RRC ID 59854
著者 Li Q, Xing W, Xu X, Wang S, He Y, Wang Y, Sun H.
タイトル Tetramethylpyrazine alleviates lipopolysaccharide-induced damage in ATDC5 cells via down-regulating MyD88.
ジャーナル Exp Mol Pathol
Abstract BACKGROUND:Tetramethylpyrazine (TMP) has been reported to play a significant role in the cardiovascular and neuronal diseases. But, the functions of TMP in osteoarthritis (OA) remain unclear. In this investigation, we intended to probe the protective effectiveness of TMP in lipopolysaccharide (LPS)-caused damage in ATDC5 cells.
METHODS:ATDC5 cells were managed with LPS (5 μg/mL) for 12 h, and then the effects of TMP on these cells were evaluated. Cell viability and apoptosis of these treated cells were detected by CCK-8 and flow cytometry methods. The secretions of IL-1β, IL-6 and TNF-α were examined via applying ELISA kits. qRT-PCR was utilized to measure cell inflammatory factors and MyD88 expression. After transfection with pc-MyD88, the above-involved cell processes were reassessed, and NF-κB and p38MAPK pathways were examined by western blot assay.
RESULTS:LPS treatment induced a series of inflammatory destructions, which reduced viability, accelerated apoptosis and cell inflammatory factors release in ATDC5 cells. However, TMP precondition clearly mitigated LPS-triggered ATDC5 cell injury. Additionally, TMP down-regulated MyD88 expression in LPS-treated ATDC5 cells, as well as overexpression of MyD88 overturned the impacts of TMP on LPS-induced cell injury in ATDC5 cells. Beyond that, TMP restrained LPS-triggered the activations of NF-κB and p38MAPK via repression of MyD88.
CONCLUSION:The above consequences exhibited that TMP exhibited a protective effect to lighten LPS-caused cell damage via mediating MyD88/NF-κB/p38MAPK pathways. These findings suggested that TMP perhaps an effective agent for the clinical treatment of OA.
巻・号 111
ページ 104317
公開日 2019-12-1
DOI 10.1016/j.yexmp.2019.104317
PII S0014-4800(19)30345-4
PMID 31655387
MeSH Animals Apoptosis / drug effects* Cells, Cultured Chondrocytes / drug effects* Chondrocytes / metabolism Chondrocytes / pathology Inflammation / drug therapy* Inflammation / metabolism Inflammation / pathology Lipopolysaccharides / toxicity* Mice Myeloid Differentiation Factor 88 / genetics Myeloid Differentiation Factor 88 / metabolism* NF-kappa B / genetics NF-kappa B / metabolism Pyrazines / pharmacology* Signal Transduction Vasodilator Agents / pharmacology* p38 Mitogen-Activated Protein Kinases / genetics p38 Mitogen-Activated Protein Kinases / metabolism
IF 2.35
引用数 1
リソース情報
ヒト・動物細胞 ATDC5(RCB0565)