这项体外研究的主要目的是防止与布比卡因相关的毒性风险,广泛应用于临床实践,通过使用镁(Mg),一个现成的和具有成本效益的元素,作为佐剂。我们假设在布比卡因诱导的LAST条件下,Mg可能在结肠细胞培养模型中表现出对细胞毒性的保护作用。我们的次要目的是研究其对遗传毒性的影响,凋亡,还有IROS.在我们的研究中使用CCD-18Co细胞。对照组(C组),布比卡因组(B组),镁组(M组),并造就布比卡因+Mg组(BM组)。在C组中孵育24小时的CCD-18Co细胞的活力被确定为100%。这些细胞被平均分配,和布比卡因以5至300μM的浓度给予B组。在M组中,添加0.625至320mEq的Mg剂量。确定在40mEq的Mg剂量下观察到最大生存力(p<0.05)。在BM组中,布比卡因以相同的浓度与Mg(40mEq)联合使用,并测量细胞活力。DNA损伤,凋亡,通过施用40mEqMg在布比卡因浓度下评估iROS。B组,CCD-18Co中的活力呈剂量依赖性下降(p<0.05,p<0.01,p<0.001)。在BM组中,与C组相比,增加浓度的细胞活力降低(p<0.05,p<0.01,p<0.001),但与B组相比,活力受到积极影响(p<0.05)。B组,DNA损伤增加(p<0.05,p<0.001)。在BM组中,DNA损伤增加(p<0.05,p<0.001)。然而,在BM组中,与B组相比,DNA损伤水平降低(p<0.05,p<0.01)。B组,细胞凋亡增加(p<0.05,p<0.001);BM组,与C组相比,细胞凋亡增加(p<0.001)。在BM组中,细胞凋亡较B组降低(p<0.05)。与C组相比,B组(p<0.05,p<0.01,p<0.01)和BM组(p<0.05,p<0.01,p<0.001)的iROS增加。在BM组中,与B组相比,iROS降低(p<0.05)。总之,Mg对布比卡因诱导的毒性具有保护作用。
The primary objective of this in vitro study was to prevent the risk of toxicity associated with
bupivacaine, widely used in clinical practice, by using magnesium (Mg), a readily available and cost-effective element, as an adjuvant. We hypothesized that Mg might exhibit a protective effect against cytotoxicity in a colon cell culture model under conditions of bupivacaine-induced LAST. Our secondary aim was to investigate its effect on genotoxicity, apoptosis, and iROS. CCD-18Co cells were used in our study. Control group (group C),
Bupivacaine group (group B), Magnesium group (group M), and
Bupivacaine+Mg group (group BM) were created. The viability of CCD-18Co cells incubated for 24 h in group C was determined to be 100%. These cells were evenly divided, and
bupivacaine was administered to group B at concentrations of 5 to 300 μM. In group M, doses of Mg at 0.625 to 320 mEq were added. It was determined that the maximum viability was observed at a Mg dose of 40 mEq (p < 0.05). In group BM,
bupivacaine was administered at the same concentrations in combination with Mg (40 mEq), and cell viability was measured. DNA damage, apoptosis, and iROS were assessed at concentrations of bupivacaine by administering 40 mEq Mg. In group B, viability decreased dose-dependently in CCD-18Co (p < 0.05, p < 0.01, p < 0.001). In group BM, the viability decreased in cells at increasing concentrations compared to group C (p < 0.05, p < 0.01, p < 0.001), but the viability was affected positively compared to group B (p < 0.05). In group B, DNA damage increased (p < 0.05, p < 0.001). In group BM, DNA damage increased (p < 0.05, p < 0.001). However, in group BM, DNA damage levels were reduced compared to group B (p < 0.05, p < 0.01). In group B, apoptosis increased (p < 0.05, p < 0.001); in group BM, apoptosis increased (p < 0.001) compared to group C. However, in group BM, apoptosis decreased compared to group B (p< 0.05). iROS increased in group B (p < 0.05, p < 0.01, p < 0.01) and group BM (p < 0.05, p < 0.01, p < 0.001) compared to the group C. However, in group BM, iROS decreased in comparison to group B (p < 0.05). In conclusion, Mg exhibits a protective effect against
bupivacaine-induced toxicity.