The Effect of Ligustilide on the Proliferation and Apoptosis of Human Cerebral Adventitia Fibroblasts Induced by Interferon-α Through lncRNA NKILA
LU Jinhua1,2*, CHENG Xi1, DAI Qingyue1
The aim of this study is to investigate the effect of ligustilide on the proliferation and apoptosis of HBVAF (human brain vascular adventitia fibroblast) induced by IFN-α (interferon-α) and its possible mechanism. HBVAF cells were induced by IFN-α to establish a cell injury model. The effect of different doses of ligustilide on the proliferation, colony formation and apoptosis of HBVAF cells induced by IFN-α were detected by MTT, plate clone formation assays and flow cytometry, respectively. qRT-PCR was used to detect the expression of lncRNA NKILA. In order to explore the effects of ligustilide and lncRNA NKILA on the proliferation and apoptosis of HBVAF cells induced by IFN-α, HBVAF cells were transfected with pcDNA and pcDNA-lncRNA NKILA, and then treated with IFN-α for 24 h. HBVAF cells were transfected with si-NC and si-lncRNA NKILA, and then co-treated with ligustilide and IFN-α for 24 h. Western blot was used to detect the expression of apoptosis-related proteins. The results showed that after ligustilide treatment, the cell survival rate and the expression of lncRNA NKILA were increased (P<0.05); the number of colonies formed was increased (P<0.05); and the apoptosis rate and the protein levels of Cleaved-caspase3, Cleaved-caspase9 were decreased (P<0.05). The effect was dose-dependent. After transfection of pcDNA-lncRNA NKILA, the cell survival rate was increased (P<0.05), the number of colonies formed was increased (P<0.05), and the apoptosis rate and the protein levels of Cleaved-caspase3, Cleaved-caspase9 were decreased (P<0.05). Transfection of si-lncRNA NKILA could attenuate the effects of ligustilide on the proliferation, colony formation and apoptosis of HBVAF cells induced by IFN-α. In conclusion, ligustilide could promote the proliferation, colony formation and inhibit the apoptosis of IFN-α-induced cerebral adventitia fibroblasts by up-regulating the expression of lncRNA NKILA.
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