Fig 1: Post-ischemia–reperfusion (IR) injury in C57BL/6J and Slit2-Tg hearts. (A) Representative images of hematoxylin–eosin (HE) staining in C57BL/6J and Slit2-Tg hearts. Scale bar = 200 μm (top) or 50 μm (bottom). The bottom panels show the magnified views of the black framed areas of the corresponding upper panels. The black framed area of the C57-IR heart section displays necrosis. The black arrows indicate ruptured cardiomyocytes; the green arrows indicate swollen cardiomyocytes. (B) Subcellular structures of cardiomyocytes as examined by TEM in C57BL/6J and Slit2-Tg hearts. Scale bar = 1 μm (top) or 500 nm (bottom). C57-non-IR, C57BL/6J hearts not subjected to IR; Slit2-non-IR, Slit2-Tg hearts not subjected to IR; C57-IR, C57BL/6J hearts subjected to IR; Slit2-IR, Slit2-Tg hearts subjected to IR. Arrows: yellow, Z-discs; blue, normal mitochondria; red, post-IR mitochondria with disappearing crista; purple, ruptured Z-discs.
Fig 2: Immunohistological stainings for Slit2 proteins. (A) Representative images of the striatal section with immunohistological stainings of SHR with different treatments (n = 5 per group). The arrow indicates the expression of Slit2 proteins. (B) Quantified results for Slit2 protein expression. The symbol, * p < 0.05, and # p < 0.05, indicate significant differences compared with the Control group and Sham group, respectively, using one-way ANOVA with Tukey’s multiple comparisons post hoc test. Control (fed with Cho diet); Taurine (fed with 45 mM taurine); Sham (fed with Cho diet); miR ATNC (injection of miR-200b-3p antagomir negative-control); miR AT (injection of miR-200b-3p antagomir).
Fig 3: The effects of quercetin on the expression of Slit-2 in sciatic nerve were detected by immunofluorescence assay. (A) The representative images of Slit-2. (B) The relative expression of Slit-2. Data are expressed as mean ± SD. **p < 0.01; ***p < 0.001.
Fig 4: Effects of recombinant Slit2 on neuronal death in brain at 5 days after GMH. TUNEL staining showed the degree of DNA breakage (A) was aggravated after GMH, which were reduced by rSlit2. “*” symbol indicates the lesion location on the representative microphotograph of brain slice. Scale bar = 100 μm. Western blotting image and quantitative analysis showed that brain cleaved caspase-3 (B) expressions increased after GMH, which were reduced by rSlit2. N = 6/group. Mean ± SEM. ANOVA, Tukey. *P < 0.05 vs. Sham, #P < 0.05 vs. GMH + Vehicle
Fig 5: Proposed cardioprotective mechanisms of Slit2 in the post-ischemia–reperfusion (IR) myocardium. Slit2 overexpression inhibits the expression of the membrane receptors Robo4 and Slamf7 but activates Robo1, which in turn blocks the nuclear translocation of NFκB p65 and impedes the release of IL-1β and IL-18 from the cells in post-IR hearts. Next, Slit2 regulates intracellular signaling pathways to attenuate the increases in myofilament-associated PKC levels and cTnI Ser43 phosphorylation in the post-IR myocardium, maintaining myofilament contractility and calcium sensitivity.
Supplier Page from Abcam for Anti-Slit2 antibody