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Fig. 4. The inhibitory effect of curcumin on brain HI damage is counteracted by VEGF overexpression in neonatal rats (n = 12 per group). (A) The VEGF expression in the sham, HI, HI + CUR, and HI + CUR + ov-VEGF groups by western blotting. (B) HI damage in brain tissues of the sham, HI, HI + CUR, and HI + CUR + ov-VEGF groups by TUNEL staining. (C) Neurological deficits evaluated in the sham, HI, HI + CUR, and HI + CUR + ov-VEGF groups by Longa’s score at 24 h and 72 h after treatment. (D) Histopathological changes of brain tissues in the sham, HI, HI + CUR, and HI + CUR + ov-VEGF groups by H&E staining (×400). (E) Cell apoptosis in the sham, HI, HI + CUR, and HI + CUR + ov-VEGF groups by TUNEL staining (×400). (F) Early and late apoptotic in brain tissues of the sham, HI, HI + CUR, and HI + CUR + ov-VEGF groups by flow cytometry. HI, hypoxic-ischemic injury; CUR, curcumin; VEGF, vascular endothelial growth factor. **p < 0.01 vs. sham group; ##p < 0.01 vs. HI group.
Korean J Physiol Pharmacol 2020;24:423-431 https://doi.org/10.4196/kjpp.2020.24.5.423
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