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  Indian J Med Microbiol
 

Figure 5: Impact of simvastatin (Sim) on nuclear factor-kB initiation in activated microglial: BV-2 cells pretreated with simvastatin for 30 min, then lipopolysaccharide was added and cultured for indicated times. The levels of phospho-IκB kinase -α/β (5 min), phospho-IκB-α (10 min) and IκB-α (20 min) assessed by Western blot. LPS-activated phosphorylation of Ikkα/β, IκB, and corruption of IκB was notably repressed by simvastatin. The α-tubulin used as an internal control (a). The expression of p65 (1 h) in nuclear assessed by Western blot and the LPS induced P65 is decreased upon simvastatin treatment. The Lamin β used as an internal control (b). After activation of BV-2 microglial cells with LPS for 20 min, MAPKs expression was observed, utilizing immune responses particular for individual phospho-MAPKs. The level of p38 phosphorylation was decreased upon simvastatin treatment, while phosphorylation of ERK and JNK was not changed significantly (c)

Figure 5: Impact of simvastatin (Sim) on nuclear factor-kB initiation in activated microglial: BV-2 cells pretreated with simvastatin for 30 min, then lipopolysaccharide was added and cultured for indicated times. The levels of phospho-IκB kinase -α/β (5 min), phospho-IκB-α (10 min) and IκB-α (20 min) assessed by Western blot. LPS-activated phosphorylation of Ikkα/β, IκB, and corruption of IκB was notably repressed by simvastatin. The α-tubulin used as an internal control (a). The expression of p65 (1 h) in nuclear assessed by Western blot and the LPS induced P65 is decreased upon simvastatin treatment. The Lamin β used as an internal control (b). After activation of BV-2 microglial cells with LPS for 20 min, MAPKs expression was observed, utilizing immune responses particular for individual phospho-MAPKs. The level of p38 phosphorylation was decreased upon simvastatin treatment, while phosphorylation of ERK and JNK was not changed significantly (c)