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白术内酯 III 对皮质酮诱导的 PC12 细胞的神经保护作用涉及线粒体凋亡途径和 MAPKs/NF-κB 炎症途径。

Involvement of mitochondrial apoptotic pathway and MAPKs/NF-κ B inflammatory pathway in the neuroprotective effect of atractylenolide III in corticosterone-induced PC12 cells.

机构信息

Modern Research Center for Traditional Chinese Medicine, Shanxi University, Taiyuan 030006, China.

Modern Research Center for Traditional Chinese Medicine, Shanxi University, Taiyuan 030006, China.

出版信息

Chin J Nat Med. 2019 Apr;17(4):264-274. doi: 10.1016/S1875-5364(19)30030-5.

Abstract

Atractylenolide III (ATL-III), a sesquiterpene compound isolated from Rhizoma Atractylodis Macrocephalae, has revealed a number of pharmacological properties including anti-inflammatory, anti-cancer activity, and neuroprotective effect. This study aimed to evaluate the cytoprotective efficiency and potential mechanisms of ATL-III on corticosterone injured rat phaeochromocytoma (PC12) cells. Our results demonstrate that ATL-III increases cell viability and reduces the release of lactate dehydrogenase (LDH). The results suggest that ATL-III protects PC12 cells from corticosterone-induced injury by inhibiting the intracellular Ca overloading, inhibiting the mitochondrial apoptotic pathway and modulating the MAPK/NF-ΚB inflammatory pathways. These findings provide a novel insight into the molecular mechanism by which ATL-III protected the PC12 cells against corticosterone-induced injury for the first time. Our results provide the evidence that ATL-III may serve as a therapeutic agent in the treatment of depression.

摘要

白术内酯 III(ATL-III)是从白术中分离得到的一种倍半萜化合物,具有多种药理活性,包括抗炎、抗癌和神经保护作用。本研究旨在评估 ATL-III 对皮质酮损伤的大鼠嗜铬细胞瘤(PC12)细胞的细胞保护效率及其潜在机制。我们的结果表明,ATL-III 能提高细胞活力,减少乳酸脱氢酶(LDH)的释放。结果提示,ATL-III 通过抑制细胞内 Ca 超载、抑制线粒体凋亡途径和调节 MAPK/NF-ΚB 炎症途径来保护 PC12 细胞免受皮质酮诱导的损伤。这些发现为 ATL-III 首次保护 PC12 细胞免受皮质酮诱导损伤的分子机制提供了新的见解。我们的结果为 ATL-III 可能作为治疗抑郁症的药物提供了证据。

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