二甲双胍对体外高糖应激下正常肝细胞乳酸代谢的影响

Xinxin Zhou, Xinliang Liu, Ling Zhang, Yong-jing Chen, Shao-Chen Guo, Yiying Yu, Zhilu Li, Pingping Yan
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引用次数: 0

摘要

目的:研究二甲双胍对体外高糖应激下肝细胞乳酸代谢的影响。方法:体外培养LO2肝细胞,肝细胞随机分为空白对照组、25 mmol/L葡萄糖溶液、27 mmol/L葡萄糖溶液、29 mmol/L葡萄糖溶液、31 mmol/L葡萄糖溶液、33 mmol/L葡萄糖溶液、35 mmol/L葡萄糖溶液处理组,确定最佳浓度为31 mmol/L后,使用30 mmol/L二甲双胍溶液,再分为空白对照组、正常肝细胞+最佳浓度葡萄糖溶液,正常肝细胞+二甲双胍溶液,正常肝细胞+。葡萄糖溶液正常肝细胞+二甲双胍溶液的最优浓度,在12 h、24 h、48 h分别计算细胞计数板上的肝细胞数量,并使用乳酸试剂盒分别测定正常肝细胞+最优浓度葡萄糖溶液和正常肝细胞+最优浓度葡萄糖溶液+二甲双胍溶液在12 h、24 h、48 h的细胞培养基乳酸值。结果:与不加二甲双胍的高血糖对照组相比,高血糖对照组乳酸浓度无明显变化,但肝细胞存活数明显增加。结论:二甲双胍对体外高糖应激下肝细胞乳酸代谢无显著影响,对高糖应激下肝细胞有保护作用。基于此,初步认为二甲双胍不是导致糖尿病乳酸酸中毒的直接因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of Metformin on Lactate Metabolism in Normal Hepatocytes under High Glucose Stress in Vitro
Objective: To study the effect of metformin on lactate metabolism in hepatocytes in vitro under high glucose stress. Method: LO2 hepatocytes was cultured in vitro, hepatocytes were randomly divided into blank control group, 25 mmol/L glucose solution, 27 mmol/L glucose solution, 29 mmol/L glucose solution, 31 mmol/L glucose solution, 33 mmol/L glucose solution, 35 mmol/L glucose solution treatment group, after determining the optimal concentration as 31 mmol/L, use 30 mmol/L metformin solution, and then divided into blank control group, normal hepatocytes + the optimal concentration of glucose solution, normal hepatocytes + metformin solution , normal hepatocytes+. The optimal concentration of glucose solution normal hepatocytes + metformin solution, calculate the number of hepatocytes on cell count plate respectively in the 12 h, 24 h, 48 h, and use the lactic acid kit to determine the lactic acid value of the cell culture medium of normal liver cells + optimal concentration glucose solution and normal liver cells + optimal concentration glucose solution + metformin solution at 12 h, 24 h, and 48 h, respectively. Results: There was no significant change in the lactic acid concentration but significant increase in the number of surviving hepatocytes in the high-glycemic control group compared with that in the high-glycemic control group without metformin. Conclusions: Metformin has no significant effect on lactic acid metabolism of hepatocytes under high glucose stress in vitro, and has a protective effect on hepatocytes under high glucose stress. Based on this, it is preliminarily believed that metformin is not the direct factor leading to diabetic lactic acidosis.
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