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Emodin attenuates apoptosis and inflammation induced by LPS through up-regulating lncRNA TUG1 in murine chondrogenic ATDC5 cells.
Biomedicine & Pharmacotherapy 2018 July
BACKGROUND: Osteoarthritis (OA) is the most frequent arthritic disease that causes disability and reduces life quality. The treatments for OA are conservative and more effective therapy remains to be identified. Herein, we mainly focused on the role of emodin in lipopolysaccharide (LPS)-induced murine chondrogenic ATDC5 cells as well as the underlying mechanisms.
METHODS: In vitro cell system to mimic OA was constructed after LPS treatments. Effects of emodin on viability, apoptosis and release of inflammatory cytokines (TNF-α, IL-6 and MCP-1) in LPS-treated ATDC5 cells were measured. Then, expression of long non-coding RNA Taurine up-regulated gene 1 (TUG1) in emodin-treated ATDC5 cells was tested by reverse transcription-quantitative PCR. Finally, the involvements of the Notch and NF-κB pathways in the emodin-associated regulation were determined by Western blot analysis. Meanwhile, whether the alteration of these two pathways was associated with TUG1 was verified.
RESULTS: The LPS-induced decrease of cell viability, increases of apoptosis and pro-inflammatory cytokines expression, and alterations of apoptosis-related proteins were all mitigated by emodin stimulation in ATDC5 cells. Then, we interestingly identified that TUG1 was up-regulated by emodin, and the Notch and NF-κB pathways were inhibited by emodin. More experiments proved that emodin inactivated these two pathways through up-regulating TUG1.
CONCLUSION: Emodin mitigated the LPS-induced apoptosis and inflammation in ATDC5 cells. Emodin might function through inhibiting the Notch and NF-κB pathways via up-regulating TUG1. Our findings might furnish a prospective therapeutic strategy using emodin for OA.
METHODS: In vitro cell system to mimic OA was constructed after LPS treatments. Effects of emodin on viability, apoptosis and release of inflammatory cytokines (TNF-α, IL-6 and MCP-1) in LPS-treated ATDC5 cells were measured. Then, expression of long non-coding RNA Taurine up-regulated gene 1 (TUG1) in emodin-treated ATDC5 cells was tested by reverse transcription-quantitative PCR. Finally, the involvements of the Notch and NF-κB pathways in the emodin-associated regulation were determined by Western blot analysis. Meanwhile, whether the alteration of these two pathways was associated with TUG1 was verified.
RESULTS: The LPS-induced decrease of cell viability, increases of apoptosis and pro-inflammatory cytokines expression, and alterations of apoptosis-related proteins were all mitigated by emodin stimulation in ATDC5 cells. Then, we interestingly identified that TUG1 was up-regulated by emodin, and the Notch and NF-κB pathways were inhibited by emodin. More experiments proved that emodin inactivated these two pathways through up-regulating TUG1.
CONCLUSION: Emodin mitigated the LPS-induced apoptosis and inflammation in ATDC5 cells. Emodin might function through inhibiting the Notch and NF-κB pathways via up-regulating TUG1. Our findings might furnish a prospective therapeutic strategy using emodin for OA.
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