Abstract
To determine whether electro-acupuncture (EA) therapy could improve the cognitive functions of amyloid precursor protein Swedish mutation (APPswe)/presenilin 1 deleted in exon 9 (PS1dE9) mice and examine whether EA treatment could attenuate neuroinflammation by targeting the toll-like receptor 4 (TLR4)/myeloid differentiation primary response factor 88 (MyD88) signaling pathway.
Twenty-seven double transgenic APPswe/PS1dE9 mice were randomly allocated into three groups: an Alzheimer's disease model group (AD group), a medication group (M group) and an EA treatment group (EA group). Each group contained nine mice, and nine wild-type mice were used in a normal group (N group). The animals in the M group were treated with oral administrations of 0.92 mg/kg donepezil hydrochloride for 15 days. For animals in the EA group, EA treatments were used on the Yintang (GV 29) and Baihui (GV 20) acupoints for 20 minutes, and the Shuigou (GV 26) acupoint was pricked without needle retention following EA treatments. Following treatments, the spatial learning and memory of the mice were measured using the Morris water maze test. The expression levels of TLR4, MyD88, nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) were analyzed by immunohistochemical staining and western blot.
The escape latencies of the M and EA groups were significantly lower than those of the AD group (vs M, P = .002; vs EA, P < .001). Moreover, compared with the AD group, the numbers of platform crossings was higher (vs M, P = .038; vs EA, P = .008) and the latency time for target quadrants was longer (vs M, P = .002; vs EA, P = .001) in the M and EA groups (P < .05). Furthermore, in the M and EA groups, the expression levels of TLR4, MyD88, NF-κB and iNOS decreased significantly compared with those of the AD group (all P < .01).
EA treatment enhanced the memory and learning abilities of APPswe/PS1dE9 mice by regulating the TLR4/MyD88 inflammatory signaling pathway.
