Fig. 5

Homer1a⁺ EVs regulated activation and nuclear translocation of NF-κB. a The expression level and quantification of NF-κB in nucleus and cytoplasm (in vivo) was detected by WB [F (3, 8) = 164.3, P < 0.0001]. b The expression level and quantification of NF-κB in nucleus and cytoplasm (in vitro) was detected by WB [F (3, 8) = 122.60, P < 0.0001]. c NF-κB-Luciferase reporter gene mice were used to detect the activation level of NF-κB. d Quantification of luciferase fluorescence intensity in panel c [F (3, 16) = 92.51, P < 0.0001]. e The regulation of ICH and Homer1a⁺ EVs on NF-κB activation was detected by double luciferase report assay in 293 T cells [F_interaction (3, 16) = 98.21, P < 0.0001]. f The regulation of ICH and Homer1a⁺ EVs on NF-κB activation was detected by double luciferase report assay in primary neurons [F_interaction (3, 16) = 25.92, P < 0.0001]. g Regulation of IL-17A by NF-κB in different treatment groups in 293 T cells [F_interaction (9, 32) = 24.05, P < 0.0001]. h Regulation of IL-17A by NF-κB in different treatment groups in primary neurons [F_interaction (9, 32) = 40.88, P < 0.0001]. i Detection of IL-17A level in vitro by ELSIA [F (3, 8) = 85.94, P < 0.0001]. j Detection of IL-17A level in vivo by ELSIA [F (3, 8) = 47.3, P < 0.0001]. k Apoptosis level of primary inflammatory neurons after treatment with DHMEQ (5 μg/mL for 48 h) and Homer1a⁺ EVs. l HE staining of brain tissue of mice treated with DHMEQ (4 mg/kg) and Homer1a⁺ EVs. m Quantification of hematoma area intensity in panel l [F (2, 6) = 86.17, P < 0.0001]. The data were analyzed using one-way (a, b, d, i, j and m) or two-way (e, f, g and h) analysis of variance and all data are expressed as the mean ± standard deviation. *P < 0.05, **P < 0.01 ***P < 0.001 and ****P < 0.0001 represents a statistically significant difference between the two groups. ns: no statistical difference. The blots are representative of other replicates in those groups