Salvianolic acid B suppresses hepatic stellate cell activation and liver fibrosis by inhibiting the NF-κB signaling pathway via miR-6499-3p/LncRNA-ROR

肝星状细胞 信号转导 细胞生长 小RNA 转录因子 癌症研究 生物 肝纤维化 分子生物学 NF-κB 细胞 纤维化 细胞生物学 化学 内分泌学 内科学 医学 生物化学 基因
作者
Rong Wang,Shengnan Li,Panpan Chen,Xin Yue,Shaozhan Wang,Yanqiu Gu,Yongfang Yuan
出处
期刊:Phytomedicine [Elsevier]
卷期号:107: 154435-154435 被引量:11
标识
DOI:10.1016/j.phymed.2022.154435
摘要

Long non-coding RNA (LncRNAs) have been reported to play an important role in liver fibrosis and are closely associated with hepatic stellate cell (HSC) activation. We previously found that salvianolic acid B (Sal B) improves liver fibrosis by regulating the NF-κB signaling pathway. However, whether the LncRNA, regulator of reprogramming (LncRNA-ROR) plays a role in Sal B-mediated anti-fibrosis effects via the NF-κB signaling pathway remain unclear.This study aimed to evaluate the effects of Sal B on HSC activation and liver fibrosis and investigate its mechanism from the perspective of LncRNA-ROR-mediated NF-κB signaling pathways.LX-2 and T6 cell lines were cultured. Animal models of liver fibrosis were established using CCl4 in male BALB/c mice. Primary HSCs were isolated from mice and cultured. Serum biochemical and liver histological analyses were performed to evaluate the effects of Sal B on liver fibrosis. The index of HSC activation and the expression of LncRNA-ROR, microRNAs (miRNAs), and inflammatory factors were determined by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) or immunofluorescence staining. Cell proliferation was measured by a Cell Counting Kit-8 (CCK-8). NF-κB signaling-associated protein levels were assessed using western blotting or immunofluorescence staining. A luciferase reporter assay was used to detect transcription activity.In this study, a lower level of LncRNA-ROR was found during Sal B attenuating HSC activation in HSCs. Mechanistically, Sal B impeded the NF-κB signaling pathway to inhibit HSC proliferation and activation by downregulating LncRNA-ROR. Additionally, Sal B upregulated miR-6499-3p to target LncRNA-ROR for degradation. Functionally, Sal B treatment ameliorated CCl4-induced liver fibrosis in mice by inhibiting HSC activation.Sal B suppresses HSC activation and liver fibrosis via regulation of miR-6499-3p/LncRNA-ROR-mediated NF-κB signaling pathway. These results reveal a new molecular mechanism of Sal B on liver fibrosis from the insight of LncRNAs.
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