Fig. 2

Both TMF-treated and AHRcKO mice showed attenuated AHR pathway proteins and AHR activities after MCAO. a Representative Western blots of the normal WT and poststroke ipsilesional hemisphere lysates from WT-vehicle and WT-TMF treated mice at 48 h after MCAO with β-actin as the loading control. b Representative Western blots of normal AHRcKO and ipsilesional AHR^flx/flx and AHRcKO brains after MCAO with β-actin as the loading control. c Quantitative levels of AHR pathway proteins in normal and poststroke brains from AHRcKO, WT, WT-vehicle, and WT-TMF mice (n = 6/each group). The AHR, IDO, ARNT, CYP1B1, and CYP1A2 proteins were increased in the WT-vehicle group after MCAO compared to the WT-normal group. The poststroke AHR^flx/flx group also had increased AHR, IDO, ARNT, CYP1B1, and CYP1A2 protein levels compared to the normal AHRcKO group. Compared to the WT-vehicle-treated group, the WT-TMF-treated group showed significantly decreased AHR pathway proteins after MCAO. Similarly, the AHRcKO group revealed downregulated AHR pathway proteins compared to the AHR^flx/flx group after MCAO. The AHR agonist activity, measured by the relative DRE-luciferase activity compared to control, was increased by treatment with the AHR agonist, FICZ, compared with control. After MCAO, the WT-vehicle-treated group showed a significant increase in AHR agonist activity compared with the normal WT group. The increased AHR agonist activity after MCAO was decreased by TMF treatment, suggesting that TMF downregulated the IDO/kynurenine/AHR activation. The results are expressed as the means ± standard error of the mean. +p < 0.05 AHRcKO-Normal compared with WT-Normal mice. #p < 0.05 compared with the respective normal controls. *p < 0.05 WT-TMF-treated mice compared with the WT-Vehicle and AHRcKO mice compared with the AHR^flx/flx mice