Research Paper Volume 12, Issue 11 pp 11004—11024

Figure 6. Mlxipl inhibited the cJun-mediated inflammatory response in microglia. (A–F) The Mlxipl expression was detected by QPCR (A–B), western blot (E) and immunofluorescence (E). The primary microglia were co-transfected with siMlxipl or LvMlxipl for 48 hr, and then treated with LPS (1 μg/ml) for 24 hr. Quantification of the western blot (D) and immunofluorescence (F). Data relative to vehicle. N = 3. ^$$$P < 0.001, ^$$P < 0.01, ^$P < 0.05 vs. LPS; ^###P < 0.001, ^##P < 0.01 vs. LPS-siNC; ***P < 0.001, **P < 0.01, *P < 0.05 vs. LPS-LvNC. (G–I) ELISA were performed to detect the expression of proinflammation cytokines. Mlxipl inhibited inflammation response in LPS-induced microglia. N = 3. ^$$$P < 0.001, ^$$P < 0.01, ^$P < 0.05 vs. LPS; ^###P < 0.001, ^##P < 0.01 vs. LPS-siNC; ***P < 0.001, **P < 0.01, *P < 0.05 vs. LPS-LvNC. (J–O) The cJun expression was detected by QPCR (J–K), western blot (L) and immunofluorescence (N). The primary microglia were co-transfected with sicJun or LvcJun for 48 hr, and then treated with LPS (1 μg/ml) for 24 hr. Knockdown of cJun inhibited the expression of Mlxipl and p-cJun. Overexpression of cJun promoted the expression of Mlxipl and p-cJun. Quantification of the western blot (M) and immunofluorescence (O). Data relative to vehicle. N = 3. ^$$$P < 0.001, ^$$P < 0.01, ^$P < 0.05 vs. LPS; ^###P < 0.001, ^##P < 0.01 vs. LPS-siNC; ***P < 0.001, **P < 0.01, *P < 0.05 vs. LPS-LvNC. (P–R) ELISA were performed to detect the expression of proinflammation cytokines. CJun promoted inflammation response in LPS-induced microglia. N = 3. ^$$$P < 0.001, ^$$P < 0.01, ^$P < 0.05 vs. LPS; ^###P < 0.001, ^##P < 0.01 vs. LPS-siNC; ***P < 0.001, **P < 0.01, *P < 0.05 vs. LPS-LvNC.