药物诱导后的人大肠癌细胞的 [Ca^(2+)]_i 的变化

CHANGES OF [Ca 2+ ] i IN COLORECTAL CANCER CELLS INDUCED BY SOME CHEMICALS

采用荧光分光光度计法检测维甲酸（ＲＡ）、１，２５（ＯＨ）２ＶＤ３及佛波酯（ＰＭＡ）诱导ＣＣＬ２２９细胞分化后［Ｃａ２＋］ｉ变化，并观察内质网（ＥＲ）特异的Ｃａ２＋－ＡＴＰａｓｅ抑制剂Ｔｈａｐｓｉｇａｒｇｉｎ（ＴＧ）、ＩＰ３受体抑制剂Ｈｅｐａｒｉｎ对ＲＡ诱导［Ｃａ２＋］ｉ变化的影响，从而探讨ＲＡ诱导［Ｃａ２＋］ｉ变化与ＥＲ的关系。结果显示：ＲＡ和１，２５（ＯＨ）２ＶＤ３在数秒内引起［Ｃａ２＋］ｉ显著升高。在ＥＧＴＡ和Ｖｅｒａｐａｍｉｌ预处理细胞条件下，ＴＧ不能抑制ＲＡ引起Ｃａ２＋从细胞内钙池中外流，ＲＡ作用后ＴＧ仍能升高［Ｃａ２＋］ｉ。另外，Ｈｅｐａｒｉｎ也不能完全抑制ＲＡ升高［Ｃａ２＋］ｉ。提示ＲＡ诱导大肠癌细胞升高［Ｃａ２＋］ｉ可能通过ＥＲ上ＩＰ３敏感性和非敏感性钙池，亦可能细胞内存在除ＥＲ外对ＲＡ敏感的钙池。

Changes of [Ca 2+ ] i in CCL229 cells induced by retinoic acid (RA), 1,25(OH) 2VD 3 and PMA were measured by spectrofluorometry. The effects of endoplasmic reticulum (ER) specific Ca 2+ ATPase inhibitor thapsigargin (TG) and IP 3 receptor inhibitor heparin on RA induced changes of [Ca 2+ ] i were observed and the relationship between RA induced changes of [Ca 2+ ] i and ER was also investigated. The results showed that [Ca 2+ ] i increased markedly in several seconds after treated by RA and 1,25(OH) 2VD 3. When cells were pretreated with EGTA and verapamil (Ca 2+ entry blocker drug), TG could not inhibit RA stimulated Ca 2+ release from intracellular calcium pools and TG could increase [Ca 2+ ] i after pretreated by RA. In addition, heparin could not completely inhibit RA induced [Ca 2+ ] i increase. The results suggest that RA might stimulate IP 3 sensitive pool or IP 3 insensitive pool on ER to increase [Ca 2+ ] i, or there might be RA sensitive calcium pools except ER in cells.