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. 2024 Jun 8;15:4913. doi: 10.1038/s41467-024-49348-0

Fig. 2. Elevated SOD3 expression is associated with the severity and experimental cerebral malaria (ECM) in murine models.

Fig. 2

a, b SOD3 is associated with cerebral malaria in WT mice. The accumulation of P. berghei iRBCs was not obvious in the mouse brains of SOD3−/− mice. However, this phenomenon was reversed in both littermate (WT) and SOD3o/e mice after infection, which showed severe sequestration of iRBCs in the brains. Overexpression of SOD3 also resulted in increased parasitemia, as reflected by increased luminescence signals in the body. The luminescence images of the mice were recorded with an AniView600 multimode in vivo animal imaging system, n = 3. Statistical tests were two-sided, and Tukey corrected for multiple comparisons. c SOD3−/− mice displayed extended survival after P. berghei infection. The survived mice in SOD3−/− group were humanely euthanized accordingly to approved criteria. d SOD3o/e mice and control mice showed similar vulnerability to the parasite infection. Five biological replicates were used for analysis. Kaplan‒Meier survival curves were calculated using the survival time for each mouse in all groups, and significance was determined by the log-rank test. e Administration of recombinant SOD3 increased the sensitivity of the SOD3−/− mice to P. berghei infection. For (ce), n indicates mouse numbers in graphs. For c and e, Kaplan-Meier survival curve p-values were performed using Log rank Mantel-COX test. Histograms present the mean ± SD. Source data are provided as a Source Data file.