PMID- 23134284
OWN - NLM
STAT- MEDLINE
DCOM- 20130610
LR  - 20191210
IS  - 1744-5116 (Electronic)
IS  - 1388-0209 (Linking)
VI  - 51
IP  - 1
DP  - 2013 Jan
TI  - Borneol alleviates oxidative stress via upregulation of Nrf2 and Bcl-2 in SH-SY5Y 
      cells.
PG  - 30-5
LID - 10.3109/13880209.2012.700718 [doi]
AB  - CONTEXT: The beta-amyloid (Abeta) peptide aggregation with accompanying oxidative 
      stress plays the major role in the pathogenesis of Alzheimer's disease (AD). Some 
      natural compounds, including borneol, shed promising light on AD treatment. 
      OBJECTIVE: The present study was designed to investigate the antioxidative, 
      antiapoptotic effects, and neuroprotection of borneol in human neuroblastoma 
      cells (SH-SY5Y). MATERIALS AND METHODS: Oxidative stress was induced by 
      administering 50 microM Abeta into SH-SY5Y cells. Neuroprotective effect of commercially 
      available borneol was examined by determining cell viability with the MTT assay. 
      Intracellular reactive oxygen species (ROS) generation was measured using a 
      fluorometer with further examination of heme oxygenase-1 (HO-1) and nuclear 
      factor-erythroid 2 p45-related factor 2 (Nrf2) expression. Apoptosis was examined 
      by measuring the ratio of B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein 
      (Bax). RESULTS: Our data indicated that Abeta-induced cell cytotoxicity was 
      inhibited by 100 microM of (-) and (+) borneol treatment. Treatment of borneol 
      significantly decreased ROS generation (P < 0.01). The expression of HO-1 and 
      nuclear translocation of Nrf2 were increased by Abeta treatment. This nuclear 
      translocation of Nrf2 was further increased by administration of borneol. 
      Compared with the Abeta treated group, the (+) borneol treated group significantly 
      increased Bcl-2 expression with decreased expression of Bax. DISCUSSION AND 
      CONCLUSION: Borneol protected SH-SY5Y cells against Abeta-induced toxicity, exerted 
      an antioxidative effect and suppressed apoptosis. It increases our knowledge 
      about neuroprotective mechanism of borneol, and it is hopeful to be a candidate 
      compound for developing therapeutic drug for the prevention and treatment of AD 
      and other Abeta-related neurodegenerative diseases.
FAU - Hur, Jinyoung
AU  - Hur J
AD  - Division of Metabolism and Functionality Research, Korea Food Research Institute, 
      Seongnam-si, Gyeonggi-do, Republic of Korea.
FAU - Pak, Sok Cheon
AU  - Pak SC
FAU - Koo, Byung-Soo
AU  - Koo BS
FAU - Jeon, Songhee
AU  - Jeon S
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121108
PL  - England
TA  - Pharm Biol
JT  - Pharmaceutical biology
JID - 9812552
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Antioxidants)
RN  - 0 (Camphanes)
RN  - 0 (NF-E2-Related Factor 2)
RN  - 0 (NFE2L2 protein, human)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Peptide Fragments)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (amyloid beta-protein (1-42))
RN  - 0 (bcl-2-Associated X Protein)
RN  - L88RA8N5EG (isoborneol)
SB  - IM
MH  - Amyloid beta-Peptides/antagonists & inhibitors/toxicity
MH  - Antioxidants/chemistry/pharmacology
MH  - Apoptosis/drug effects
MH  - Camphanes/chemistry/*pharmacology
MH  - Cell Line, Tumor
MH  - Cell Survival/drug effects
MH  - Fluorometry
MH  - Humans
MH  - NF-E2-Related Factor 2/genetics
MH  - Neuroblastoma/metabolism
MH  - Neuroprotective Agents/chemistry/*pharmacology
MH  - Oxidative Stress/*drug effects
MH  - Peptide Fragments/antagonists & inhibitors/toxicity
MH  - Proto-Oncogene Proteins c-bcl-2/genetics/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Up-Regulation/drug effects
MH  - bcl-2-Associated X Protein/genetics/metabolism
EDAT- 2012/11/09 06:00
MHDA- 2013/06/12 06:00
CRDT- 2012/11/09 06:00
PHST- 2012/11/09 06:00 [entrez]
PHST- 2012/11/09 06:00 [pubmed]
PHST- 2013/06/12 06:00 [medline]
AID - 10.3109/13880209.2012.700718 [doi]
PST - ppublish
SO  - Pharm Biol. 2013 Jan;51(1):30-5. doi: 10.3109/13880209.2012.700718. Epub 2012 Nov 
      8.