Role of FAK in Syk-mediated neuroprotective effects under LLLT treatment. (A) LPS-activated BV-2 cells pretreated with or without 10 μM PP1, followed by LLLT treatment. Western blot analysis of the treated cells was performed to detect phospho-Ty861-FAK, phospho-Tyr397-FAK, and total FAK at indicated time. (B) Quantitative analysis of the levels of phospho-Ty861-FAK, phospho-Tyr397-FAK, and total FAK in treated cells. Data represent mean ± SEM (n = 4; *P <0.05 and **P <0.05 versus corresponding control cells, #P <0.05 versus indicated cells). (C) BV-2 cells were transfected with GFP-FRNK (FRNK, an endogenous inhibitor of FAK). G418-resistant cells were collected for LPS (100 ng/ml) stimulation and LLLT (20 J/cm2) treatment. Immediately thereafter, SH-SY5Y cells were subjected to microglia cytotoxicity assay as previous described. Data represent mean ± SEM (n = 4; *P <0.05 versus control cells, #P <0.05 versus indicated cells). (D) Western blot analysis of the transfected cells received LPS stimulation and LLLT treatment to detect phospho-Tyr397-FAK, phospho-Tyr519/520-Syk, total MyD88, and total iNOS. Data were the representative graph (n = 4). iNOS, inducible nitric oxide synthase; LLLT, low-level laser therapy; LPS, lipopolysaccharide.