxi Cardiovascular Hospital, Taiyuan, Shanxi, China.
FAU - Wei, Xiao-Na
AU  - Wei XN
AUID- ORCID: 0000-0003-1954-4246
AD  - Department of Neurology, Shanxi Cardiovascular Hospital, Taiyuan, Shanxi, China.
FAU - Ma, Yi-Peng
AU  - Ma YP
AUID- ORCID: 0000-0001-8997-6015
AD  - Department of Neurology, Shanxi Cardiovascular Hospital, Taiyuan, Shanxi, China.
FAU - Wu, Jian-Kun
AU  - Wu JK
AUID- ORCID: 0000-0003-1112-559X
AD  - Department of Neurology, Shanxi Cardiovascular Hospital, Taiyuan, Shanxi, China.
LA  - eng
PT  - Journal Article
DEP - 20220713
PL  - United States
TA  - Parkinsons Dis
JT  - Parkinson's disease
JID - 101539877
PMC - PMC9300292
COIS- The authors declare that they have no conflicts of interest.
EDAT- 2022/07/26 06:00
MHDA- 2022/07/26 06:01
PMCR- 2022/07/13
CRDT- 2022/07/25 03:39
PHST- 2022/03/10 00:00 [received]
PHST- 2022/06/07 00:00 [revised]
PHST- 2022/06/22 00:00 [accepted]
PHST- 2022/07/25 03:39 [entrez]
PHST- 2022/07/26 06:00 [pubmed]
PHST- 2022/07/26 06:01 [medline]
PHST- 2022/07/13 00:00 [pmc-release]
AID - 10.1155/2022/6813017 [doi]
PST - epublish
SO  - Parkinsons Dis. 2022 Jul 13;2022:6813017. doi: 10.1155/2022/6813017. eCollection 
      2022.