Ultrasound in medicine & biology · 2026
Targeted microbubble cavitation has no therapeutic effect on atherosclerotic plaques of the aorta in diabetic ApoE-/- mice.
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Korn Amber, Simsek Suat, Fiet Mitchell D, Waas Ingeborg S E, Kooiman Klazina, Niessen Hans W M, Krijnen Paul A J
Аннотация
AIMS: Diabetes mellitus (DM) increases plaque instability via inflammation. Ultrasound-activated microbubble cavitation has previously reduced intra-plaque neovascularisation in non-DM models. Here we studied how ultrasound-activated microbubbles targeted against intercellular adhesion molecule-1 and CD90 affect atherosclerotic plaques in a DM model.
METHODS: DM was induced in C57BL/6 ApoE-/- mice via streptozotocin injection. Sixteen weeks later, either 5 × 107 targeted microbubbles or the vehicle was applied, followed by 1 min of 1 MHz pulsed thoracic ultrasound with 100 kPa peak negative acoustic pressure and a 1 kHz pulse repetition frequency (10% duty cycle). Aortic root plaque characteristics were examined via (immuno)histochemical analyses 4 wk post-treatment. Circulating monocyte subsets were assessed with flow cytometry in blood samples obtained within 3 d pre- and post-treatment, and 4 wk post-treatment.
RESULTS: Targeted microbubble cavitation did not significantly affect atherosclerotic plaque size or intra-plaque inflammation, despite a positive trend in intra-plaque CD45+ leukocytes and Ly6G+ neutrophils. Ultrasound-activated microbubble cavitation significantly increased the percentage of inflammatory classical monocytes within 3 d post-treatment.
CONCLUSIONS: Targeted microbubble cavitation induced a significant but temporary increase in circulating pro-inflammatory monocytes under mild exposure conditions in diabetic ApoE-/- mice without atherosclerotic plaque alterations.
METHODS: DM was induced in C57BL/6 ApoE-/- mice via streptozotocin injection. Sixteen weeks later, either 5 × 107 targeted microbubbles or the vehicle was applied, followed by 1 min of 1 MHz pulsed thoracic ultrasound with 100 kPa peak negative acoustic pressure and a 1 kHz pulse repetition frequency (10% duty cycle). Aortic root plaque characteristics were examined via (immuno)histochemical analyses 4 wk post-treatment. Circulating monocyte subsets were assessed with flow cytometry in blood samples obtained within 3 d pre- and post-treatment, and 4 wk post-treatment.
RESULTS: Targeted microbubble cavitation did not significantly affect atherosclerotic plaque size or intra-plaque inflammation, despite a positive trend in intra-plaque CD45+ leukocytes and Ly6G+ neutrophils. Ultrasound-activated microbubble cavitation significantly increased the percentage of inflammatory classical monocytes within 3 d post-treatment.
CONCLUSIONS: Targeted microbubble cavitation induced a significant but temporary increase in circulating pro-inflammatory monocytes under mild exposure conditions in diabetic ApoE-/- mice without atherosclerotic plaque alterations.