目的研究阿克替苷对大鼠前列腺增生的组织形态及Bax和Bcl-2表达的影响。方法大鼠予以50 mg·kg~(-1)丙酸睾丸,隔日皮下注射,连续4周,构建前列腺增生模型。建模成功后,将其分为模型组、对照组和低、中、高3个剂量实验组,每组各10只。另取,10只正常大鼠作为空白组。空白组和模型组均予以等剂量0.9%Na Cl,灌胃;对照组予以0.8 mg·kg~(-1)非那雄胺,灌胃;低、中、高3个剂量实验组分别予以20,40,80 mg·kg~(-1)阿克替苷,灌胃。6组大鼠每天灌胃1次,连续6周。取各组大鼠前列腺组织并称重,计算前列腺指数。用组织切片观察各组大鼠前列腺组织的病理形态,用免疫印迹法检测各组大鼠前列腺Bax和Bcl-2蛋白的表达。结果空白组、模型组、对照组、低、中、高3个剂量实验组的前列腺湿重分别为(815.52±262.68),(1220.49±353.52),(1075.25±174.03),(1103.00±106.23),(816.12±132.87)和(815.37±106.81)mg,前列腺指数分别为(2.43±0.85)%,(3.74±0.78)%,(3.15±0.28)%,(3.10±0.22)%,(2.53±0.41)%和(2.48±0.37)%,Bax分别为(11.41±2.72)%,(8.49±2.01)%,(10.17±2.87)%,(9.09±1.98)%,(11.01±2.04)%和(11.10±1.91)%,Bcl-2分别为(7.79±1.74)%,(13.79±3.59)%,(10.23±2.74)%,(12.18±2.10)%,(8.53±2.62)%和(8.61±1.99)%,模型组、低剂量实验组的上述指标与中、高2个剂量实验组比较,差异均有统计学意义(均P<0.05)。结论阿克替苷能显著抑制前列腺增生,其机制可能是通过调节Bcl-2和Bax的表达,从而促进良性前列腺增生的细胞凋亡。 Objective To study the effect of acteoside on the histomorphology and Bax and Bcl-2 expression of benign prostatic hyperplasia in rats. Methods Rats (50 mg · kg -1) propionate were injected subcutaneously every other day for 4 consecutive weeks to establish a model of benign prostatic hyperplasia. After the successful modeling, it was divided into model group, control group and low, medium and high doses of three experimental groups, each group of 10. Another take, 10 normal rats as a blank group. The rats in the blank group and model group were treated with 0.9% NaCl at an equal dose. The rats in the control group were given finasteride 0.8 mg · kg -1, and were given gavage. The low, medium and high dose groups were given 20 , 40,80 mg · kg -1 acteoside, gavage. Six groups of rats were given gavage once daily for 6 weeks. Prostate tissue of each group was taken and weighed to calculate the prostate index. The histopathology of prostatic tissue in each group was observed by histological sections. The expressions of Bax and Bcl-2 protein in prostate were detected by Western blotting. Results The wet weight of the prostatic glands in the blank, the model group and the control group were (815.52 ± 262.68), (1220.49 ± 353.52), (1075.25 ± 174.03) and (1103.00 ± 106.23), respectively (816.12 ± 132.87) and (815.37 ± 106.81) mg respectively, and the indexes of prostate were (2.43 ± 0.85)%, (3.74 ± 0.78)%, (3.15 ± 0.28)%, (3.10 ± 0.22)% and (2.53 ± 0.41) (11.41 ± 2.72)%, (8.49 ± 2.01)%, (10.17 ± 2.87)%, (9.09 ± 1.98)%, (11.01 ± 2.04)%, and Bcl-2 was significantly higher than that of Bcl-2 cells (1.91%), (12.7 ± 2.10)%, (8.53 ± 2.62)% and (8.61 ± 1.99)%, , The model group, low-dose experimental group of the above indicators and the high dose of two experimental groups, the difference was statistically significant (P <0.05). Conclusion Acteoside can significantly inhibit the proliferation of benign prostatic hyperplasia, and its mechanism may be through the regulation of Bcl-2 and Bax expression, thereby promoting benign prostatic hyperplasia apoptosis.