The Relationship Study on Inflammation Factors, Trx and Neuronapoptosis on Multiplealzheimer’s Disease Rat Model
|Course||Human Anatomy and Embryology|
|Keywords||Alzheimer’s disease Thioredoxin Inflammation factors Apoptosis ERK|
Objective：According to the Aβ1-42and D-galactose induced aging theory, on the basisof subacute aging model，we established a multiple Alzheimer disease animal modelthrough injecting Aβ1-42to the lateral ventricle. Based on this, we were to observe thelearning and memory ability of these rats; to study and compare the expression ofinflammation factors between the control group rats and the AD model group rats; todiscuss the correlation between inflammation factors and AD; and to investigate therelationship between the expression of Trx in the AD model group rats brain and the nervecell apoptosis pathway. We try to find some new evidences in the scientific theory for thepathogenesis of neurodegenerative diseases and clinical prevention.Methods:(1) Injected D-Galactose peritoneally combined with injected Aβ1-42to lateralventricle to establish a multiple Alzheimer disease animal model (B group). And normalrats were selected as the control group (A group).(2) Behavior test. Using Morris water maze test two groups of rats’ learning andmemory ability(3) Morphological observation. Using the hematoxylin eosin staining method toobserve the changes of neurons form and quantity(4) Histology observation. Observe the changes of Tau protein quantity.(5) Using ELISA to assay the expression of the inflammatory factors (CRP，IL-1β，IL-6and TNF-α) in brain cortex、hippocampus、striatum、cerebellum and periodontaltissue.(6) Immunohistochemical detection. Detect the expressions of Trx、 ERK andp38MAPK in different area of brain tissue(7) Biological information verification on the relationship between Trx、MAPKpathway and AD. Results:(1) Study of behavior experiments showed that: compared with the control group, thememory ability of AD model group were significantly decreased (P<0.01).(2) HE staining experiment results showed that: compared with the control group, thenumber of neurons in the AD model group had considerable reduced with statisticallysignificant difference (P<0.01). Morphological changes were visible, such as nuclearpyknosis、smaller cell body, etc.(3) Immunohistochemical detection results showed that: compared with group A,group B of the Tau protein expression significantly increased.(4) Immunohistochemical detection results showed that: in the cortex、hippocampus、serum and the periodontal tissue of AD model group, the expressions of inflammatoryfactors associated (CRP，IL-1β，IL-6and TNF-α) increased significantly in statistics(P<0.05or P <0.01) versus the control group; The expression differences of theseinflammatory factors in the striatum and cerebellum were not obvious or not statisticallysignificant versus the control group.(5) The expression differences of Trx、ERK and p38MAPK between model group andcontrol group were statistically significant; Biological information was verified withregulating the relationship between them.Conclusion:(1) It is more successful in establishing a multiple Alzheimer disease animal model onthe basis of aging, preliminary study the potential relationship between aging and AD.(2) On the basis of D-galactose subacute aging model, established the multipleAlzheimer disease animal model with beta-amyloid. This model can well simulate thepathological feature of ADs in behavior、biochemical indicators and histologically. It cannot only to be used for fundamental research of the old dementia, but also to investigate theprevention and cure of the old dementia.(3) Base of the multiple Alzheimer disease animal model established by D-galactoseand Aβ1-42, the expression of Trx and ERK in brain regions were significantly decreased,and the expression of p38MAPK was significantly increased. These may hint an importantrelationship between Turks and cell apoptosis in ADs.(4) Base of the multiple Alzheimer disease animal model established by D-galactoseand Aβ1-42, the expression of inflammatory factors associated (CRP，IL-1β，IL-6and TNF-α) significantly increased. And the increase of inflammatory cytokines, in turn,accelerated the process of AD. Therefore, inhibition of inflammation may be one ofimportant factors should be considered in the clinical treatment of ADs.