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目的:观察氧化苦参碱(OM)对过氧化氢(Hn 2On 2)处理的大鼠胰腺腺泡AR42J细胞株高迁移率族蛋白B1(HMGB1)表达和释放的影响。n 方法:应用MTT法检测不同浓度Hn 2On 2处理对AR42J细胞生存率的影响。将体外培养的AR42J细胞分为对照组、Hn 2On 2组、Hn 2On 2＋OM组。Hn 2On 2组及Hn 2On 2＋OM组加入等容积的Hn 2On 2(终浓度0.16 mmol/L)，对照组加入等容积三蒸水，Hn 2On 2＋OM组在加入Hn 2On 2前0.5 h加入OM(终浓度0.5 g/L)，培养24 h后收取细胞及细胞上清液。采用蛋白免疫印迹法检测细胞HMGB1蛋白表达，酶联免疫吸附试验检测细胞上清液HMGB1蛋白水平，免疫荧光法检测HMGB1蛋白在细胞内的定位分布。n 结果:Hn 2On 2组细胞HMGB1蛋白表达量、分泌到细胞上清液中HMGB1蛋白量、细胞质HMGB1蛋白占细胞总HMGB1蛋白的比例均显著高于对照组[1.04±0.04比0.69±0.02，(4.84±0.13)μg/L比(2.68±0.07)μg/L，(35.7±2.5)%比(10.7±1.9)%]，差异均有统计学意义(n P值均<0.05)；应用OM干预后，细胞HMGB1蛋白表达及分泌量、细胞质中HMGB1蛋白占比分别为0.82±0.02、(3.97±0.10)μg/L、(27.3±1.7)%，均显著低于Hn 2On 2组，差异均有统计学意义(n P值均<0.05)。n 结论:Hn 2On 2能够诱导大鼠胰腺腺泡细胞HMGB1的表达和释放，OM干预可减轻Hn 2On 2致AR42J细胞氧化应激损伤的程度。n “,”Objective:To observe the effects of oxymatrine(OM) on the expression and release of high mobility group box 1(HMGB1) in rat pancreatic acinar cell line AR42J stimulated by hydrogen peroxide.Methods:MTT method was used to detect the effects of Hn 2On 2 in different concentrations on the survival of AR42J cells. AR42J cells cultured n in vitro were divided into control group, Hn 2On 2 group and Hn 2On 2+ OM group. An equal volume of Hn 2On 2(final concentration 0.16 mmol/L) was added in Hn 2On 2 group and Hn 2On 2+ OM group, respectively, while an equal volume of triple distilled water was added in control group. In Hn 2On 2+ OM group, OM(final concentration 0.5 g/L)was added 0.5 h before the addition of Hn 2On 2, and cell samples and supernatant were collected after 24 h culture. The expression of HMGB1 protein was detected by Western blotting, the level of HMGB1 protein in cell supernatant was detected by enzyme-linked immunosorbent assay, and the intracellular distribution of HMGB1 protein was detected by immunofluorescence.n Results:In the Hn 2On 2 group, the expression of HMGB1, the secretion of HMGB1 in the supernatant and the proportion of cytoplasmic HMGB1 in the total HMGB1 were significantly higher than those in the control group[1.04±0.04 n vs 0.69±0.02, (4.84±0.13)μg/Ln vs (2.68±0.07)μg/L, (35.7±2.5)%n vs (10.7±1.9)%], and all the differences were statistically significant (all n P<0.05). After OM intervention, HMGB1 protein expression, secretion and cytoplasmic proportion were [0.82±0.02, (3.97±0.10)μg/L and (27.3±1.7)%], respectively, which were obviously lower than those in the Hn 2On 2 group, and all the differences were statistically significant (all n P<0.05).n Conclusions:Hn 2On 2 can induce the expression and release of HMGB1 in rat pancreatic acinar cells; OM treatment could alleviate the severity of oxidative stress injuries induced by Hn 2On 2 in AR42J cells.n