Abstract
BackgroundThe purpose of present study was to explore the mechanism of nuclear factor-kappa B (NF-κB), phosphatidylinositol 3-kinase (PI3K)/protein kinase B(PKB/Akt) and mitogen-activated protein kinase (MAPK) signaling pathways after intervention of advanced glycosylation end products (AGEs) on rat bone-marrow stromal cells (BMSCs).MethodsPrepare and identify AGEs. BMSCs were isolated from 16 SD rats and cultured with different concentration of AGEs. Cell viability was detected by cell counting kit-8 (CCK-8). BMSCs were cultured with AGEs (0.25 mg/ml) for 30 min, 12 h, 24 h, 72 h and 120 h. In addition, BMSCs were cultured with AGEs, AGEs + JNK inhibitor and AGEs + P38 inhibitor for 24 h and 48 h, respectively. Western blotting and RT-PCR were used to determine the protein and mRNA expression levels, respectively.ResultsCell viability of BMSCs was significantly correlated with concentration and effect time of AGEs (P < 0.05), and the most appropriate concentration was 0.25 mg/ml. AGEs stimulation significantly increased the protein expression levels of NF-κB p65, JNK, p38 (P < 0.05), decreased IκB (P < 0.05), but had no effect on the protein expression of Akt in BMSCs (P > 0.05). At the mRNA level, JNK and p38 inhibitors significantly reduced the levels of NF-κB p65, p38 and JNK, increased IκB (P > 0.05), but had no effect on Akt in BMSCs (P > 0.05). At the protein level, JNK and p38 inhibitors notably decreased the expression of NF-κB p65, p38, p-JNK, P-IκB and JNK (P < 0.001), and increased IκB (P < 0.05).ConclusionAdvanced glycosylation end products can inhibit the proliferation of bone-marrow stromal cells through activating MAPK pathway.
Highlights
The purpose of present study was to explore the mechanism of nuclear factor-kappa B (NF-κB), phosphatidylinositol 3-kinase (PI3K)/protein kinase B(PKB/Akt) and mitogen-activated protein kinase (MAPK) signal‐ ing pathways after intervention of advanced glycosylation end products (AGEs) on rat bone-marrow stromal cells (BMSCs)
The change of biomembrane ecosystem of subgingival plaque and the increase of adipocytokine secretion caused by diabetes related obesity and dyslipidemia play a synergistic role, leading to the loss of metabolism balance of periodontal tissue, which is manifested in the increase of periodontal tissue damage and tissue repair function damage, that is, rapid progress and serious periodontitis [10]
It was confirmed that AGEs could inhibit BMSCs proliferation and nuclear factor-κB (NF-κB) expression
Summary
The purpose of present study was to explore the mechanism of nuclear factor-kappa B (NF-κB), phosphatidylinositol 3-kinase (PI3K)/protein kinase B(PKB/Akt) and mitogen-activated protein kinase (MAPK) signal‐ ing pathways after intervention of advanced glycosylation end products (AGEs) on rat bone-marrow stromal cells (BMSCs). Under the condition of hyperglycemia, advanced glycosylation end products (AGEs) and its main signal receptor RAGE interact with each other, which can lead to the abnormal function of immune cells, change the phenotype and function of other important cells in periodontal tissues, and increase the expression of pro-inflammatory cytokines (Interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α) [7]. Li et al Eur J Med Res (2021) 26:94 hyperglycemia increases the over expression of reactive oxygen species (ROS) and causes oxidative stress [8]. It can directly or indirectly change the quantity and quality of various cytokines through the AGEs/RAGE response axis. The change of biomembrane ecosystem of subgingival plaque and the increase of adipocytokine secretion caused by diabetes related obesity and dyslipidemia play a synergistic role, leading to the loss of metabolism balance of periodontal tissue, which is manifested in the increase of periodontal tissue damage and tissue repair function damage, that is, rapid progress and serious periodontitis [10]
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