Siji Antiviral Mixture Protects against CA16 Induced Brain Injury through Inhibiting PERK/STAT3/NF-κB Pathway

Figure 8

SAM inhibited the inflammatory response through the PERK/STAT3/ NF-κB pathway. (a) SH-SY5Y cells were transfected with PERK, STAT3, and NF-κB-specific siRNA (15 nM), respectively, and then subjected CA16 infection. Total proteins were extracted and PERK, P-PERK, NF-κB(p-65), P-elF2α, and elF2α expression levels were detected by Western blotting with the corresponding antibodies. ^##P<0.01 versus control group; ^∗P<0.05; ^∗∗P<0.01 versus siCON group. (b) SH-SY5Y cells were overexpressed PERK with PERK lentiviral activation particles as the protocol direction and then subjected to CA16 infection and treated with SAM (2.4 mg/mL). PERK, P-PERK, NF-κB(p-65), P-elF2α, and elF2α expression levels were detected by Western blotting; survival rate and LDH release rate were also detected by kits. ^##P<0.01 versus control group; ^∗P<0.05; ^∗∗P<0.01 versus model group; ^&&P<0.01 versus SAM treatment group.

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