Protective and proliferative effect of Aesculus indica extract on stressed human adipose stem cells via downregulation of NF-κB pathway
0301 basic medicine
Cell biology
NFKB1
Science
Phytochemicals
Anti-Inflammatory Agents
Aesculus
Down-Regulation
Adipose tissue
FOS: Basic medicine
Plant Science
Signal transduction
Biochemistry
Gene
NF-κB
Agricultural and Biological Sciences
03 medical and health sciences
Cell Movement
Biochemistry, Genetics and Molecular Biology
Humans
Molecular Biology
Biology
Cells, Cultured
Cell Proliferation
Inflammation
Stem cell
Biological Activities of Prenylated Flavonoids
Plant Extracts
Superoxide Dismutase
Q
R
NF-kappa B
Life Sciences
Mesenchymal Stem Cells
Downregulation and upregulation
Iodoacetic Acid
3. Good health
Oxidative Stress
Chemistry
Adipose Tissue
Bioavailability and Health Effects of Curcumin
Medicine
Molecular Medicine
Transcription factor
Research on Citrus Flavonoids and Health Benefits
Research Article
Signal Transduction
DOI:
10.1371/journal.pone.0258762
Publication Date:
2021-10-22T20:24:27Z
AUTHORS (7)
ABSTRACT
Inflammatory microenvironment after transplantation affects the proliferation and causes senescence of adipose-derived mesenchymal stem cells (hADMSCs) thus compromising their clinical efficacy. Priming with herbal extracts is considered very promising to improve viability in inflammatory milieu. Aesculus indica (A. indica) used treat many diseases Asia for decades. Herein, we explored protective role A. extract on human Mesenchymal Stem Cells against Monosodium Iodoacetate (MIA) induced stress vitro. ameliorated injury as depicted by significantly enhanced proliferation, viability, improved cell migration superoxide dismutase activity. Furthermore, reduced lactate dehydrogenase activity, reactive oxygen species release, senescent apoptotic were detected primed hADMSCs. Downregulation NF-κB pathway associated genes, p65/RelA p50/NF-κB 1, Interleukin 6 (IL-6), 1 (IL-1β), Tumor necrosis factor alpha (TNF-α) matrix metalloproteinase 13 (MMP-13) observed hADMSCs compared stressed Complementary gene expression, priming release transcription p65, inhibitory-κB kinase (IKK) α β, IL-1β TNF-α proteins expression. Our data elucidates that preconditioning rescued oxidative therapeutic potential relieving inflammation through regulation pathway.
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