Fig. 9

AKI of mice can be relieved by AMSC-Exo-342 through promoting autophagy. Notes: Four hours after establishment of sepsis-associated AKI mouse models by CLP, mouse models were injected with 100 µg AMSC-Exo-342 or AMSC-Exo-67 by the tail vein. Then, 72 h later, the kidney tissues and blood samples were collected. qRT-PCR was applied to measure the expression of miR-342-5p in kidney tissues of mice (A), qRT-PCR (B) and western blot (C) to detect the expression of TLR9 in kidney tissues of mice, and H&E staining to evaluate the damage of kidney (D). The levels of BUN (E), SCr (F), TNF-α (G), IL-1β (H), IL-6 (I), and MCP-1 (J) in mouse serum were inspected by ELISA. The protein expression levels of autophagy-related proteins LC3-II/LC3-I (L), p62 (M), and Beclin-1 (N) were determined by western blot (K). The expression of p-p65 (O, P) in kidney tissues was measured by western blot. ^* P < 0.05, ^** P < 0.01, ^*** P < 0.001, compared to the Sham, CLP, CLP + AMSC-Exo-67, or CLP + AMSC-Exo-342 group; AMSCs, adipose-derived mesenchymal stem cells; Exo, exosome; AKI, acute kidney injury; CLP, cecal ligation and puncture. Data were analyzed using one-way analysis of variance and Tukey test was used for post hoc analysis. Data were generated from three independent experiments