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Toxicity Mechanism of Emodin on Interstitial Cells of Cajal

机译:大黄素对Cajal间质细胞的毒性机制。

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Aim: To explore the emodin’s toxicity and action mechanism on the function of interstitial cells of Cajal (ICC) cultured in vitro. Methods: ICC of KM mouse was cultured in vitro. The minimum toxicity concentration and critical time points of emodin were investigated with Uniform Design methodology and MTT assay. The cell enzymology assay and enzyme immunoassay (EIA) were applied to observe the effect of emodin on membrane stability, cellular internal environment, energy metabolism and second messenger of ICC. Results: The minimum toxicity concentration was 0.001%, and the critical time points were 30 s, 1 min, 30 min, and 60 min. After administration of emodin, the damage on cells aggravated with time prolonging. The activity of malonaldehyde (MDA), lactate dehydrogenase (LDH), and phosphatase in the cell was raised significantly (P + and Ca2+ were increased but K+ concentration was decreased. The Na+-K+-ATPase activity was promoted but Ca2+-ATPase descended. Second messenger as IP3 and cAMP also became more active. All these changes had statistical significance (P Conclusion: Emodin had toxicity function on ICC which can lead to membrane damage, energy metabolism disorder. This mechanism could be related to electrolytes concentration disorder, inhibited activity of Na+-K+-ATPase and Ca2+-ATPase, and raised activity of IP3 and cAMP.
机译:目的:探讨大黄素对体外培养的Cajal(ICC)间质细胞功能的毒性和作用机制。方法:体外培养KM小鼠ICC。大黄素的最低毒性浓度和临界时间点采用统一设计方法和MTT法进行了研究。应用细胞酶学测定和酶免疫测定(EIA)观察大黄素对膜稳定性,细胞内部环境,能量代谢和ICC第二信使的影响。结果:最低毒性浓度为0.001%,临界时间为30 s,1 min,30 min和60 min。大黄素给药后,对细胞的损害随着时间的延长而加剧。细胞内丙二醛(MDA),乳酸脱氢酶(LDH)和磷酸酶的活性显着升高(P +和Ca2 +升高,但K +浓度降低; Na + -K + -ATPase活性升高,而Ca2 + -ATPase降低。 IP3和cAMP等第二信使也变得更加活跃,所有这些变化都具有统计学意义(P结论:大黄素对ICC具有毒性作用,可导致膜损伤,能量代谢紊乱。此机制可能与电解质浓度紊乱,活性抑制有关Na + -K + -ATPase和Ca2 + -ATPase的合成,并提高IP3和cAMP的活性。

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