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. 2022 Jul 22;7(14):e158523. doi: 10.1172/jci.insight.158523

Figure 1. Remote ischemic preconditioning (RIPC) protects the murine kidney from IRI by HMGB1 signaling in vivo.

Figure 1

After induction of general anesthesia WT mice received either 3 cycles of 5-minute RIPC by inflation of a blood pressure cuff (200 mmHg) positioned to upper leg of the hind limb interrupted by 5-minute reperfusion intervals following cuff deflation. In the control group, the cuff was inflated to 20 mmHg, not resulting in limb ischemia. IRI was induced in WT mice by clamping of the renal pedicles for 32 minutes. Twenty-four hours after the surgery, mice were sacrificed. (A) The recruitment of neutrophils (PMNs) into the kidney was analyzed by flow cytometry (n = 5). (B) Serum creatinine levels were measured by a photometric assay (n = 5). (C and D) Exemplary histological images and quantification of histological tubular injury (n = 4–5). Scale bar: 100 µm. (E and F) Plasma HMGB1 levels and urinary HMGB1 levels were analyzed before and after RIPC or control procedure (n = 6). Some mice received either BoxA or a vehicle control before inducing RIPC prior to renal IRI. Twenty-four hours after IRI, mice were sacrificed. (G) The recruitment of neutrophils (PMNs) into the kidney was analyzed by flow cytometry (n = 4-6). (H) Serum creatinine levels were measured by a photometric assay (n = 4-6). Mann-Whitney U test (D) and 1-way ANOVA followed by Bonferroni testing (A, B, and E–H) were used for statistical analysis; *P < 0.05.