Fig. 8. The role of CISD1 overexpression in autophagy and neurological impairment in vivo.
A The ideograph of ORF-CISD1 lentivirus injection site. B The protein expression of CISD1 increased after injection of ORF-CISD1 lentivirus. C TTC staining of rat brains. Scale bar = 1 cm. D Infarcts were quantified by planimetry and expressed as a percentage of risk zones. E Zea-longa score of HI rats. F Grip times were assessed in 1 d, 3 d, and 7 d after HI. G Time on rotarod was assessed in 38 d after HI. H Number of crossing was recorded in 38 d after HI. I Latency to platforms were assessed in 30 d, 31 d, 32 d, 33 d, and 34 d after HI. J, K Reduction of right cerebral blood flow after HI. L Representative EM images of autophagic vacuoles were shown. Scale bar = 250 nm. The arrows depict autophagosomes. M–Q The expression of ATG12, P62, Beclin-1 LC3I, and LC3II were detected by western blotting. Representative immunoblot for conversion of LC3I to LC3II in Sham group, HI group, ORF-NC group and ORF-CISD1 group. The densitometric analysis of WB of LC3II is shown. Data are shown as mean ± s.d. *P < 0.05, **P < 0.01 with one-way ANOVA, n = 6. CISD1 CDGSH iron-sulfur domain-containing protein 1, HI hypoxia ischemia, ORF-NC negative control overexpression, ORFCISD1 CISD1 overexpression, H hours, S seconds.