Fig. 5

Engagement of σ-1R and JNK/p38 in LPS-induced HECTD1 upregulation. a Pretreatment of astrocytes with BD1047 inhibited LPS-induced increase of HECTD1 expression. b Pretreatment of astrocytes with BD1047 inhibited LPS-induced increase of p-JNK expression. c Pretreatment of astrocytes with BD1047 inhibited LPS-induced increase of p-p38 expression. d The effect of BD1047 on p-Akt expression post LPS. All the data are presented as mean ± SEM of three individual experiments. *p < 0.05, **p < 0.01, and ***p < 0.01 vs. the control group; #p < 0.05 vs. the LPS-treated control group. e Pretreatment of primary mouse astrocytes with BD1047, SB203580, and SP600125 resulted in inhibition of the LPS-mediated HECTD1 elevation. f Pretreatment of primary mouse astrocytes with BD1047, SB203580, or SP600125 resulted in inhibition of the LPS-mediated GFAP elevation. All the data are presented as mean ± SEM of three individual experiments. **p < 0.01 vs. the control group; #p < 0.05, ##p < 0.01 vs. the LPS-treated control group. g Pretreatment of primary mouse astrocytes with siRNA of σ-1R, JNK, or p38 resulted in inhibition of the LPS-mediated HECTD1 elevation. All the data are presented as mean ± SEM of three individual experiments. ***p < 0.001 vs. the control group; ##p < 0.01 vs. the LPS-treated control group. h Pretreatment of primary mouse astrocytes with siRNA of σ-1R, JNK, or p38 resulted in inhibition of the LPS-mediated GFAP elevation. All the data are presented as mean ± SEM of three individual experiments. **p < 0.01 vs. the control group; #p < 0.05 vs. the LPS-treated control group