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. 2016 Jun 1;12(2):823–828. doi: 10.3892/etm.2016.3413

Figure 2.

Figure 2.

CCM inhibited the increased expression of (A) TLR-4, (B) MyD88, (C) NF-κB (p65) and (D) caspase-3 in LPS-stimulated BV2 microglia. Cells were pretreated with LPS for 0.5 h, followed by incubation with 5 µg/ml CCM for 24 h. The lysates were probed by immunoblotting with antibodies against TLR-4, MyD88, NF-κB and caspase-3 and GAPDH individually. Results are the mean ± standard error. Each experiment was derived from at least three independent cultures. *P<0.05 vs. the Ctrl group; **P<0.05 vs. the LPS group. TLR-4, Toll-like receptor 4; MyD88, myeloid differentiation primary response 88; NF, nuclear factor; LPS, lipopolysaccharide; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; Ctrl, control; CCM, curcumin.