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Objective: To evaluate the anti-inflammatory property of both glycyrrhizic acid(GA)and glabridin in reducing inflammation to accelerate wound regeneration on 3T3-L1 and NIH-3T3 fibroblast cell lines.Methods: Cell proliferation and viability assay(MTT assay), scratch wound healing assays,and quantitative real-time PCR were conducted to investigate the effects on cell proliferation,cell migration, and expression of CXC chemokine ligand 5 inflammation gene respectively.Results: Results showed that at a low concentration of 1 × 10~(-8)mol/L, glabridin down regulated cell proliferation in NIH-3T3 significantly, suggesting its involvement in ERK1/2 signaling pathway. GA and glabridin significantly accelerated cell migration through wound healing in both 3T3-L1 and NIH-3T3 and significantly down regulated the expression of CXC chemokine ligand 5 in 3T3-L1 at concentration 1 × 10~(-8)mol/L,indicating the possible involvement of nuclear factor-k B and cyclooxygenase 2 transcriptions modulation.Conclusions: Both GA and glabridin can serve as potential treatment for chronic inflammatory disease, and glabridin as an oncogenic inhibitor due to its anti-proliferative property.
Objective: To evaluate the anti-inflammatory property of both glycyrrhizic acid (GA) and glabridin in reducing inflammation to accelerate wound regeneration on 3T3-L1 and NIH-3T3 fibroblast cell lines. Methods: Cell proliferation and viability assay (MTT assay) wound healing assays, and quantitative real-time PCR were conducted to investigate the effects on cell proliferation, cell migration, and expression of CXC chemokine ligand 5 inflammasome respectively. Results: Results showed that at a low concentration of 1 × 10 ~ 8) mol / L, glabridin down regulated cell proliferation in NIH-3T3 significantly, suggesting its involvement in ERK1 / 2 signaling pathway. GA and glabridin significantly accelerated cell migration through wound healing in both 3T3-L1 and NIH-3T3 and significantly decreased regulated the expression of CXC chemokine ligand 5 in 3T3-L1 at concentration 1 × 10 ~ (-8) mol / L, indicating the possible involvement of nuclear factor-k B and cyclooxygenase 2 transcriptions modulatio n.Conclusions: Both GA and glabridin can serve as potential treatment for chronic inflammatory disease, and glabridin as an oncogenic inhibitor due to its anti-proliferative property.