Objective: To observe the effect of electroacupuncture (EA) on motor function, calpain and calpastatin expression in rats with spinal cord injury, so as to explore the mechanism of EA underlying improvement of acute spinal cord injury.
Methods: Thirty male SD rats were randomly divided into sham operation group, model group and EA group, with 10 rats in each group. The acute moderate spinal cord injury model was established by using a NYU spinal cord impactor. EA was applied to "Jizhong"(GV6) and "Mingmen" (GV4) for 30 min, once daily for 28 d. The Basso, Beattie and Bresnahan (BBB) rating scale (0 to 21 points) was used to assess changes of locomotor function. Histopathological changes of the injured spinal cord were observed after sectioning and Nissl staining, and the expression levels of calpain1, calpain2 and calpastatin mRNA and protein in the spinal cord tissues were detected by using quantitative real-time PCR and Western blot, respectively.
Results: The BBB score of the model group was significantly lower than that of the sham operation group (<0.01), and was significantly higher in the EA group than that of the model group on 14th and 28th day (<0.01). Compared with the sham operation group, the number of neurons in the model group decreased, and Nissl body stained cells decreased or even disappeared, which was evidently milder in the EA group. Compared with the sham operation group, the expression levels of calpain1 mRNA and protein in the spinal cord of the model group were significantly increased (<0.01), while the expression levels of calpastatin mRNA and protein were significantly reduced (<0.01). Following EA intervention, in contrast to the model group, the expression levels of calpain1 mRNA and protein in the EA group were significant down-regulated (<0.01), calpastatin mRNA and protein expression levels were significantly up-regulated(<0.01). There was no significant difference in calpain2 mRNA and protein expression among the 3 groups(>0.05).
Conclusion: EA can improve the locomotor function of rats with spinal cord injury, which may be related to its effect in inhibiting the activity of calpain in the injured spinal cord.
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http://dx.doi.org/10.13702/j.1000-0607.200102 | DOI Listing |
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Department of Microbiology, Immunology, and Cell Biology, School of Medicine, West Virginia University, Morgantown, WV 26506, USA.
The complex set of interactions between the immune system and metabolism, known as immunometabolism, has emerged as a critical regulator of disease outcomes in the central nervous system. Numerous studies have linked metabolic disturbances to impaired immune responses in brain aging, neurodegenerative disorders, and brain injury. In this review, we will discuss how disruptions in brain immunometabolism balance contribute to the pathophysiology of brain dysfunction.
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