PMID- 36394770
OWN - NLM
STAT- MEDLINE
DCOM- 20221230
LR  - 20230103
IS  - 1476-3524 (Electronic)
IS  - 1029-8428 (Print)
IS  - 1029-8428 (Linking)
VI  - 40
IP  - 6
DP  - 2022 Dec
TI  - Epigallocatechin-3-gallate Enhances Cognitive and Memory Performance and Protects 
      Against Brain Injury in Methionine-induced Hyperhomocysteinemia Through 
      Interdependent Molecular Pathways.
PG  - 2103-2116
LID - 10.1007/s12640-022-00605-4 [doi]
AB  - Brain injury and cognitive impairment are major health issues associated with 
      neurodegenerative diseases in young and aged persons worldwide. 
      Epigallocatechin-3-gallate (EGCG) was studied for its ability to protect against 
      methionine (Met)-induced brain damage and cognitive dysfunction. Male mice were 
      given Met-supplemented in drinking water to produce hyperhomocysteinemia 
      (HHcy)-induced animals. EGCG was administered daily concurrently with Met by 
      gavage. EGCG attenuated the rise in homocysteine levels in the plasma and the 
      formation of amyloid-beta and tau protein in the brain. Cognitive and memory 
      impairment in HHcy-induced mice were significantly improved by EGCG 
      administration. These results were associated with improvement in glutamate and 
      gamma-aminobutyric acid levels in the brain. EGCG maintained the levels of 
      glutathione and the activity of antioxidant enzymes in the brain. As a result of 
      the reduction of oxidative stress, EGCG protected against DNA damage in 
      Met-treated mice. Moreover, maintaining the redox balance significantly 
      ameliorated neuroinflammation evidenced by the normalization of IL-1beta, IL-6, 
      tumor necrosis factor alpha, C-reactive protein, and IL-13 in the same animals. The 
      decreases in both oxidative stress and inflammatory cytokines were significantly 
      associated with upregulation of the antiapoptotic Bcl-2 protein and 
      downregulation of the proapoptotic protein Bax, caspases 3 and 9, and p53 
      compared with Met-treated animals, indicating a diminution of neuronal apoptosis. 
      These effects reflect and explain the improvement in histopathological 
      alterations in the hippocampus of Met-treated mice. In conclusion, the beneficial 
      effects of EGCG may be due to interconnecting pathways, including modulation of 
      redox balance, amelioration of inflammation, and regulation of antiapoptotic 
      proteins.
CI  - (c) 2022. The Author(s).
FAU - Mostafa, Mostafa D
AU  - Mostafa MD
AD  - Zoology Department, Faculty of Science, Mansoura University, Mansoura, Egypt.
FAU - ElKomy, Magda A
AU  - ElKomy MA
AD  - Zoology Department, Faculty of Science, Mansoura University, Mansoura, Egypt.
FAU - Othman, Azza I
AU  - Othman AI
AD  - Zoology Department, Faculty of Science, Mansoura University, Mansoura, Egypt.
FAU - Amer, Maggie E
AU  - Amer ME
AD  - Zoology Department, Faculty of Science, Mansoura University, Mansoura, Egypt.
FAU - El-Missiry, Mohamed A
AU  - El-Missiry MA
AUID- ORCID: 0000-0002-4566-0497
AD  - Zoology Department, Faculty of Science, Mansoura University, Mansoura, Egypt. 
      elmissiry@mans.edu.eg.
LA  - eng
PT  - Journal Article
DEP - 20221117
PL  - United States
TA  - Neurotox Res
JT  - Neurotoxicity research
JID - 100929017
RN  - AE28F7PNPL (Methionine)
RN  - BQM438CTEL (epigallocatechin gallate)
RN  - 0 (Apoptosis Regulatory Proteins)
RN  - 8R1V1STN48 (Catechin)
RN  - 73JWT2K6T3 (Racemethionine)
SB  - IM
MH  - Mice
MH  - Male
MH  - Animals
MH  - Methionine/pharmacology
MH  - *Hyperhomocysteinemia/chemically induced/complications/drug therapy
MH  - Oxidative Stress
MH  - Cognition
MH  - Apoptosis Regulatory Proteins
MH  - *Catechin/pharmacology/therapeutic use
MH  - Racemethionine/pharmacology
MH  - *Brain Injuries
PMC - PMC9797462
OTO - NOTNLM
OT  - Epigallocatechin-3-gallate
OT  - Hyperhomocysteinemia
OT  - Methionine
OT  - Morris water maze
OT  - Neurotoxicity
COIS- The authors declare no competing interests.
EDAT- 2022/11/18 06:00
MHDA- 2022/12/31 06:00
PMCR- 2022/11/17
CRDT- 2022/11/17 13:58
PHST- 2022/09/15 00:00 [received]
PHST- 2022/11/08 00:00 [accepted]
PHST- 2022/10/25 00:00 [revised]
PHST- 2022/11/18 06:00 [pubmed]
PHST- 2022/12/31 06:00 [medline]
PHST- 2022/11/17 13:58 [entrez]
PHST- 2022/11/17 00:00 [pmc-release]
AID - 10.1007/s12640-022-00605-4 [pii]
AID - 605 [pii]
AID - 10.1007/s12640-022-00605-4 [doi]
PST - ppublish
SO  - Neurotox Res. 2022 Dec;40(6):2103-2116. doi: 10.1007/s12640-022-00605-4. Epub 
      2022 Nov 17.