Objective:To explore the mechanism of acupuncture intervention on anti-neuronal apoptosis in heroindependent rats based on the PI3K/AKT signaling pathway.Methods:A total of 30 SD rats were randomly divided into a normal group,a model group and an acupuncture group,10 rats in each one.In the model group and the acupuncture group,the heroin relapse rat model was established by intramuscular incremental injection of heroin.In the model group,no any intervention was applied.In the acupuncture group,after modeling,acupuncture was applied at Bǎihuì (百会 GV20) and Dàzhuī (大椎 GV14).Transmission electron microscope (TEM) was adopted to observe neuronal apoptosis in the rats.The effect of acupuncture on anti-neuronal apoptosis was compared.Using reverse transcription-polymerase chain reaction (RT-PCR) and west blot methods,the mRNA and protein expressions of PI3K and AKT were detected in ventral tegmental area (VIA).Results:It was found that edema was presented in VTA neuronal cytoplasm and organelles basically disappeared in the heroin relapse rats,nuclear chromatin aggregation,condensation and increased neuronal apoptosis were presented as well.After acupuncture at Bǎihuì(百会 GV20) and Dàzhuī (大椎 GV14),a small amount of mitochondria,rough endoiplasmic reticulum and glycogen granules were visible in the cytoplasm of VTA neurons.The nuclear membrane structure was clear and the chromatin in the nucleus was basically normal.The fluorescence quantitative polymerase chain reaction (PCR) and west blot methods were adopted to detect mRNA and protein expressions of PI3K and AKT.It was found that the mRNA and protein expressions of PI3K and AKT in the brain of the rats in the model group were lower than those in the normal group (all P ＜ 0.05).Compared with the model group,the mRNA and protein expressions of PI3K and AKT in the acupuncture group were increased (all P ＜ 0.05),tending to the levels as the normal group.Conclusion:The effect of acupuncture on anti-brain cell apoptosis in heroin relapse rats may be related to the inhibition of PI3K/AKT signaling pathway.