[Electroacupuncture improves learning-memory ability by down-regulating expression of hippocampal Aβ1-42 and Tau and NF-κB proteins in diabetic rats with cognitive impairment].

OBJECTIVE

To observe the effect of electroacupuncture(EA) on the expression of nuclear transcription factors κB (NF-κB) and Tau protein and content of amyloid (Aβ) in diabetic rats with cognitive impairment, so as to explore its mechanism underlying improvement of learning-memory ability.

METHODS

Male SD rats were randomly divided into normal control (=9), model (=9) and EA (=9) groups. The diabetic mellitus model was established by feeding the rats with high fat and high sugar for 1 month and intraperitoneal injection of STZ (25 mg·kg-1·d-1) for 2 days. EA was applied to "Zusanli"(ST36) and "Neiting"(ST44) for 20 min, alternatively on both side every day, and "Yishu"(EX-B3) was stimulated by twirling the acupuncture needle with uniform reinforcing-reducing method for 1 min, followed by retaining it for 20 min. The treatment was conducted 6 times a week for 4 weeks. The learning-memory ability was evaluated by using Morris water maze swimming test. The blood glucose level was randomly detected by using a glucometer, the content of Aβ1-42 in the hippocampal tissue was detected by ELISA, and the relative expression levels of hippocampal Tau and NF-κB p65 proteins and mRNAs were determined by Western blot and fluorescence quantitative real-time PCR, separately.

RESULTS

After modeling, the blood glucose, escape latency, Aβ1-42 content and the expression levels of Tau and NF-κB p65 proteins and mRNAs in the model group were significantly increased (<0.01, <0.05) in comparison with the normal control group. Following EA intervention, the modeling induced increase of blood glucose, escape latency, Aβ1-42 content and the expression levels of Tau and NF-κB p65 proteins and mRNAs were reversed (<0.05, <0.01).

CONCLUSION

EA can improve the learning-memory ability in rats with diabetic cognitive impairment, which may be related to its function in down-regulating the levels of hippocampal Aβ1-42, Tau and NF-κB proteins.