Neuroprotective Effect of Kaempferol Glycosides against Brain Injury and Neuroinflammation by Inhibiting the Activation of NF-κB and STAT3 in Transient Focal Stroke
Figure 6
KRS and KGS inhibited the activation of NF-κB and STAT3 in tMCAO rats.
(A) Representative photomicrographs of the immunohistochemical expression of p-NF-κB p65 and p-STAT3 (brown staining) in the cortical ischemic penumbra. (B) Immunoreactivity of p-NF-κB p65 and p-STAT3 measured using the integrated optical density (IOD) of the immunostained-positive cells (n = 6 each group). (C) Representative immunoblots of NF-κB p65, Lamin B, p-STAT3, and STAT3. The data are expressed as mean ± SEM. (D, E) Immunoblot expression measured using densitometry. The data are expressed as mean ± SEM (n = 3 each group). The loaded protein amount was normalized to Lamin B or STAT3, and the data are expressed as a percentage of the mean value in the sham-operated group. Treatment with KRS or KGS significantly reduced the phosphorylation of STAT3 at Tyr705, phosphorylation of NF-κB p65 at Ser536 and the nuclear content of NF-κB p65. *p<0.05, **p<0.01, compared with the vehicle-treated group.