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Acacetin inhibits expression of matrix metalloproteinases via a MAPK-dependent mechanism in fibroblast-like synoviocytes.

Chen WP, Yang ZG, Hu PF, Bao JP, Wu LD - J. Cell. Mol. Med. (2015)

Bottom Line: We found that acacetin inhibits p38 and JNK phosphorylation and reduces MMP-1, MMP-3 and MMP-13 expression in interleukin-1β-induced FLSs.Our results suggest that acacetin has antiarthritic effects in FLSs.Thus, acacetin should be further studied for the treatment of arthritis.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopedic Surgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, China.

No MeSH data available.


Related in: MedlinePlus

Effect of acacetin on IL-1β-induced phosphorylation of MAPKs in FLSs. Western blotting was performed to detect the phosphorylation levels of JNK, ERK1/2 and p38 in cells pre-treated with acacetin for 2 hrs before stimulation with IL-1β for 30 min. (A). The ratio between the intensity of the phosphorylated and non-phosphorylated band are shown in B. Cells were treated with a p38 inhibitor or a JNK inhibitor for 2 hrs before stimulation with IL-1β for 30 min., and MMP-1, MMP-3 and MMP-13 expression were assessed (C). *P < 0.05 compared with cells stimulated with IL-1β in the absence of acacetin.
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fig04: Effect of acacetin on IL-1β-induced phosphorylation of MAPKs in FLSs. Western blotting was performed to detect the phosphorylation levels of JNK, ERK1/2 and p38 in cells pre-treated with acacetin for 2 hrs before stimulation with IL-1β for 30 min. (A). The ratio between the intensity of the phosphorylated and non-phosphorylated band are shown in B. Cells were treated with a p38 inhibitor or a JNK inhibitor for 2 hrs before stimulation with IL-1β for 30 min., and MMP-1, MMP-3 and MMP-13 expression were assessed (C). *P < 0.05 compared with cells stimulated with IL-1β in the absence of acacetin.

Mentions: As MAPK pathways are involved in the regulation of MMP expression as well as the inflammatory process, the effects of acacetin on MAPKs were investigated. IL-1β significantly induced the phosphorylation of ERK1/2, p38 and JNK within 30 min. The phosphorylation of p38 and JNK was inhibited by acacetin, whereas the phosphorylation of ERK1/2 was not affected (Fig.4A). The ratio between the intensity of the phosphorylated and non-phosphorylated band are shown in Figure4B. Furthermore, pre-treatment of FLSs with either a p38 inhibitor (SB203580; 10 μM) or a JNK inhibitor (SP600125, 10 μM) for 2 hrs before stimulation with IL-1β for 30 min. reduced IL-1β-induced protein expressions of MMP-1, MMP-3 and MMP-13 (Fig.4C).


Acacetin inhibits expression of matrix metalloproteinases via a MAPK-dependent mechanism in fibroblast-like synoviocytes.

Chen WP, Yang ZG, Hu PF, Bao JP, Wu LD - J. Cell. Mol. Med. (2015)

Effect of acacetin on IL-1β-induced phosphorylation of MAPKs in FLSs. Western blotting was performed to detect the phosphorylation levels of JNK, ERK1/2 and p38 in cells pre-treated with acacetin for 2 hrs before stimulation with IL-1β for 30 min. (A). The ratio between the intensity of the phosphorylated and non-phosphorylated band are shown in B. Cells were treated with a p38 inhibitor or a JNK inhibitor for 2 hrs before stimulation with IL-1β for 30 min., and MMP-1, MMP-3 and MMP-13 expression were assessed (C). *P < 0.05 compared with cells stimulated with IL-1β in the absence of acacetin.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4549041&req=5

fig04: Effect of acacetin on IL-1β-induced phosphorylation of MAPKs in FLSs. Western blotting was performed to detect the phosphorylation levels of JNK, ERK1/2 and p38 in cells pre-treated with acacetin for 2 hrs before stimulation with IL-1β for 30 min. (A). The ratio between the intensity of the phosphorylated and non-phosphorylated band are shown in B. Cells were treated with a p38 inhibitor or a JNK inhibitor for 2 hrs before stimulation with IL-1β for 30 min., and MMP-1, MMP-3 and MMP-13 expression were assessed (C). *P < 0.05 compared with cells stimulated with IL-1β in the absence of acacetin.
Mentions: As MAPK pathways are involved in the regulation of MMP expression as well as the inflammatory process, the effects of acacetin on MAPKs were investigated. IL-1β significantly induced the phosphorylation of ERK1/2, p38 and JNK within 30 min. The phosphorylation of p38 and JNK was inhibited by acacetin, whereas the phosphorylation of ERK1/2 was not affected (Fig.4A). The ratio between the intensity of the phosphorylated and non-phosphorylated band are shown in Figure4B. Furthermore, pre-treatment of FLSs with either a p38 inhibitor (SB203580; 10 μM) or a JNK inhibitor (SP600125, 10 μM) for 2 hrs before stimulation with IL-1β for 30 min. reduced IL-1β-induced protein expressions of MMP-1, MMP-3 and MMP-13 (Fig.4C).

Bottom Line: We found that acacetin inhibits p38 and JNK phosphorylation and reduces MMP-1, MMP-3 and MMP-13 expression in interleukin-1β-induced FLSs.Our results suggest that acacetin has antiarthritic effects in FLSs.Thus, acacetin should be further studied for the treatment of arthritis.

View Article: PubMed Central - PubMed

Affiliation: Department of Orthopedic Surgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang Province, China.

No MeSH data available.


Related in: MedlinePlus