PMID- 23821590
OWN - NLM
STAT- MEDLINE
DCOM- 20140124
LR  - 20171116
IS  - 1477-0903 (Electronic)
IS  - 0960-3271 (Linking)
VI  - 32
IP  - 7
DP  - 2013 Jul
TI  - Serrapeptase and nattokinase intervention for relieving Alzheimer's disease 
      pathophysiology in rat model.
PG  - 721-35
LID - 10.1177/0960327112467040 [doi]
AB  - Serrapeptase (SP) and nattokinase (NK) are proteolytic enzymes belonging to 
      serine proteases. In this study, we hypothesized that SP and NK could modulate 
      certain factors that are associated with Alzheimer's disease (AD) pathophysiology 
      in the experimental model. Oral administration of aluminium chloride (AlCl3) in a 
      dose of 17 mg/kg body weight (bw) daily for 45 days induced AD-like pathology in 
      male rats with a significant increase in brain acetylcholinesterase (AchE) 
      activity, transforming growth factor beta (TGF-beta), Fas and interleukin-6 (IL-6) 
      levels. Meanwhile, AlCl3 supplementation produced significant decrease in 
      brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-1 (IGF-1) 
      when compared with control values. Also, AlCl3 administration caused significant 
      decline in the expression levels of disintegrin and metalloproteinase domain 9 
      (ADAM9) and a disintegrin and metalloproteinase domain 10 (ADAM10) genes in the 
      brain. Histological investigation of brain tissue of rat model of AD showed 
      neuronal degeneration in the hippocampus and focal hyalinosis with cellular as 
      well as a cellular amyloid plaques formation. Oral administration of SP or NK in 
      a rat model of AD daily for 45 days resulted in a significant decrease in brain 
      AchE activity, TGF-beta, Fas and IL-6 levels. Also, the treatment with these enzymes 
      produced significant increase in BDNF and IGF-1 levels when compared with the 
      untreated AD-induced rats. Moreover, both SP and NK could markedly increase the 
      expression levels of ADAM9 and ADAM10 genes in the brain tissue of the treated 
      rats. These findings were well confirmed by the histological examination of the 
      brain tissue of the treated rats. The present results support our hypothesis that 
      the oral administration of proteolytitc enzymes, SP and/or NK, would have an 
      effective role in modulating certain factors characterizing AD. Thus, these 
      enzymes may have a therapeutic application in the treatment of AD.
FAU - Fadl, N N
AU  - Fadl NN
AD  - Medical Physiology Department, National Research Centre, Dokki, Cairo, Egypt.
FAU - Ahmed, H H
AU  - Ahmed HH
FAU - Booles, H F
AU  - Booles HF
FAU - Sayed, A H
AU  - Sayed AH
LA  - eng
PT  - Journal Article
PL  - England
TA  - Hum Exp Toxicol
JT  - Human & experimental toxicology
JID - 9004560
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Disintegrins)
RN  - 0 (Interleukin-6)
RN  - 0 (Transforming Growth Factor beta)
RN  - 0 (fas Receptor)
RN  - 67763-96-6 (Insulin-Like Growth Factor I)
RN  - EC 3.1.1.8 (Cholinesterases)
RN  - EC 3.4.- (Peptide Hydrolases)
RN  - EC 3.4.21.- (Subtilisins)
RN  - EC 3.4.24.- (ADAM Proteins)
RN  - EC 3.4.24.- (Adam9 protein, rat)
RN  - EC 3.4.24.81 (ADAM10 Protein)
RN  - EC 3.4.24.81 (ADAM10 protein, rat)
RN  - H81695M5OP (nattokinase)
RN  - NL053ABE4J (serratiopeptidase)
SB  - IM
MH  - ADAM Proteins/genetics
MH  - ADAM10 Protein
MH  - Alzheimer Disease/*drug therapy/metabolism
MH  - Animals
MH  - Brain/drug effects/metabolism/pathology
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cholinesterases/metabolism
MH  - Disease Models, Animal
MH  - Disintegrins/genetics
MH  - Insulin-Like Growth Factor I/metabolism
MH  - Interleukin-6/metabolism
MH  - Male
MH  - Peptide Hydrolases/pharmacology/*therapeutic use
MH  - Rats
MH  - Subtilisins/pharmacology/*therapeutic use
MH  - Transforming Growth Factor beta/metabolism
MH  - fas Receptor/metabolism
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - nattokinase
OT  - proteolytic enzymes
OT  - rats
OT  - serrapeptase
EDAT- 2013/07/04 06:00
MHDA- 2014/01/25 06:00
CRDT- 2013/07/04 06:00
PHST- 2013/07/04 06:00 [entrez]
PHST- 2013/07/04 06:00 [pubmed]
PHST- 2014/01/25 06:00 [medline]
AID - 32/7/721 [pii]
AID - 10.1177/0960327112467040 [doi]
PST - ppublish
SO  - Hum Exp Toxicol. 2013 Jul;32(7):721-35. doi: 10.1177/0960327112467040.