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Diclofenac inhibits 27-hydroxycholesterol-induced inflammation
Bo-Young Kim1, Yonghae Son1, Seong-Kug Eo2
1Department of Pharmacology, Pusan National University - School of Medicine, Yangsan, Gyeongnam 50612, Republic of Korea.
Biochemical and Biophysical Research Communications
|August 31, 2016
Summary
Diclofenac effectively reduces inflammation caused by 27-hydroxycholesterol (27OHChol), a cholesterol oxidation product. This study shows diclofenac suppresses key inflammatory markers and cell migration in response to 27OHChol.
Area of Science:
- Biochemistry
- Immunology
- Pharmacology
Background:
- 27-Hydroxycholesterol (27OHChol) is a cholesterol oxidation product known to promote inflammation.
- Understanding the mechanisms by which 27OHChol induces inflammation is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the anti-inflammatory effects of diclofenac on 27OHChol-induced responses in human monocyte/macrophage (THP-1) cells.
- To determine the impact of diclofenac on chemokine production, cell migration, and matrix metalloproteinase activity.
Main Methods:
- Utilized human THP-1 cells to model 27OHChol-induced inflammation.
- Assessed the effects of varying diclofenac concentrations on chemokine (CCL2, CCL3, CCL4) transcription and secretion.
- Measured monocytic cell and T cell migration, as well as MMP-9 activity.
Main Results:
- Diclofenac significantly attenuated the 27OHChol-induced transcription and secretion of CCL2, CCL3, and CCL4 chemokines in a dose-dependent manner.
- Diclofenac reduced the migration of monocytic cells and CCR5-positive Jurkat T cells.
- The drug also inhibited 27OHChol plus LPS-induced CCL2 overproduction, monocytic cell migration, and MMP-9 activity.
Conclusions:
- Diclofenac demonstrates potent anti-inflammatory properties against 27OHChol-induced responses.
- These findings suggest diclofenac can suppress inflammation in environments characterized by cholesterol oxidation products.
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