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目的 为了减少肝细胞在微囊化过程中的缺氧损伤， 研究在缺氧状态下果糖对肝细胞的保护作用。方法 将ＳＤ大鼠分为三组：Ａ 组， 细胞分离的灌流液和消化液中均加果糖２０ ｍ ｍｏｌ／Ｌ，Ｂ、Ｃ两组不加果糖； 细胞分离及微囊化后， 检测细胞的活率； 微囊化肝细胞行体外培养，Ｃ组培养液中加果糖１０ ｍ ｍｏｌ／Ｌ，Ａ、Ｂ两组不加。测定三组肝细胞的乳酸脱氢酶（ＬＤＨ） 漏出率（ ％ ） 及培养上清液中的总蛋白质。结果 Ａ组的细胞活率显著高于Ｂ、Ｃ 两组（ Ｐ＜ ０ ．０１） ， 而Ａ 组的ＬＤＨ 漏出率显著低于Ｂ、Ｃ组（ Ｐ＜ ０ ．０１） ，Ａ 组蛋白质合成功能的恢复显著优于Ｂ、Ｃ 组（ Ｐ＜ ０ ．０１） 。结论 果糖在缺氧状态下能有效延缓肝细胞的缺氧损伤， 但应在缺氧状态发生之前给予才能发挥作用。
Aim To reduce the hypoxic injury of hepatocytes during microencapsulation, the protective effect of fructose on hepatocytes under hypoxia condition was studied. Methods The SD rats were divided into three groups: group A, fructose added 20 m mol / L in perfusate and digestive juice; group B and C did not add fructose; cells were isolated and microencapsulated, The viability of microencapsulated hepatocytes was cultured in vitro. Fructose 10 m mol / L was added to the culture medium of group C, without addition of A and B groups. Lactate dehydrogenase (LDH) leakage rate (%) and total protein in the culture supernatant of the three groups of hepatocytes were measured. Results The cell viability of group A was significantly higher than that of group B and C (P <0.01), while the leakage rate of LDH in group A was significantly lower than that of group B and C (P <0.01) Of the recovery was significantly better than B, C group (P <0 .01). Conclusion Fructose can effectively delay the hypoxic injury of hepatocytes in hypoxic condition, but should be given before hypoxia.