PMID- 35815397
OWN - NLM
STAT- MEDLINE
DCOM- 20240304
LR  - 20240304
IS  - 1563-5279 (Electronic)
IS  - 0020-7454 (Linking)
VI  - 134
IP  - 3
DP  - 2024 Jun
TI  - Sinomenine exerts a neuroprotective effect on PD mouse model through inhibiting 
      PI3K/AKT/mTOR pathway to enhance autophagy.
PG  - 301-309
LID - 10.1080/00207454.2022.2100780 [doi]
AB  - BACKGROUND: Parkinson's disease (PD), as a chronic and progressive 
      neurodegenerative disease, is associated with autophagy. This study focused on 
      the regulation of sinomenine (SN) on autophagy in PD and its related mechanism. 
      METHODS: The PD mouse model was constructed by MPTP inducement, and the mouse 
      motor function after modeling and SN treatment was examined by rotarod, grip 
      strength, and foot printing tests. Tyrosine hydroxylase (TH)/LC3B-positive 
      neurons in the substantia nigra pars compacta of mouse brains were detected by 
      immunofluorescence. The expressions of proteins related to autophagy (Beclin1, 
      p62, LC3-I and LC3-II) and phosphorylated phosphoinositide 3-kinase 
      (PI3K)/AKT/mechanistic target of rapamycin kinase (mTOR) signaling pathway were 
      measured by western blot. Rescue experiments were performed to determine the 
      effects of MHY1485 (mTOR activator) on SN-treated PD mice. RESULTS: SN 
      potentiated the motor ability in PD mice, promoted the survival of dopaminergic 
      neurons, increased the protein expression level of Beclin1, LC3-II/LC3-I ratio 
      and LC3B-positive neurons, lowered the protein expression level of p62 and 
      inactivated PI3K/AKT/mTOR pathway in the substantia nigra tissue of mouse brains. 
      Moreover, MHY1485 reversed the above effects of SN on PD mice via reactivating 
      PI3K/AKT/mTOR pathway. CONCLUSION: SN augments the autophagy of dopaminergic 
      neurons via inhibiting the PI3K/AKT/mTOR pathway and exerts a neuroprotective 
      effect on PD mice.
FAU - Bao, Xi
AU  - Bao X
AD  - Department of Geriatrics, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese 
      Medical University, Hangzhou, Zhejiang, China.
FAU - He, Yingchun
AU  - He Y
AD  - Department of Geriatrics, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese 
      Medical University, Hangzhou, Zhejiang, China.
FAU - Huang, Lin
AU  - Huang L
AD  - Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
FAU - Li, Haichang
AU  - Li H
AD  - Zhejiang Chinese Medical University, Hangzhou, Zhejiang, China.
FAU - Li, Qiang
AU  - Li Q
AD  - Department of Geriatrics, Hangzhou TCM Hospital Affiliated to Zhejiang Chinese 
      Medical University, Hangzhou, Zhejiang, China.
FAU - Huang, Yun
AU  - Huang Y
AD  - Department of Chinese Medicine Gynecology, Hangzhou TCM Hospital, Zhejiang 
      Chinese Medical University, Hangzhou, Zhejiang, China.
LA  - eng
PT  - Journal Article
DEP - 20220718
PL  - England
TA  - Int J Neurosci
JT  - The International journal of neuroscience
JID - 0270707
RN  - EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
RN  - 0 (Neuroprotective Agents)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
RN  - 63LT81K70N (sinomenine)
RN  - EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
RN  - 0 (Beclin-1)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
RN  - 0 (Morphinans)
SB  - IM
MH  - Animals
MH  - Mice
MH  - Phosphatidylinositol 3-Kinase
MH  - *Neuroprotective Agents/pharmacology
MH  - Phosphatidylinositol 3-Kinases
MH  - Proto-Oncogene Proteins c-akt
MH  - Beclin-1
MH  - *Neurodegenerative Diseases
MH  - *Parkinson Disease
MH  - TOR Serine-Threonine Kinases
MH  - Autophagy
MH  - Disease Models, Animal
MH  - Dopaminergic Neurons
MH  - *Morphinans
OTO - NOTNLM
OT  - PI3K/AKT/mTOR signaling pathway
OT  - Parkinson's disease
OT  - autophagy
OT  - sinomenine
EDAT- 2022/07/12 06:00
MHDA- 2024/03/04 06:46
CRDT- 2022/07/11 04:34
PHST- 2024/03/04 06:46 [medline]
PHST- 2022/07/12 06:00 [pubmed]
PHST- 2022/07/11 04:34 [entrez]
AID - 10.1080/00207454.2022.2100780 [doi]
PST - ppublish
SO  - Int J Neurosci. 2024 Jun;134(3):301-309. doi: 10.1080/00207454.2022.2100780. Epub 
      2022 Jul 18.