The β-amyloid protein induces S100 β expression in rat hippocampus through a mechanism that involves IL-1

Objective To explore the effect of β-amyloid protein （Aβ） on S100β expression in rat hippocampus and its mechanisms. Methods At 7 days after bilateral stereotaxls injection of different dose of fibrillar Aβ25--35 and interluekin-1 receptor antagonist （IL-1ra） into the rat CA1 region, the learning and memory abilities of rats were tested with passive avoidance task. Amyloid deposition was detected by using Congo red staining technique. Nlssl staining and immunohlstochemical techniques were used to analyze the number of neurons, and GFAP and the S100β expression in hippocampal CA1 region , respectively. Results After fibrillar Aβ injection, the step-through latency of rats was significantly shortened compared to that of the control group. The GFAP positive astrocytes were found surrounding amyloid deposition. Neuronal loss occurred in the pyramidal cell layer of CA1 region. The number of S100β positive cells in Aβ-treated group was significantly increased compared with that in the control group. After IL-1ra injection, the number of S100β positive cells was significantly decreased. Conclusion Intrahippocampal injection of Aβ25 - 35 could cause similar pathologic changes of Alzheimer＇s disease. Aβ 25- 35 was capable of up-regulating S100β expression in a dose-dependent manner. The injection of IL-1ra could attenuate the effect of Alton S100β expression.