Why the study?
Mesenchymal stem cells have emerged as an attractive therapeutic agent, motivating investigation into the effect of human umbilical cord MSCs on atherosclerotic plaque formation and lesion progression.
Does human umbilical cord mesenchymal stem cell treatment reduce atherosclerotic plaque formation in a high-fat diet rabbit model?
Does human umbilical cord mesenchymal stem cell treatment reduce atherosclerotic plaque formation in a high-fat diet rabbit model?
Human umbilical cord mesenchymal stem cells alleviate atherosclerotic plaque burden and inflammation in a high-fat diet rabbit model, potentially mediated by regulation of intestinal flora and TMAO levels.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating in rabbits; human trials needed before considering stem cell therapy for atherosclerosis.
BACKGROUND: Atherosclerosis (AS) is a complex disease caused in part by dyslipidemia and chronic inflammation. AS is associated with serious cardiovascular disease and remains the leading cause of mortality worldwide. Mesenchymal stem cells (MSCs) have evolved as an attractive therapeutic agent in various diseases including AS. Human umbilical cord MSCs (UCSCs) have been used in cell therapy trials due to their ability to differentiate and proliferate. The present study aimed to investigate the effect of UCSCs treatment on atherosclerotic plaque formation and the progression of lesions in a high-fat diet rabbit model. METHODS: in 500 μL phosphate buffered saline) after 1 month of high-fat diet, once every 2 weeks, for 3 months. The model group was given PBS only. We analyzed serum biomarkers, used ultrasound and histopathology to detect arterial plaques and laser Doppler imaging to measure peripheral blood vessel blood filling, and analyzed the intestinal flora and metabolism. RESULTS: Histological analysis showed that the aortic plaque area was significantly reduced in the treatment group. We also found a significant decrease in macrophage accumulation and apoptosis, an increase in expression of scavenger receptors CD36 and SRA1, a decrease in uptake of modified low-density protein (ox-LDL), and a decrease in levels of pro-inflammatory cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-α following UCSCs treatment. We also found that anti-inflammatory cytokines IL-10 and transforming growth factor (TGF)-β expression increased in the aorta atherosclerotic plaque of the treatment group. UCSCs treatment improved the early peripheral blood filling, reduced the serum lipid level, and inhibited inflammation progression by regulating the intestinal flora dysbiosis caused by the high-fat diet. More specifically, levels of the microbiota-dependent metabolite trimethylamine-N-oxide (TMAO) were down-regulated in the treatment group. CONCLUSIONS: UCSCs treatment alleviated atherosclerotic plaque burden by reducing inflammation, regulating the intestinal flora and TMAO levels, and repairing the damaged endothelium.
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Li et al. (2021) studied this question.
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