Zhang, X., Lu, Y., Wu, Q., Dai, H., Li, W., Lv, S., Zhou, X., Zhang, X., Hang, C. and Wang, J. (2019). Astaxanthin mitigates subarachnoid hemorrhage injury primarily by increasing sirtuin 1 and inhibiting the Toll-like receptor 4 signaling pathway. The FASEB Journal, 33: 722-737. https://doi.org/10.1096/fj.201800642RR The original paper of this article contains an error in Figure 6K for the SAH + vehicle (KO) group. The corrected Figure 6 is presented below. The mistake does not change the results or conclusions of the study. The authors apologize for the error. FIGURE 6. Effects of ATX on neuronal death, brain edema, and neurologic function at 24-h post-SAH. ATX (0.1 mM) was administered to rats via intracerebroventricular injection at 30 min after SAH. (A) Western blot analysis for Bcl2, Bax, and caspase-3. (B) Quantification of Western blots showed that ATX significantly decreased levels of cleaved caspase-3 and Bax, and enhanced levels of Bcl2. (C, D) Representative photomicrographs of immunofluorescence staining for caspase-3 and TUNEL staining in the indicated experimental groups. (E, F) Quantification showed that SAH rats treated with ATX had significantly fewer caspase-3-positive and TUNEL-positive neurons than did the vehicle-treated SAH group. *p < .05, n = 6/group. (G) Representative photomicrographs of FJC staining. (H) Quantification showed that ATX reduced the number of FJC-positive cells after SAH. (I) ATX treatment significantly alleviated brain water content after SAH. (J-L) ATX improved neurologic scores after SAH. Representative photomicrographs (K) and quantitative analysis (L) of TUNEL staining in WT and TLR4 KO mouse groups. TLR4 KO mice exhibited fewer TUNEL-positive neurons. Nevertheless, treatment with ATX reduced the number of TUNEL-positive neurons in both genotypes. (M) ATX significantly ameliorated SAH-induced neurologic impairment in WT mice but not in TLR4 KO mice. ns, not significant. *p < .05 (n = 6/group).

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