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. 2022 Apr 7;11(4):728. doi: 10.3390/antiox11040728

Figure 6.

Figure 6

ZO-1 deficiency attenuated protective effects of HSYA during cerebral ischemic injury. Male C57BL/6J mice were injected with AAV2/br1-TIE-mir30-m-Tjp1 and AAV2/br1-TIE-NC (negative control) viruses to build ZO-1 deficiency mice. Additionally, the mice were administrated with HSYA for 3 consecutive days: (A) immunofluorescence staining of ZO-1 protein expression in the peri-infarct zones of brain tissue (scale bar: 50 μm). Green: CD31, red: ZO-1; (B) Evans blue staining was used to observe the permeability of blood–brain barrier in mouse brain tissue. After injection of 2% Evans blue for 2 h, the brain tissue of the mice was removed and photographed; (C) immunofluorescence of Iba1 in the peri-infarct zones of brain tissue (scale bar: 500 μm); (D) bEnd.3 cells were transfected with siRNA against ZO-1 (siTjp1) or control siRNA (siNC) and then treated with HSYA in the presence of LPS. TEER values, and the absorbance of FITC–dextran across the bEnd.3 monolayer cells were measured. All data are presented from five independent experiments. ### p < 0.001 vs. indicated group, * p < 0.05, *** p < 0.001 vs. LPS group.