Dihydroergotamine ameliorates liver fibrosis by targeting transforming growth factor β type II receptor

Figure 2 Treatment inhibiting the activation of LX-2 cells. A and B: After LX-2 cell was activated with transforming growth factor β 1 (TGFβ1) (5 ng/mL) for 24 h, different concentrations of lifitegrast and phenytoin were added for 24 h, and the protein levels of collagen III and α-SMA were detected by western blot; C and D: After LX-2 was activated with TGFβ1 (5 ng/mL) for 24 h, different concentrations of darifenacin and dihydroergotamine (DHE) were added for further treatment for 24 h, and the protein levels of collagen III, α-SMA, and p-SMAD3 were detected by western blot; E: Real-time polymerase chain reaction (RT-PCR) was performed to detect the expression of COL1A1, COL1A2, COL3A1, and α-SMA of LX-2 after different concentrations of darifenacin treatment (n = 6); F: RT-PCR was performed to detect the expression of COL1A1, COL1A2, COL3A1, and α-SMA of LX-2 after different concentrations of DHE treatment (n = 5-6). All data are presented as means ± standard error of the mean. One-way ANOVA test was performed. ^aP < 0.05, ^bP < 0.01, ^cP < 0.001, and ^dP < 0.0001. TGFβ: Transforming growth factor β; TGFβR: Transforming growth factor β receptor; DHE: Dihydroergotamine.