Abstract
Abstract AMD is the main cause of visual impairment in people over 50 years of age and the most common cause of blindness. In recent years, the use of bevacizumab to treat neovascular AMD has become a preferred treatment in the United States. However, whether bevacozumab is available for RPE or AMD patients is unknown. We firstly indicate that Pam3CSK4 (P3C) activates TLR2 pathway during ARPE-19 apoptosis as determined by western blotting. And then, the expression of MyD88, NF-κB, p-IKK in primary RPE cells from AMD patients is significantly down-regulated after treatment with 50 µg L−1 Bevacizumab. Therefore, our data shows that MyD88 is involved in the TLR2 pathway in ARPE-19 cell apoptosis resulting from Pam3CSK4 (P3C). And more importantly, our findings suggested that Bevacizumab cured age-related macular degeneration (AMD) via down-regulate Toll—like receptor 2 (TLR2) pathway in RPE from AMD patients.
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