Abstract

To investigate the effect of allicin on the expression of α-smooth muscle actin (α-SMA) in airway smooth muscle cells (ASMC), and to evaluate the mechanism of allicin on inhibition of airway remodeling. The human ASMCs were treated for 48 hours with 0, 2.5, 5.0, and 10.0 μmol/L allicin, respectively, and the total RNA and protein of the cells were collected. The mRNA expression of α-SMA was determined by real-time polymerase chain reaction (PCR) analysis. The protein expression of α-SMA and phosphorylation Smad1 (p-Smad1) were assessed by Western blotting analysis. After the treatment with allicin for 48 hours in a dose of 0, 2.5, 5.0, and 10.0 μmol/L respectively, the mRNA expression of α-SMA was down-regulated (0.543±0.121, 0.354±0.072, 0.223±0.058, and 0.191±0.034, respectively), with statistically significant difference among groups (all P<0.05), and the protein expression of α-SMA and p-Smad1 was also gradually down-regulated in a dose-dependent manner [α-SMA protein (grad value ratio): 0.96±0.02, 0.72±0.16, 0.54±0.11, and 0.31±0.14, respectively; p-Smad1 protein (grad value ratio): 0.94±0.03, 0.76±0.13, 0.62±0.11, and 0.43±0.12, respectively), with statistically significant difference among groups (all P<0.05). Allicin depresses the mRNA and protein expression of α-SMA, and inhibits p-Smad1 in a dose-dependent manner, thus interrupts the transforming growth factor-β and Rho kinase signal pathway.

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