PMID- 30338822
OWN - NLM
STAT- MEDLINE
DCOM- 20191212
LR  - 20191217
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 22
IP  - 19
DP  - 2018 Oct
TI  - Neuroprotective effects of alpha-lipoic acid on long-term experimental autoimmune 
      encephalomyelitis.
PG  - 6517-6528
LID - 16066 [pii]
LID - 10.26355/eurrev_201810_16066 [doi]
AB  - OBJECTIVE: Experimental autoimmune encephalomyelitis (EAE) is an animal model 
      commonly used in research on the acute phase of multiple sclerosis (MS), but 
      studies on the pathology and pathogenesis of EAE with a long disease course are 
      seldom conducted. Besides its antioxidant properties, the comprehensive 
      mechanisms through which alpha-lipoic acid (LA) affects EAE remain obscure. We here 
      conducted the study to explore the possible mechanisms. MATERIALS AND METHODS: In 
      this study, the following methods were used for investigating the effects of LA 
      on long-term EAE: hematoxylin-eosin staining (HE) and electron microscopic 
      examinations of pathological changes; Western blotting of beta-amyloid precursor 
      protein (beta-APP) and myelin basic protein (MBP); Enzyme-linked immunosorbent assay 
      (ELISA) of tumor necrosis factor-alpha (TNF-alpha), transforming growth factor-beta (TGF-beta), 
      superoxide dismutase (SOD), malondialdehyde (MDA) as well as flow cytometry of 
      CD4+CD25+FoxP3+ regulatory T cells (Tregs). RESULTS: The results showed: (1) 
      diverse pathological features of long-term relapsing-remitting EAE; (2) 
      relatively increased MBP and reduced beta-APP expression in LA recipients 180 days 
      after onset; (3) down-regulated TNF-alpha and up-regulated TGF-beta levels in LA 
      recipients 7 days after onset; (4) lower MDA and higher SOD levels in LA 
      recipients 180 days after onset; (5) increased Treg levels in LA recipients 7 
      days after onset. CONCLUSIONS: Aside from oxidative stress, LA possessed 
      anti-inflammatory and immunomodulatory effects on EAE. LA might be a promising 
      candidate for MS treatment.
FAU - Li, B
AU  - Li B
AD  - Department of Neurology, the Second Hospital of Hebei Medical University, 
      Shijiazhuang, Hebei, China. guoli6@163.com.
FAU - Tan, G-J
AU  - Tan GJ
FAU - Lin, H-Q
AU  - Lin HQ
FAU - Zhang, J-N
AU  - Zhang JN
FAU - Guo, L
AU  - Guo L
FAU - Chen, L-P
AU  - Chen LP
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antioxidants)
RN  - 0 (Immunologic Factors)
RN  - 0 (Mbp protein, mouse)
RN  - 0 (Myelin Basic Protein)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 73Y7P0K73Y (Thioctic Acid)
SB  - IM
MH  - Amyloid beta-Protein Precursor/metabolism
MH  - Animals
MH  - Anti-Inflammatory Agents/pharmacology
MH  - Antioxidants/pharmacology
MH  - Encephalomyelitis, Autoimmune, 
      Experimental/immunology/metabolism/pathology/*prevention & control
MH  - Immunologic Factors/pharmacology
MH  - Mice, Inbred C57BL
MH  - Myelin Basic Protein/metabolism
MH  - Neuroprotective Agents/*pharmacology
MH  - Oxidative Stress/drug effects
MH  - Spinal Cord/*drug effects/immunology/metabolism/pathology
MH  - T-Lymphocytes, Regulatory/drug effects/immunology/metabolism
MH  - Thioctic Acid/*pharmacology
MH  - Time Factors
MH  - Transforming Growth Factor beta/metabolism
MH  - Tumor Necrosis Factor-alpha/metabolism
EDAT- 2018/10/20 06:00
MHDA- 2019/12/18 06:00
CRDT- 2018/10/20 06:00
PHST- 2018/10/20 06:00 [entrez]
PHST- 2018/10/20 06:00 [pubmed]
PHST- 2019/12/18 06:00 [medline]
AID - 16066 [pii]
AID - 10.26355/eurrev_201810_16066 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2018 Oct;22(19):6517-6528. doi: 
      10.26355/eurrev_201810_16066.