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丹参酮 IIA 从丹参通过抑制促纤维化因子水平对心肌成纤维细胞和大鼠心脏组织发挥抗纤维化作用:miR-618 的关键作用。

Tanshinone IIA from Salvia miltiorrhiza exerts anti-fibrotic effects on cardiac fibroblasts and rat heart tissues by suppressing the levels of pro-fibrotic factors: The key role of miR-618.

机构信息

Second Department of Cardiology, Ganzhou People's Hospital, Ganzhou, China.

Department of Cardiology, Ganzhou Municipal Hospital, Ganzhou, China.

出版信息

J Food Biochem. 2022 Feb;46(2):e14078. doi: 10.1111/jfbc.14078. Epub 2022 Jan 10.

Abstract

Tanshinone IIA (TAN) is widely employed for handling cardiovascular disorders. The current study explored the potential role of miRs in the antifibrotic effect of TAN on heart. Fibrotic features were induced in cardiac fibroblasts (CFs) and in rat hearts, and then handled with TAN. MicroRNAs (miRs) responding to TAN were determined using a microarray assay. The selected miR was modulated to verify its role in antifibrotic effects of TAN. TAN suppressed the viability and the production of α-SMA in CFs, which was associated with 101 miR being upregulated and 223 miR being downregulated. MiR-618 was selected as the potential target of TAN. Ang II inhibited miR-618 level and resulted in the upregulation of pro-fibrosis factors, which was reversed by TAN. The antifibrotic effect of TAN was weakened by miR-618 inhibition. TAN inhibits hypertrophy and collagen deposition in heart tissues, which is associated with the increased level of miR-618. PRACTICAL APPLICATIONS: The findings outlined in the current study show that the antifibrotic function of TAN is closely related to the function of miRs: the induction of miR-618 is indispensable for the function of TAN against the fibrotic process after heart injury, which will promote the application of TAN as an adjuvant therapy for improving heart function.

摘要

丹参酮 IIA(TAN)广泛用于处理心血管疾病。本研究探讨了 miR 在 TAN 抗心脏纤维化作用中的潜在作用。在心脏成纤维细胞(CFs)和大鼠心脏中诱导纤维化特征,然后用 TAN 处理。使用微阵列分析测定对 TAN 有反应的 microRNAs(miRs)。调节选定的 miR 以验证其在 TAN 的抗纤维化作用中的作用。TAN 抑制 CFs 的活力和 α-SMA 的产生,这与 101 个 miR 上调和 223 个 miR 下调有关。miR-618 被选为 TAN 的潜在靶标。Ang II 抑制 miR-618 水平并导致促纤维化因子上调,TAN 可逆转该作用。miR-618 抑制削弱了 TAN 的抗纤维化作用。TAN 抑制心脏组织中的肥大和胶原沉积,这与 miR-618 水平的增加有关。实际应用:本研究中的发现表明,TAN 的抗纤维化功能与 miR 的功能密切相关:miR-618 的诱导对于 TAN 在心脏损伤后对抗纤维化过程的功能是必不可少的,这将促进 TAN 的应用作为改善心脏功能的辅助治疗。

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