TLR4 Signaling Is Involved in Brain Vascular Toxicity of PCB153 Bound to Nanoparticles
Figure 1
PCB153-NP-induced enhancement of infarct volume following ischemia/reperfusion is reduced in TLR4-deficient mice.
Mice were exposed to PCB153-NPs (5 ng PCB153/g body weight bound to 1.04×105 silica NPs) by infusion into the internal carotid artery (ICA). Control mice were infused with the same amounts of NPs, PCB153 or vehicle (PBS). After 24 h, all animals were subjected to a 40 min occlusion of the middle cerebral artery (MCA), followed by a 24 h reperfusion. The infarct area was detected by 2,3,5-triphenyltetrazolium chloride (TTC) staining and the image illustrates the representative results. The loss of tissue viability is reflected by unstained (white) areas. Quantified results are depicted in a bar graph. Results are means ± SEM, n = 5. Significantly different as compared to vehicle treatment in mice with normal TLR4 expression at ***p<0.001. Results in the TLR4-deficient mice treated with PCB153-NPs are statistically different from those in control animals exposed to PCB153-NPs at ###p<0.001.