Abstract Title:

Tetramethylpyrazine alleviates lipopolysaccharide-induced damage in ATDC5 cells via down-regulating MyD88.

Abstract Source:

Exp Mol Pathol. 2019 Dec ;111:104317. Epub 2019 Oct 23. PMID: 31655387

Abstract Author(s):

Qiang Li, Wanying Xing, Xiong Xu, Sulong Wang, Yisha He, Yueshu Wang, Hongbin Sun

Article Affiliation:

Qiang Li


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.

Study Type : In Vitro Study

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