Abstract: Objective To explore the role of Bcl-2 and Bax in pathogenesis of the autism. Methods Female Sprague-Dawley rats were given a single intraperitoneal injection of sodium valproate (VPA, 600 mg/kg) on 12.5 d after pregnancy, their offspring were as the model group; while the other pregnancy rats were given normal saline, their offspring were as the control group. Both groups were observed with the Nissl staining, immunohistochemistry of Bcl-2 and Bax and image analysis 1 d, 7 d, 14 d, 28 d, 56 d after birth. Results Compared with the control group, Nissl staining showed the number of cortical neurons decreased on 1 d and 7 d after birth in the model group, rapidly increased on 14 d after birth, and maintained in high level on 28d , 56 d after birth. For immunohistochemistry, the integrated optical density (IOD) of Bcl-2 and Bax decreased in cortex on 1~14 d after birth (P<0.001) in both groups, and were stable 28 d after birth (P>0.05). Compared with the control group, the IOD of Bcl-2 decreased much more at every time point (P<0.001) in the model group, but the IOD of Bax increased on 1 d, 7 d (P<0.001), decreased on 14 d (P<0.001), similar 28 after birth(P>0.05). The ratio of Bcl-2/Bax was the most on 1 d after birth, and then decreased to approximately 1 in the control group, while it was the least on 7 d, most on 14 d, and decrease to less than 128 d after birth. Conclusion Apoptosis of cerebral cortex neurons increases in the autism model rats, especially in the early time.

Key words: autism, apoptosis, Bcl-2, Bax, rats