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
HE Chao, YUAN Ai-hong, YANG Jun, et al. 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[J]. Acupuncture research, 2022, 47(6): 485-490.
HE Chao, YUAN Ai-hong, YANG Jun, et al. 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[J]. Acupuncture research, 2022, 47(6): 485-490. DOI: 10.13702/j.1000-0607.20210707.
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(n=9)
model(n=9) and EA(n=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)·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(P
<
0.01
P
<
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(P
<
0.05
P
<
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