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血脂康,一种红曲米提取物,通过抑制内质网应激介导的细胞凋亡和炎症来减缓易损斑块的进展。

Xuezhikang, an extract from red yeast rice, attenuates vulnerable plaque progression by suppressing endoplasmic reticulum stress-mediated apoptosis and inflammation.

作者信息

Shen Linghong, Sun Zhe, Chu Shichun, Cai Zhaohua, Nie Peng, Wu Caizhe, Yuan Ruosen, Hu Liuhua, He Ben

机构信息

Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

Department of Cardiology, Renji Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.

出版信息

PLoS One. 2017 Nov 30;12(11):e0188841. doi: 10.1371/journal.pone.0188841. eCollection 2017.

Abstract

Xuezhikang (XZK), an extract of red yeast rice, is a traditional Chinese medicine widely used for the treatment of cardiovascular diseases in China and other countries. However, whether XZK treatment can improve atherosclerotic plaque stability is not fully understood. Based on our previously developed mouse model of spontaneous vulnerable plaque formation and rupture in carotid arteries in ApoE-/- mice. We showed that low-dose (600 mg/kg/d) XZK improved plaque stability without decreasing plaque area, whereas high-dose (1200 mg/kg/d) XZK dramatically inhibited vulnerable plaque progression accompanied by decreased plaque area. Mechanistically, XZK significantly suppressed lesional endoplasmic reticulum (ER) stress in mouse carotid arteries. In vitro, XZK inhibited 7-KC-induced activation of ER stress in RAW264.7 macrophages, as assessed by the reduced levels of p-PERK, p-IRE1α, p-eIF2α, c-ATF6, s-XBP1, and CHOP. Compared to controls, the XZK-treated group displayed dramatically decreased apoptotic cell numbers (shown by decreased TUNEL- and cleaved caspase3-positive cells), lower necrotic core area and ratio, and reduced expression of NF-κB target gene. In RAW264.7 cells, XZK inhibited 7-KC-induced upregulation of apoptosis, protein expression of apoptotic markers (cleaved caspase-3 and cleaved PARP), and NF-κB activation (shown by target gene transcription and IκBα reduction). Collectively, our results suggest that XZK effectively suppresses vulnerable plaque progression and rupture by mitigating macrophage ER stress and consequently inhibiting apoptosis and the NF-κB pro-inflammatory pathway, thereby providing an alternative therapeutic strategy for stabilizing atherosclerotic plaques.

摘要

血脂康(XZK)是红曲米提取物,是一种在中国及其他国家广泛用于治疗心血管疾病的传统中药。然而,血脂康治疗是否能改善动脉粥样硬化斑块稳定性尚未完全明确。基于我们之前建立的ApoE基因敲除小鼠颈动脉自发易损斑块形成和破裂的小鼠模型,我们发现低剂量(600毫克/千克/天)血脂康可改善斑块稳定性而不减小斑块面积,而高剂量(1200毫克/千克/天)血脂康则显著抑制易损斑块进展并伴有斑块面积减小。机制上,血脂康显著抑制小鼠颈动脉病变部位的内质网(ER)应激。在体外,通过降低p-PERK、p-IRE1α、p-eIF2α、c-ATF6、s-XBP1和CHOP的水平评估,血脂康抑制7-KC诱导的RAW264.7巨噬细胞内质网应激激活。与对照组相比,血脂康治疗组凋亡细胞数量显著减少(通过TUNEL和裂解的caspase3阳性细胞减少显示),坏死核心面积和比例降低,NF-κB靶基因表达减少。在RAW264.7细胞中,血脂康抑制7-KC诱导的凋亡上调、凋亡标志物(裂解的caspase-3和裂解的PARP)蛋白表达以及NF-κB激活(通过靶基因转录和IκBα减少显示)。总体而言,我们的结果表明,血脂康通过减轻巨噬细胞内质网应激,进而抑制细胞凋亡和NF-κB促炎途径,有效抑制易损斑块进展和破裂,从而为稳定动脉粥样硬化斑块提供了一种替代治疗策略。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74ad/5708751/40a3c3e83892/pone.0188841.g001.jpg

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