The Beneficial Effect of Melatonin in Brain Endothelial Cells against Oxygen-Glucose Deprivation Followed by Reperfusion-Induced Injury
Figure 5
The measurement of JNK, Akt, and Bax expression in brain endothelial cells after OGD/R-induced injury. (a) Western blotting showed that the relative protein level of phosphor-Akt was reduced in EC compared to the NC group. The protein level of phosphor-Akt was increased in Mel (100 nM) groups, compared to the EC group. The bar graph shows the quantification of phosphor-Akt/Akt protein in all groups. (b) Western blotting showed that the relative protein expression of phosphor-JNK increased in the EC group, compared to the NC group. The relative level of phosphor-JNK decreased in Mel 10 nM and Mel 100 nM groups, compared to the EC group. The bar graph shows the quantification of phosphor-JNK/JNK protein in all groups. (c) Western blotting showed that the relative protein expression of Bax increased in the EC group, compared to the NC group. The protein level of Bax decreased in Mel 10 nM and Mel 100 nM groups, compared to the EC group. The bar graph shows the quantification of Bax protein in all groups. (d) Western blotting showed the relative protein expression of Bax by melatonin and 100 nM Akt inhibitor pretreatment under OGD/R injury. The expression of Bax was increased in the EC treatment group, compared to the NC group. The protein level of Bax was increased in Mel 10 nM and Mel 100 nM groups with 100 nM Akt inhibitor copretreatment, compared to the EC group. The bar graph shows the quantification of Bax in all groups. β-Actin was used as an internal control. Data are expressed as mean ± S.E.M. (#, *, and **). Protein kinase B (Akt), phosphorylated Akt (p-Akt), c-Jun N-terminal kinases (JNK), and phosphorylated JNK (p-JNK).
