Early administration of cold water and adipose derived mesenchymal stem cell derived exosome effectively protects the heart from ischemia-reperfusion injury.
Chai HT., Sheu JJ., Chiang JY., Shao PL., Wu SC., Chen YL.
Laboratory Study with a reported sample of 30 on Systemic / IV, published in Am J Transl Res (2019) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Laboratory Study
- Journal
- Am J Transl Res (2019)
- Country
- United States
- Reported sample size
- 30
- Source database
- PubMed
- PMID
- 31632517
Abstract (original English)
This study tested the hypothesis that early administration with cold water (CW)-assisted adipose-derived mesenchymal stem cell (ADMSC)-derived exosome (Exo) therapy was superior to either one on protecting the heart against ischemia-reperfusion (IR) (i.e., by ligation of 50 minutes and relieved by day 5 prior to euthanizing the animals) injury. Adult-male SD rats (n=30) were equally categorized into groups 1 (sham-operated control), 2 (IR), 3 (IR + CW), 4 (IR + Exo) and 5 (IR + CW-Exo). The left ventricular ejection fraction (LVEF) was highest in group 1, lowest in group 2, and significantly higher in group 5 than in groups 3 and 4, but no difference between groups 3 and 4 (all P<0.001). The protein expressions of oxidative-stress (NOX-1/NOX-2/NOX-4/oxidized protein), apoptotic/mitochondrial-damaged (mitochondrial-Bax/caspase 3/PARP/p53/cytosolic-cytochrome-C) and inflammatory (IL-1β/TNF-α/NF-κB/MMP-9) biomarkers, and cellular-stress response signaling (PI3K/Akt/GSK3β and p-m-TOR) showed an opposite pattern, whereas the anti-oxidants (SIRT1/SIRT3), anti-inflammation (IL-10) and IKB-α/p-AMKP/mitochondrial-cytochrome-C exhibited an identical pattern to the LVEF among the five groups (all P<0.0001). The cellular expressions of inflammation (CD68), total cellular ROS (i.e., stained by H 2 DCFDA) and the LV infarct/fibrotic/collagen-deposition areas displayed an opposite pattern, wh
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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