Chen Chung-Yi, Li Yi-Wen, Kuo Soong-Yu
Department of Medical Technology, School of Medicine and Health Sciences, Fooyin University, Kaohsiung County 83101 Taiwan.
Molecules. 2009 Mar 2;14(3):959-69. doi: 10.3390/molecules14030959.
The effect of [10]-gingerol on cytosol free Ca(2+) concentration (Ca(2+)) and viability is large unknown. This study examines the early signaling effects of [10]-gingerol on human colorectal cancer cells. It was found that this compound caused a slow and sustained rise of Ca(2+) in a concentration-dependent manner. [10]-Gingerol also induced a Ca(2+) rise when extracellular Ca(2+) was removed, but the magnitude was reduced by 38%. In a Ca(2+)-free medium, the [10]-gingerol-induced Ca(2+) rise was partially abolished by depleting stored Ca(2+) with thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor). The elevation of [10]-gingerol-caused Ca(2+) in a Ca(2+)-containing medium was not affected by modulation of protein kinase C activity. The [10]-gingerol-induced Ca(2+) influx was insensitive to L-type Ca(2+) channel blockers. At concentrations of 10-100 mM, [10]-gingerol killed cells in a concentration-dependent manner. These findings suggest that [10]-gingerol induces Ca(2+) rise by causing Ca(2+) release from the endoplasmic reticulum and Ca(2+) influx from non-L-type Ca(2+) channels in SW480 cancer cells.
[10]-姜辣素对细胞质游离钙离子浓度（[Ca(2+)]i）及细胞活力的影响尚不清楚。本研究检测了[10]-姜辣素对人结肠癌细胞的早期信号传导作用。结果发现，该化合物可引起[Ca(2+)]i缓慢且持续升高，呈浓度依赖性。去除细胞外钙离子时，[10]-姜辣素仍可诱导[Ca(2+)]i升高，但幅度降低了38%。在无钙培养基中，用毒胡萝卜素（一种内质网钙离子泵抑制剂）耗尽储存的钙离子后，[10]-姜辣素诱导的[Ca(2+)]i升高部分被消除。在含钙培养基中，[10]-姜辣素引起的[Ca(2+)]i升高不受蛋白激酶C活性调节的影响。[10]-姜辣素诱导的钙离子内流对L型钙离子通道阻滞剂不敏感。浓度为10 - 100 mM时，[10]-姜辣素可浓度依赖性地杀死细胞。这些发现表明，[10]-姜辣素通过引起内质网释放钙离子以及非L型钙离子通道内流，诱导SW480癌细胞内[Ca(2+)]i升高。
