Intravitreal Injection of Amyloid β1–42 Activates the Complement System and Induces Retinal Inflammatory Responses and Malfunction in Mouse

Abstract

To investigate whether intravitreal injection of amyloid β1–42 (Aβ1–42) activates the complement system and induces retinal inflammatory responses and malfunction, Aβ1–42 was applied intravitreally in mice. The expressions of key components of complement system were determined by real-time PCR. Retinal function was assessed by electroretinography. We found interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in Aβ1–42 treated mice retinas increased from day 1 to day 7. Compared with control group, mRNA expression of C1qa and C3 in the Aβ1–42 treated retinas increased at days 1 and 7. The level of CFB, CFD, or CFH increased at day 4 and day 7. Regulator of membrane attack complex (MAC), CD59a, increased from day 1 to day 7. The expression of the main complement components in Aβ1–42 treated eyes increased at days 4 and 7. Therefore, our results suggested that exogenous Aβ1–42 activated CP and AP of the complement system in mice retinas, induced retinal inflammatory responses, and caused retinal malfunction.