PMID- 33300068
OWN - NLM
STAT- MEDLINE
DCOM- 20210504
LR  - 20230407
IS  - 1791-3004 (Electronic)
IS  - 1791-2997 (Print)
IS  - 1791-2997 (Linking)
VI  - 23
IP  - 2
DP  - 2021 Feb
TI  - Neuroprotective effect of emodin against Alzheimer's disease via Nrf2 signaling 
      in U251 cells and APP/PS1 mice.
LID - 108 [pii]
LID - 10.3892/mmr.2020.11747 [doi]
AB  - Emodin is a naturally‑occurring medicinal herbal ingredient that possesses 
      numerous pharmacological properties, including anti‑inflammatory and antioxidant 
      effects. In the present study, potential neuroprotective effects associated with 
      the antioxidant activity of emodin were assessed in U251 cells that were 
      subjected to beta‑amyloid peptide (Abeta)‑induced apoptosis and in amyloid precursor 
      protein (APP)/presenilin‑1 (PS1) double‑transgenic mice. U251 is a type of human 
      astroglioma cell line (cat. no. BNCC337874; BeNa Culture Collection). In 
      apoptotic U251 cells, 3‑h emodin pre‑treatment prior to 24‑h Abeta co‑exposure 
      improved cell viability, suppressed lactate dehydrogenase leakage and caspase‑3, 
      ‑8 and ‑9 activation to inhibit apoptosis. Compared with those after Abeta exposure 
      alone, emodin ameliorated the dissipation of the mitochondrial membrane 
      potential, inhibited the over‑accumulation of reactive oxygen species, enhanced 
      the expression levels of nuclear factor‑erythroid‑2‑related factor 2 (Nrf2), 
      haemeoxygenase‑1, superoxide dismutase 1, Bcl‑2 and catalase in addition to 
      decreasing the expression levels of Bax. In APP/PS1 mice, an 8‑week course of 
      emodin administration improved spatial memory and learning ability and decreased 
      anxiety. Emodin was also found to regulate key components in the Nrf2 pathway and 
      decreased the deposition of Abeta, phosphorylated‑tau and 4‑hydroxy‑2‑nonenal in 
      APP/PS1 mice. Taken together, the present data suggest that emodin may serve as a 
      promising candidate for the treatment of Alzheimer's disease.
FAU - Li, Zhiping
AU  - Li Z
AD  - Department of Pharmacy, The First Hospital of Jilin University, Changchun, Jilin 
      130021, P.R. China.
FAU - Bi, Hui
AU  - Bi H
AD  - Department of Anesthesiology, Hospital of Stomatology, Jilin University, 
      Changchun, Jilin 130021, P.R. China.
FAU - Jiang, Hongbo
AU  - Jiang H
AD  - School of Life Sciences, Jilin University, Changchun, Jilin 130012, P.R. China.
FAU - Song, Jingjing
AU  - Song J
AD  - School of Life Sciences, Jilin University, Changchun, Jilin 130012, P.R. China.
FAU - Meng, Qingfan
AU  - Meng Q
AD  - School of Life Sciences, Jilin University, Changchun, Jilin 130012, P.R. China.
FAU - Zhang, Yizhi
AU  - Zhang Y
AD  - Department of Neurology, The Second Hospital of Jilin University, Jilin 
      University, Changchun, Jilin 130041, P.R. China.
FAU - Fei, Xiaofang
AU  - Fei X
AD  - School of Life Sciences, Jilin University, Changchun, Jilin 130012, P.R. China.
LA  - eng
PT  - Journal Article
DEP - 20201210
PL  - Greece
TA  - Mol Med Rep
JT  - Molecular medicine reports
JID - 101475259
RN  - 0 (APP protein, human)
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NFE2L2 protein, human)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (PSEN1 protein, human)
RN  - 0 (Presenilin-1)
RN  - KA46RNI6HN (Emodin)
SB  - IM
EIN - Mol Med Rep. 2023 May;27(5):. PMID: 37026528
MH  - Alzheimer Disease/*drug therapy/genetics/metabolism/pathology
MH  - Amyloid beta-Protein Precursor/genetics/*metabolism
MH  - Animals
MH  - Apoptosis/drug effects/genetics
MH  - Cell Line, Tumor
MH  - Emodin/*pharmacology
MH  - Humans
MH  - Mice
MH  - Mice, Transgenic
MH  - NF-E2-Related Factor 2/genetics/*metabolism
MH  - Neuroprotective Agents/*pharmacology
MH  - Presenilin-1/genetics/*metabolism
PMC - PMC7723071
OTO - NOTNLM
OT  - emodin
OT  - Alzheimer's disease
OT  - beta‑amyloid peptide
OT  - nuclear factor‑erythroid‑2‑related factor 2
OT  - oxidative stress
EDAT- 2020/12/11 06:00
MHDA- 2021/05/05 06:00
PMCR- 2020/12/02
CRDT- 2020/12/10 05:59
PHST- 2020/04/10 00:00 [received]
PHST- 2020/08/17 00:00 [accepted]
PHST- 2020/12/10 05:59 [entrez]
PHST- 2020/12/11 06:00 [pubmed]
PHST- 2021/05/05 06:00 [medline]
PHST- 2020/12/02 00:00 [pmc-release]
AID - 108 [pii]
AID - MMR-0-0-11747 [pii]
AID - 10.3892/mmr.2020.11747 [doi]
PST - ppublish
SO  - Mol Med Rep. 2021 Feb;23(2):108. doi: 10.3892/mmr.2020.11747. Epub 2020 Dec 10.