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Codonopsis lanceolata Contributes to Ca2+ Homeostasis by Mediating SOCE and PLC/IP3 Pathways in Vascular Endothelial and Smooth Muscle Cells
Planta Medica ( IF 2.1 ) Pub Date : 2020-07-30 , DOI: 10.1055/a-1214-6718
Min Kyung Kim 1 , A Young Han 1 , You Kyoung Shin 1 , Kwang-Won Lee 2 , Geun Hee Seol 1
Affiliation  

Codonopsis lanceolata has been widely used as an anti-inflammatory and anti-lipogenic agent in traditional medicine. Recently, C. lanceolata was reported to prevent hypertension by improving vascular function. This study evaluated the effects of C. lanceolata and its major component lancemaside A on cytosolic calcium concentration in vascular endothelial cells and vascular smooth muscle cells. Cytosolic calcium concentration was measured using fura-2 AM fluorescence. C. lanceolata or lancemaside A increased the cytosolic calcium concentration by releasing Ca2+ from the endoplasmic reticulum and sarcoplasmic reticulum and by Ca2+ entry into endothelial cells and vascular smooth muscle cells from extracellular sources. The C. lanceolata- and lancemaside A-induced cytosolic calcium concentration increases were significantly inhibited by lanthanum, an inhibitor of non-selective cation channels, in both endothelial cells and vascular smooth muscle cells. Moreover, C. lanceolata and lancemaside A significantly inhibited store-operated Ca2+ entry under pathological extracellular Ca2+ levels. In Ca2+-free extracellular fluid, increases in the cytosolic calcium concentration induced by C. lanceolata or lancemaside A were significantly inhibited by U73122, an inhibitor of phospholipase C, and 2-APB, an inositol 1,4,5-trisphosphate receptor antagonist. In addition, dantrolene treatment, which inhibits Ca2+ release through ryanodine receptor channels, also inhibited C. lanceolata- or lancemaside A-induced increases in the cytosolic calcium concentration through the phospholipase C/inositol 1,4,5-trisphosphate pathway. These results suggest that C. lanceolata and lancemaside A increase the cytosolic calcium concentration through the non-selective cation channels and phospholipase C/inositol 1,4,5-trisphosphate pathways under physiological conditions and inhibit store-operated Ca2+ entry under pathological conditions in endothelial cells and vascular smooth muscle cells. C. lanceolata or lancemaside A can protect endothelial cells and vascular smooth muscle cells by maintaining cytosolic calcium concentration homeostasis, suggesting possible applications for these materials in diets for preventing vascular damage.

中文翻译:

党参通过介导血管内皮细胞和平滑肌细胞中的 SOCE 和 PLC/IP3 通路促进 Ca2+ 稳态

党参在传统医学中被广泛用作抗炎和抗脂肪生成剂。最近,C. lanceolata 被报道通过改善血管功能来预防高血压。本研究评估了 C. lanceolata 及其主要成分 lancemaside A 对血管内皮细胞和血管平滑肌细胞中细胞溶质钙浓度的影响。使用 fura-2 AM 荧光测量细胞溶质钙浓度。C. lanceolata 或 lancemaside A 通过从内质网和肌质网释放 Ca2+ 以及通过从细胞外来源进入内皮细胞和血管平滑肌细胞的 Ca2+ 来增加细胞溶质钙浓度。C. lanceolata 和 lancemaside A 诱导的细胞溶质钙浓度增加被镧显着抑制,内皮细胞和血管平滑肌细胞中非选择性阳离子通道的抑制剂。此外,在病理性细胞外 Ca2+ 水平下,C. lanceolata 和 lancemaside A 显着抑制了存储操作的 Ca2+ 进入。在不含 Ca2+ 的细胞外液中,由 C. lanceolata 或 lancemaside A 诱导的细胞溶质钙浓度增加受到磷脂酶 C 抑制剂 U73122 和肌醇 1,4,5-三磷酸受体拮抗剂 2-APB 的显着抑制。此外,通过 ryanodine 受体通道抑制 Ca2+ 释放的丹曲林治疗也通过磷脂酶 C/肌醇 1,4,5-三磷酸途径抑制 C.lanceolata 或 lancemaside A 诱导的细胞溶质钙浓度增加。这些结果表明 C. lanceolata 和 lancemaside A 在生理条件下通过非选择性阳离子通道和磷脂酶 C/肌醇 1,4,5-三磷酸途径增加细胞溶质钙浓度,并在病理条件下抑制内皮细胞和血管平滑肌细胞中钙库操作的 Ca2+ 进入. C. lanceolata 或 lancemaside A 可以通过维持细胞溶质钙浓度稳态来保护内皮细胞和血管平滑肌细胞,这表明这些材料可能在饮食中用于预防血管损伤。
更新日期:2020-07-30
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