Extracorporeal Shockwave Effectively Attenuate Brain Infarct Size Improve Neurological Function in Rat Mode

Extracorporeal Shockwave Effectively Attenuate Brain Infarct Size Improve Neurological Function in Rat Mode
Chun-Man Yuen, Han-Kan Yip

Institution:
Kaohsiung Chang Gung Memorial Hospital; Taiwan

Device and producing company:
none

Introduction:
We tested hypothesis that extracorporeal shock wave (ECSW) therapy effectively attenuated rat brain ischemic area (BIA) and improved neurological function in acute ischemic stroke (AIS) that was induced by occlusion of distal left internal carotid artery.

Methods:
Adult-male SD rats (n=20) were divided into AIS, and AIS-ECSW (energy dosage of 0.15mJ/mm2/300 impulses) and sacrificed by day 21 after the procedure. Results: In normal animals, the intra-cranial pressure was found to be increased from 5 mmHg (baseline) to 15 mmHg during applying the ECSW to the rat skull. Additionally, the brain protein levels of apoptotic (cleaved caspase 3 and PRAP) and DNA-damaged (γ-H2A) markers did not differ between with and without ECSW therapy. Furthermore, p- S6K and focal adhesion molecule (FAK) were the earliest proteins to be activated (2 hr post-ECSW), followed by heat shock protein 70 and the brain glial cells (≥ 16 hr after ECSW application).
By day 21, brain MRI demonstrated that that BIA was larger in AIS than in AIS-ECSW (p<0.001). Sensorimotor functional test (Corner test) identified a higher frequency of turning movement to left in AIS than in AIS-ECSW (p<0.05). The cellular and protein expressions of angiogenesis biomarkers in BIA (CD31, VEGF, CXCR4, SDF-1α) were higher in AIS-ECSW than in AIS animals (all p<0.001). Number of apoptotic nuclei on TUNEL assay and protein expressions of cleaved caspase 3 and PRAP, and γ-H2A, MMP-9, and TNF-α were significantly higher in AIS-ECSW than in AIS animals (all p<0.001).

Discussion:
none

Conclusion:
Application of ESCW with energy dosage of 0.15mJ/mm2/300 to the rat brain was safe and effectively reduced BIA and improved neurological function through inhibiting inflammation and cellular apoptosis and enhancing angiogenesis.