Evaluation of aβ deposits in hippocampus of ad rat model after intravenous injection of hadscs by immuno- and thioflavin s- costaining
Mina Eftekharzadeh,
1,* Maryam doshmanziari,
2 Marjan shariatpanahi,
3 Arash sarveazad3,
4 Fatemeh moradi,
5
1. Department of Anatomy, Iran University of Medical Sciences, Tehran, Iran
2. Department of Anatomy, Iran University of Medical Sciences, Tehran, Iran
3. Department of Toxicology & Pharmacology, School of Pharmacy, International Campus, Iran University of Medical Sciences, Tehran, Iran
4. Colorectal Research Center, Iran University of Medical Sciences, Tehran, Iran
5. Department of Anatomy, Iran University of Medical Sciences, Tehran, Iran
Abstract
Introduction
Alzheimer,s disease (ad) is a progressive neuropsychiatry disorder that
gradually deteriorates memory and behavioral functions. amyloid beta (aβ) is
considered as the most toxic substances in the ad brain. aβ immunofluorecent
staining distinguishes fibrillar and non-fibrillar aβ, whereas thioflavin-s (thio-s)
identifies the β-pleated fibrillar amyloid form of ad. the present study was designed to
evaluate aβ deposits in hippocampus of ad rat model after intravenous injection of
human adipose derived stem cells (hadscs).
Methods
Twenty-four male rats were used in 4 groups; control, sham, ad rat model,
and hadscs treatment group. the hadscs characterization was confirmed by
flowcytometry technique. an immuno- and thioflavin s- costaining (double staining
method) wasutilized for detecting aβ plaques in ad rat model following injection of
hadscs.
Results
Statistical analysis revealed that administration of hadscs significantly
decreased immunoreactive and thio-s positive plaques number in ad group (###pvalue<
0.001). we also found that the plaques detected by anti-beta amyloid antibody
were significantly more than plaques which distinguished by thio-s in all the groups (f
[3, 40] = 0.15, p =0.928). conclusion: consequently, our results showed that the
hadscs had effective role in decreasing amyloid aggregation following migration to
the site of injury.
Conclusion
As aβ toxicity is the major reason of neuronal death in ad, hadsc
may be a promising candidate for ad therapy due to its high potential for clearance of
aβ deposits.
Keywords
Alzheimer ,s disease; thioflavin; amyloid beta-protein; stem cell transplantation