Effect of electroacupuncture on neuronal apoptosis in rats with traumatic brain injury based on PI3K/Akt signaling pathway

Abstract

To observe the effect of electroacupuncture (EA) on neuronal apoptosis in rats with traumatic brain injury (TBI), and to explore the action mechanism of EA on improving the brain nerve function of TBI. A total of 88 6-week-old SD rats were randomly divided into a sham operation group, a model group, an EA group and a LY294002+EA group, 22 rats in each group. The TBI model on the left side was established by the improved Feeney's free fall method. After modeling for 24 h, the rats in the EA group and LY294002+EA group were treated with acupuncture at "Baihui" (GV 20) for 10 min and pricking acupuncture at "Shuigou" (GV 26) for 20 s; EA was applied at "Neiguan" (PC 6) and "Zusanli" (ST 36) on the right side (discontinuous wave, 2 Hz of frequency, 1 mA of intensity) for 10 min, once a day for 3 days. After 3 days of intervention, the TUNEL method was used to detect the level of neuron apoptosis in left cerebral cortex; the Western blot method was used to detect the expression of Akt, p-Akt, Bcl-2, Bax, Cyt-C and Caspase-9 in the left cerebral cortex. After 3-day treatment, compared with the sham group, the number of neuronal apoptosis in the left cortex was increased in the model group (P<0.01), and the expression of Bax, Cyt-C and Caspase-9 protein was increased (P<0.01), and the expression of p-Akt/Akt, Bcl-2 was decreased (P<0.01). Compared with the model group, the number of neuronal apoptosis in the left cortex was decreased in the EA group (P<0.01), and the expression of Bax, Cyt-C and Caspase-9 was decreased (P<0.01), and the expression of p-Akt/Akt and Bcl-2 was increased (P<0.01). Compared with the LY294002+EA group, the number of neuronal apoptosis in the left cortex was decreased in the EA group (P<0.01), and the expression of Bax, Caspase-9 and Cyt-C was decreased (P<0.01, P<0.05), and the expression of p-Akt/Akt and Bcl-2 was increased (P<0.01). EA could significantly reduce the neuronal apoptosis in rats with TBI, and its mechanism may be related to the activation of PI3K/Akt signaling pathway.