Influence of electroacupuncture therapy of tonifying the kidney and regulating governor vessel on Aβ related degradation enzymes in the hippocampus of a rat model of Alzheimer's disease induced by Aβ1-42.

Abstract Objective To explore influence of electroacupuncture (EA) therapy of tonifying the kidney and regulating governor vessel on amyloid beta (Aβ) related degradation enzymes in the hippocampus of a rat model of Alzheimer's disease (AD) induced by Aβ 1-42. Methods Forty Wistar male rats were randomly divided into 4 groups: a normal group, a sham operation group, a model group and an EA group, 10 rats in each one. The rats in normal group were normally fed. The rats in sham operation group were bilaterally injected in the hippocampus with 5 µL of saline and they were normally fed after the injection. The rats in the model group and the EA group were bilaterally injected in the hippocampus with 5 µL of Aβ 1-42 on each side. Rats in the EA group received EA of 5 Hz continuous wave at the "Băihuì (百会 GV20)" and bilateral "Shènshū (肾俞 BL23)" for a duration of 15 min per time every day and continuously for 15 days. After 15 days, the hippocampal expression levels of insulin degrading enzyme (IDE), lipoprotein (LPL), transthyretin (TTR), apolipoprotein E (APoE), α2 macroglobulin (α 2 M) and Aβ 1-42 of the 4 groups were tested by Western blot. Results Compared with the sham operation group, the expression levels of IDE, LPL, TTR, APoE and α2M in the hippocampus were significantly lower (P < 0.05, P < 0.01) and the expression of Aβ 1-42 was significantly higher(P < 0.01) in the model group. Compared with the model group, the expression levels of IDE, LPL, TTR, APoE and α2M in the hippocampus of these rats were significantly lower (P < 0.05, P < 0.01), the expression of Aβ 1-42 was significantly higher(P < 0.01) in the EA group. Conclusion EA therapy of tonifying the kidney and regulating governor vessel can enhance the expression of IDE, LPL, TTR, APoE, and α 2 M in the hippocampus of AD rats injected by Aβ 1-42 , and may consequently promote the degradation of aβ 1-42 to help improve the pathological manifestations of AD and therefore delay its progression. [ABSTRACT FROM AUTHOR]