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Abstract: PO2239

Efficacy of Low-Intensity Pulsed Ultrasound on CKD-Associated Cachexia and Muscle Wasting Prevention in a Mouse Model

Session Information

Category: Pathology and Lab Medicine

  • 1601 Pathology and Lab Medicine: Basic

Authors

  • Liu, Shing-Hwa, Institute of Toxicology, National Taiwan University, Taipei, Taiwan
  • Hung, Kuan-Yu, Superintendent Office, National Taiwan University Hospital Hsin-Chu Branch, Hsinchu, Taiwan
  • Chiang, Chih-Kang, Institute of Toxicology, National Taiwan University, Taipei, Taiwan
Background

Low-intensity pulsed ultrasound (LIPUS), a therapeutic ultrasound, is recognized to elevate the bone fracture repair process and help in some soft tissue healing. Here, we tested the prevention of chronic kidney disease (CKD)-associated cachexia and sarcopenia by LIPUS in a renal ischemia/reperfusion injury (IRI) mouse model.

Methods

Adult C57BL/6J male mice were used. A model of unilateral IRI with nephrectomy of the contralateral kidney with or without LIPUS treatment (3 MHz, 0.1 W/cm2, 20 minutes/day) 5 days before and 14 days after surgery was performed. The CKD-related cachexia/muscle wasting in mice was evaluated. Mice were euthanized 14 days after IRI.

Results

LIPUS treatment significantly alleviated the decrease in the serum albumin/globulin (A/G) ratio and the increases in the serum levels of blood urea nitrogen (BUN), creatinine, cystatin C, and fibroblast growth factor (FGF)-23, and the renal pathological changes and fibrosis in CKD mice (p<0.05, n=8; for A/G ratio and FGF-23). The development of epithelial-mesenchymal transition and the induction of senescence-related molecular signals and the decreased protein expressions of α-Klotho and endogenous antioxidant enzymes in the kidneys of CKD mice were significantly alleviated by LIPUS treatment (p<0.05, n=4). LIPUS treatment could also significantly reverse the decreased muscle mass, grip strength, and cross-section areas (CSA) of muscle fibers (p<0.05, n=8; for soleus muscle weight, hindlimb grip strength), and the increased muscular protein expressions of atrogenes, Atrogin1 and MuRF1, and phosphorylated AMP-activated protein kinase (AMPK), and the decreased muscular protein expressions of phosphorylated Akt, peroxisome proliferator-activated receptor-γ coactivator 1-α (PGC-1α), and mitochondrially encoded cytochrome c oxidase I (MT-CO1) in CKD mice (p<0.05, n=5 or 6).

Conclusion

LIPUS treatment showed the benefits for renal and muscular protection in a CKD mouse model via inhibition of renal fibrosis, restoration of antioxidant enzymes, and attenuation renal senescence/aging, and muscle mass loss via prevention of muscular mitochondrial dysfunction, AMPK activation, and Akt downregulation. LIPUS treatment may be potentially applied to an alternative non-invasive therapeutic intervention on CKD-associated cachexia/muscle wasting therapy.