[Effects of Electroacupuncture Intervention on Oxygen Free Radicals and Expression of Apoptosis-related Proteins in Rats with Ischemic Learning and Memory Disorder].

Abstract

OBJECTIVE:

To observe the effect of electroacupuncture (EA) therapy on levels of oxygen free radicals (OFR) and hippocampal apoptosis-related protein expression in ischemic learning-memory disorder rats so as to investigate its mechanisms underlying improvement of ischemic learning-memory impairment.

METHODS:

A total of 60 SD rats were randomly divided into sham operation (sham), model, medication, and EA groups, with 15 rats in each group. The learning-memory disorder model was made by occlusion of bilateral carotid arteries. EA (2- 3 Hz, 2 mA) was applied to "Zhi San Zhen" ["Shenting" (GV 24) and bilateral "Benshen" (GB 13)] for 30 min, once a day for 3 weeks. The rats of the medication group were treated by lavage of Aricept (0.03 mg . kg(-1) . d(-1)), once daily for 3 weeks. The rats' learning-memory ability was detected by Morris water maze tests and the state of hippocampal apoptosis cells was observed by light microscope after TUNEL staining and the expression of hippocampal Bcl-2, Bax and Caspase-3 proteins was detected by immunohistochemistry. Serum and hippocampal superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity and malondialdehyde (MDA) contents were detected by chemical colorimetric analysis.

RESULTS:

Compared with the sham group, the escape latencies (place-navigation) after modeling were evidently prolonged, and the times of target-platform crossing in 90 sec (spatial probe test) considerably reduced in the model group (P<0.01), suggesting an impairment of learning-memory ability. After the treatment for 21 d, the increased escape latency and the reduced target-platform crossing time in both EA and medication groups were reversed in comparison with the model group (P<0.01), suggesting an improvement of memory ability, and the effect of the EA group was significantly superior to that of the medication group (P<0.05). Compared with the sham group, the number of apoptotic cells in hippocampal CA 1- CA 3 regions, and the expression levels of hippocampal Bcl-2, Bax and Caspase-3 proteins, and serum and hippocampal MDA contents were significantly increased in the model group (P<0.01), while serum and hippocampal SOD and GSH-Px levels obviously decreased in the model group (P<0.01). After the treatment for 21 days, compared to the model group, the number of the apoptotic cells, the expression levels of hippocampal Bax and Caspase--3 proteins, and the contents of serum and hippocampal MDA were notably decreased in the EA and medication groups (P<0.01), whereas, Bcl-2 protein expression levels, and serum and hippocampal SOD and GSH-Px activity were notably up-regulated in the EA and medication groups (P<0.01). The effects of EA group were obviously superior to those of medication group in increasing hippocampal Bcl-2 immunoactivity, serum SOD and GSH-Px and hippocampal GSH-Px activity and in down-regulating serum MDA level (P<0.01, P<0.05).

CONCLUSION:

Electroacupuncture intervention can improve learning-memory ability in ischemic learning-memory disorder rats which may be associated with its effects in reducing blood and hippocampal OFR contents and hippocampal cellular apoptosis.

• Authors: Zhi-tao Hou, Zhong-ren Sun, Song-tao Liu, Sheng-biao Xiong, Yi-tian Liu, Xiao-xia Han, Hong-fang Sun, Yu-sheng Han, Hong-na Yin, Jin-qiao Xu, Dong-dong Li
• Journal: Zhen ci yan jiu = Acupuncture research (Zhen Ci Yan Jiu) Vol. 40 Issue 6 Pg. 431-8 (Dec 2015) ISSN: 1000-0607 [Print] China
• PMID: 26887202 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Apoptosis Regulatory Proteins
• Reactive Oxygen Species
• Malondialdehyde
• Glutathione Peroxidase
• Superoxide Dismutase

Topics

• Acupuncture Points
• Animals
• Apoptosis Regulatory Proteins (genetics, metabolism)
• Electroacupuncture
• Glutathione Peroxidase (metabolism)
• Humans
• Ischemia (complications, psychology)
• Learning
• Learning Disabilities (etiology, genetics, metabolism, therapy)
• Male
• Malondialdehyde (metabolism)
• Memory
• Memory Disorders (etiology, genetics, metabolism, therapy)
• Rats
• Rats, Sprague-Dawley
• Reactive Oxygen Species (metabolism)
• Superoxide Dismutase (metabolism)