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2022, Vol. 26 ›› Issue (7): 1080-1084Mechanism by which allicin inhibits proliferation and promotes apoptosis of rat vascular endothelial cellsZhang Yujie1, 2, Yang Jiandong2, Cai Jun2, Zhu Shoulei2, Tian Yuan2
Abstract: BACKGROUND: Allicin has anti-fibrosis and anti-angiogenesis effects. Previous studies have confirmed the inhibitory effect of allicin on the proliferation of fibroblasts, but the effect and exact mechanism of allicin on the proliferation and apoptosis of vascular endothelial cells are still unclear. OBJECTIVE: To observe the effect of allicin on the morphology, proliferation and apoptosis of vascular endothelial cells and its possible mechanism, and provide a theoretical basis for the next clinical application of allicin. METHODS: Vascular endothelial cells were routinely cultured to logarithmic phase in vitro, and the cells were divided into control group (0 mg/L), low concentration group (25 mg/L), medium concentration group (50 mg/L), and high concentration group (100 mg/L) according to the concentration of allicin in the medium. After 24 hours of intervention, CCK-8 assay was used to detect cell viability. Inverted phase contrast microscope was used to observe cell morphological changes. AO/EB double staining method and AnnexinV-FITC double staining method were used to detect apoptosis rate. PI/RNase method was used to detect cell cycle. Reverse-transcription PCR and western blot assay were used to measure the expression levels of PCNA, Bax and BcL-2 proteins and genes. RESULTS AND CONCLUSION: After treated with allicin at concentrations of 0, 25, 50 and 100 mg/L for 24 hours, the viability of vascular endothelial cells significantly decreased in a time-dose-dependent manner, with an IC50 value of 103.27 mg/L at 24 hours. As the concentrations of allicin increased, the apoptosis rate of vascular endothelial cells rose up (P < 0.01); the cell numbers at G1 phase decreased (P < 0.01); and at G2 phase increased (P < 0.01). Compared with control group, the expression of PCNA and Bcl-2 decreased (P < 0.01), while the expression of Bax increased significantly in the allicin group (P < 0.01). The results suggested that allicin inhibited the proliferation of vascular endothelial cells and induced their apoptosis. The action mechanism may be achieved by regulating the expression of PCNA, Bcl-2 and Bax. Key words:vascular endothelial cells, allicin, proliferation, apoptosis, factor, mechanism, epidural scar |