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. Author manuscript; available in PMC: 2018 Dec 1.
Published in final edited form as: J Neuroimmune Pharmacol. 2017 May 2;12(4):624–660. doi: 10.1007/s11481-017-9746-5

Figure 13. The therapeutic effect of DAS in ameliorating activation of redox sensitive kinases and ALS markers in the LPS treated mice.

Figure 13

DAS suppresses LPS-induced upregulation of redox sensitive kinases and ALS dysfunction in the SNpc. Mice were treated as indicated in fig 12. (A) Representative immunoblot images showing relative levels of c-Abl and phospho-c- Abl (Y245 and Y412) in the SN of mice at 6h post LPS treatment. Densitometric scanning analysis revealed that LPS treatment caused hyperphosphorylation of c-Abl tyosine kinase at both activation sites (Y245 and Y412), which was blocked significantly by DAS pre-treatment. Similarly, a marked increase in phosphorylation of PKCδ at Y311 residue was evidenced in LPS treated mice while DAS pretreated mice demonstrated a significant reduction in the phosphorylation of PKCδ. Levels of β actin was used an internal loading control. The p-c-Abl and p-PKCδ band intensity were normalized to c-Abl and PKCδ, respectively, and c-Abl and PKCδ were normalized to β actin. Data expressed as the mean ± S.E.M. (N=3-4) of % control. *p<0.05 and **p<0.01 versus saline-treated control group; #p<0.05 versus LPS group. (B) DAS protects against LPS-induced ALS dysfunction by decreasing beclin-1 levels and increasing TFEB levels in the substantia nigra of LPS treated mice. Whole cell lysates were prepared from the SNpc and immunoblotted for beclin-1 and TFEB. Densitometric scanning reveals DAS significantly (p<0.05) ameliorated ALS dysfunction. The bands were normalized to β actin. Data represented as the mean ± S.E.M. (N=3-4). **p<0.01 versus saline-treated control group; #p<0.05 versus LPS group.