Fig 2: Intranasal delivery of dendritic cell-derived EVs loaded with Cy5-miR-124 inhibits cocaine-mediated upregulation of TLR4, MYD88, STAT3 and NF-kB p65 in vivo. Wild-type C57BL/6N, mice were administered either cocaine (20 mg/kg; i.p.) or saline for seven consecutive days. On the fifth, sixth, and seventh days, mice were intranasally administered dendritic cell-derived EVs loaded with Cy5-miR-124 or Cy5-scrambled miRNAs or were left unloaded, followed by cocaine injection. (A–D) Western blot images depicting the effect of EV-miR-124 on the expression of TLR4, MYD88, STAT3 and NF-kB p65. Actin served as a loading control. Quantification of western blots is shown under each blot. Data are shown as mean ± SEM (n = 4/group, *p < 0.05 vs. saline+ EV control, #p < 0.05 vs. cocaine+ EV control group).

Fig 3: QWZK alleviated the pathological characteristics of lung in ALI rats induced by LPS. (A) The images of lung in different groups, which was stained with H&E. Images are representatives of independent experiments. The scale bar in the figures represents a distance of 100 µm. (B) Statistical results of alveolar wall percentage in different groups. Data were presented as the mean ± SEM, n = 10. (C) Statistical results of lung injury score in different groups. Data were presented as the median ± SEM, n = 10. # p < 0.05 vs. control group, ## p < 0.01 vs. control group, ### p < 0.001 vs. control group. *p < 0.05 vs. LPS group, **p < 0.01 vs. LPS group, ***p < 0.001 vs. LPS group.

Fig 4: QWZK recovered the WBC counts and classification in ALI rats induced by LPS. (A) The number of WBC in BALF was detected by globulimeter. (B, C) Globulimeter was used to detect the number and ratio of neutrophils in BALF. (D, E) The number and ratio of lymphocyte were detected by a globulimeter in different groups. (F, G) The globulimeter was used to detect the number and ratio of monocyte in different groups. Data were presented as the mean ± SEM, n = 8. # p < 0.05 vs. control group, ## p < 0.01 vs. control group, ### p < 0.001 vs. control group. *p < 0.05 vs. LPS group, ** p < 0.vs. LPS group, *** p < 0.001 vs. LPS group.

Fig 5: Effects of Pterosin B on Ang II-activated HMGB1 secretion. H9c2 cells were treated with 300 nM Ang II with or without Pterosin B. (A) Protein expression levels of AT1R and RAGE in H9c2 cells-treated with 300 nM Ang II with or without Pterosin B for 48 h. (B,C) Quantification of AT1R and RAGE expression levels shown in (A). The protein levels were normalized to GAPDH. * p < 0.05, ** p < 0.01, *** p < 0.001. n = 6. (D) H9c2 cells were treated with Ang II for 10 min and HMGB1 expression level was detected by Western blot from cell lysate and culture medium. (E) Quantification of intracellular HMGB1 protein levels and amount of secreted HMGB1 shown in (D). * p < 0.05, ** p < 0.01, *** p < 0.001. NS vs. control. n = 4. (F) H9c2 cells were treated with Ang II with or without Pterosin B for 48 h. Western blot was performed to detect protein expression levels of TLR2, TLR4, and MyD88. (G–I) Quantification of protein levels shown in (F). * p < 0.05, *** p < 0.001. TLR2 (n = 6), TLR4 (n = 6), and MyD88 (n = 3).