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Palmitate triggers inflammatory response by upregulating fatty acid translocase in THP-1 macrophages / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12): 393-398, 2018.
Article in Chinese | WPRIM | ID: wpr-701133
ABSTRACT

AIM:

To investigate the role of fatty acid translocase(FAT/CD36)on palmitate-induced inflam-mation in human monocyte-derived macrophage THP-1.

METHODS:

THP-1 cells were treated with palmitate(0,0.1 and 0.2 mmol/L)for 24 h.Transwell chamber assay was used to examine the migration ability of THP-1 cells.The mRNA ex-pression of CD36,tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)and monocyte chemotactic protein 1(MCP-1) was measured by real-time PCR.The protein levels of TNF-αand IL-6 in the supernatant of cultured cells were measured by ELISA.The protein level of CD36 was examined by Western blot.Small interfering RNA(siRNA)targeting CD36 (siCD36)was used to inhibit the expression of CD 36 in the THP-1 cells,and the changes of the cell migration and inflam-matory response were monitored as mentioned above.

RESULTS:

Palmitate increased the expression of CD36 in the THP-1 cells(P<0.05).Palmitate also up-regulated inflammatory cytokine and chemokine levels,and the differences were sta-tistically significant(P<0.05).Compared with control group,palmitate promoted migration of THP-1 cells.siCD36 was transfected into the THP-1 cells and the silencing efficiency was approximately 54%.The protein levels of TNF-αand IL-6 were also decreased in siCD36 group compared with scrambled RNA(scrRNA)group,and the differences were statisti-cally significant(P<0.05).The migrated cells in siCD36 group were significantly less than those in scrRNA group(P<0.05).

CONCLUSION:

Palmitate promotes migration ability and triggers inflammatory response in the THP-1 macropha-ges by upregulating CD36 expression.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2018 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 2018 Type: Article