Tanshinone IIA通过SKP2/BKCA轴抑制了内侧前庭核细胞中缺氧诱导的凋亡。
摘要来源：
curr pharm des。 2020 Jun 2。 Wu, Xiang Chen, Ting-Ting Jiang, Xin-Qian Li, Jing-Min Li, Yong Yan, Xue-Jun Wu, Yu-Ying Liu, Pin Dong
Article Affiliation:Jing-Jing Zhu
Abstract:BACKGROUND: The aim of the present study was to investigate the protective effects of Tanshinone IIA (Tan IIA) on hypoxia induced injury in medial vestibular nucleus (MVN) cells.
METHODS: An in vitro hypoxia model was established using MVN cells exposed to hypoxia.通过评估细胞活力，凋亡和AP的表达来证实缺氧引起的细胞损伤Optosis相关蛋白。 Oxidative stress and related indicators were also measured following hypoxia modeling and Tan IIA treatment, and the genes potentially involved in the response were predicted using multiple GEO datasets.
RESULTS: The results of the present study showed that Tan IIA significantly increased cell viability, decreased cell apoptosis and decreased the ratio of缺氧治疗的细胞中的BAX/BCL-2。此外，缺氧治疗增加了MVN细胞中的氧化应激，用棕褐色的Ia治疗减少了氧化应激。在缺氧治疗的细胞中，S期激酶相关蛋白2（SKP2）的表达上调，而TAN IIA治疗降低了SKP2的表达。 Mechanistically, SKP2 interacted with large conductance Ca2+ -activated K+ channels (BKCa), regulating its expression, and BKCa knockdown alleviated the protective effects of Tan IIA on hypoxia induced cell apoptosis.
结论： 本研究的结果表明，tan iiA通过其抗凋亡和抗氧化活性通过SKP2/BKCA轴对缺氧诱导的细胞损伤具有保护作用。这些发现表明，棕褐色可能是治疗缺氧引起的眩晕的潜在治疗方法。