A Fermented Whole Grain Prevents Lipopolysaccharides-Induced Dysfunction in Human Endothelial Progenitor Cells.
Laura GiustiMorena GabrieleGiuseppe PennoMonia GarofoloVincenzo LongoStefano Del PratoDaniela LucchesiLaura PucciPublished in: Oxidative medicine and cellular longevity (2017)
Endogenous and exogenous signals derived by the gut microbiota such as lipopolysaccharides (LPS) orchestrate inflammatory responses contributing to development of the endothelial dysfunction associated with atherosclerosis in obesity, metabolic syndrome, and diabetes. Endothelial progenitor cells (EPCs), bone marrow derived stem cells, promote recovery of damaged endothelium playing a pivotal role in cardiovascular repair. Since healthy nutrition improves EPCs functions, we evaluated the effect of a fermented grain, Lisosan G (LG), on early EPCs exposed to LPS. The potential protective effect of LG against LPS-induced alterations was evaluated as cell viability, adhesiveness, ROS production, gene expression, and NF-kB signaling pathway activation. Our results showed that LPS treatment did not affect EPCs viability and adhesiveness but induced endothelial alterations via activation of NF-kB signaling. LG protects EPCs from inflammation as well as from LPS-induced oxidative and endoplasmic reticulum (ER) stress reducing ROS levels, downregulating proinflammatory and proapoptotic factors, and strengthening antioxidant defense. Moreover, LG pretreatment prevented NF-kB translocation from the cytoplasm into the nucleus caused by LPS exposure. In human EPCs, LPS increases ROS and upregulates proinflammatory tone, proapoptotic factors, and antioxidants. LG protects EPCs exposed to LPS reducing ROS, downregulating proinflammatory and proapoptotic factors, and strengthening antioxidant defenses possibly by inhibiting NF-κB nuclear translocation.
Keyphrases
- lps induced
- inflammatory response
- endothelial cells
- high glucose
- anti inflammatory
- signaling pathway
- oxidative stress
- metabolic syndrome
- toll like receptor
- gene expression
- dna damage
- stem cells
- cell death
- diabetic rats
- reactive oxygen species
- endoplasmic reticulum
- type diabetes
- insulin resistance
- cardiovascular disease
- pi k akt
- pluripotent stem cells
- nitric oxide
- dna methylation
- mesenchymal stem cells
- epithelial mesenchymal transition
- induced apoptosis
- nuclear factor
- induced pluripotent stem cells
- immune response
- bone marrow
- risk assessment
- mouse model
- weight gain
- cardiovascular risk factors
- cell proliferation
- climate change
- high fat diet induced