To observe the expression of peroxisome proliferator-activated receptor γ (PPARγ) and CD40/CD40L pathway in patients with acute coronary syndrome (ACS) who were treated with tirofiban.

One hundred and twenty ACS patients in cardiology department of Handan No.1 hospital were selected from December 2016 to July 2017.All patients were randomly divided into control group and tirofiban groups according to random number table, blood samples of patients in tirofiban groups were collected 12 h, 24 h and 36 h after percutaneous coronary intervention (PCI). The protein expression levels of CD40, CD40L and PPARγ were measured by enzyme-linked immunosorbent assay (ELISA). CD40, CD40L and PPARγ mRNA levels were assayed by reverse transcription-polymerase chain reaction (RT-PCR).

In tirofiban groups, CD40 and CD40L protein expression decreased, the levels of CD40 and CD40L were (0.86±0.08)μg/L, (0.46±0.05)μg/L, (0.40±0.05)μg/L and (0.92±0.04)μg/L, (0.54±0.04)μg/L, (0.40±0.05)μg/L, respectively.PPARγ expression increased, (0.94±0.04)μg/L, (1.40±0.01)μg/L and (1.48±0.01)μg/L, respectively.Compared with control group, the differences were statistically significant (F=1 977.39, 5 071.39, 4 719.81, all P<0.01). The expression of CD40 (0.98±0.07, 0.50±0.02, 0.41±0.01) and CD40L (1.02±0.06, 0.50±0.02, 0.40±0.01) mRNA decreased, and PPARγ increased (0.74±0.04, 1.31±0.01, 1.49±0.01). The differences also had statistical significance (F=5 781.52, 5 935.29, 4 683.59, all P<0.01).

Tirofiban could up-regulate the expression of PPARγ, and inhibit the activation of CD40/CD40L signaling pathway so that it can suppress inflammation and stabilize atheromatous plaque.