To observe the effects of electropuncture(EA) on myoelectric activity and apoptosis of posterior cervical muscle cells in rats with chronic cervical muscle injury.Methods:Seven Wistar rats were randomly selected from 34 Wistar rats and assigned to the blank group，and the remaining rats were used to establish a chronic cervical muscle injury model(as detected by ultrasonic diagnosis，six rats failed for model induction and were excluded).The model rats were randomly divided into a model group，an EA group，and a meloxicam group，with seven rats in each group.The rats in the EA group received EA treatment at bilateral Fengchi(GB 20)，25 min each time，once a day，for 10 consecutive days as a course of treatment，with a two-day interval between the two courses of treatment，for a total of two courses.An ultrasonic diagnostic system was used to detect the morphological changes in rat posterior cervical muscle tissues，and electrophysiological records presented the changes in rat cervical muscle myoelectricity.Cell apoptosis rate was detected using the TUNEL method，and protein expression levels of B-cell lymphoma 2(Bcl-2)，Bcl-2-associated X protein(Bax)，cysteinyl aspartate-specific protease 3(Caspase-3)，and cysteinyl aspartate-specific protease 9(Caspase-9) were detected by immunohistochemistry.Results:The results of the ultrasonic examination showed that the arrangement of muscle fibers was orderly and the muscle thickness increased after EA treatment as compared with the conditions in the model group.The results of the electrophysiological test showed that the amplitude and frequency of myoelectricity in the model group were significantly attenuated，and the amplitude and frequency of myoelectricity after EA were significantly higher than those in the model group.TUNEL results showed that the number of apoptotic cells in the EA group was significantly reduced compared with that in the model group(P<0.05).Immunohistochemical results showed that the number of Bcl-2 positive cells in the model group was lower and the number of Bax，Caspase-3，and Caspase-9 positive cells was higher than those in the blank group(P<0.05).The number of Bcl-2 positive cells in the EA group was higher，and the number of Bax，Caspase-3，and Caspase-9 positive cells was lower than those in the model group(P<0.05).Conclusion:EA can repair chronic cervical muscle injury，and its mechanism may be attributed to increasing the amplitude of cervical muscle electromyography and inhibiting apoptosis in rats with chronic cervical muscle injury，which may be realized by inhibiting the activity of the mitochondrial pathway.