CAJ | 학술논문

目的探讨当归贝母苦参丸对良性前列腺增生(BPH)模型小鼠的影响及作用机理.方法将60只雄性小鼠,按照随机数字表法随机分为6组:空白组,模型组,阳性对照组,高、中、低剂量治疗组.空白组给予腹腔注射12.5 mg/kg·d-1橄榄油,其他各组采用腹腔注射内酸睾酮原液制作小鼠BPH模型,同时高、中、低剂量治疗组分别予高、中、低剂量当归贝母苦参丸水煎溶液灌胃,阳性对照组灌胃前列康水混悬液600 mg/kg.给药第21天处死,观察前列腺指数(PI)的变化;HE染色光镜观察前列腺病理改变;免疫组化方法检测PCNA、bcl-2和bax表达的变化.结果当归贝母苦参丸治疗组PI低于模型组;PCNA、bcl-2表达IOD值低于模型组;bax表达高于模型组.治疗组高、中、低剂量组比较差异无统计学意义,三个治疗组与阳性对照组比较差异无统计学意义.结论当归贝母苦参丸可抑制模型小鼠BPH,其机理可能与下调细胞增殖蛋白PCNA和凋亡抑制蛋白bcl-2、增加baX的表达相关.
목적 탐토당귀패모고삼환대량성전렬선증생(BPH)모형소서적영향급작용궤리.방법 장60지웅성소서,안조수궤수자표법수궤분위6조:공백조,모형조,양성대조조,고、중、저제량치료조.공백조급여복강주사12.5 mg/kg·d-1감람유,기타각조채용복강주사내산고동원액제작소서BPH모형,동시고、중、저제량치료조분별여고、중、저제량당귀패모고삼환수전용액관위,양성대조조관위전렬강수혼현액600 mg/kg.급약제21천처사,관찰전렬선지수(PI)적변화;HE염색광경관찰전렬선병리개변;면역조화방법검측PCNA、bcl-2화bax표체적변화.결과 당귀패모고삼환치료조PI저우모형조;PCNA、bcl-2표체IOD치저우모형조;bax표체고우모형조.치료조고、중、저제량조비교차이무통계학의의,삼개치료조여양성대조조비교차이무통계학의의.결론 당귀패모고삼환가억제모형소서BPH,기궤리가능여하조세포증식단백PCNA화조망억제단백bcl-2、증가baX적표체상관.
Objective To study the effect of Danggui-beimu-kushen Pill on benign prostatic hyperplasia (BPH) and its possible mechanism. Methods BPH model mouse was produced by intraperitoneal injection of testosterone propionate. The high, medium and low dose treatment group was fed high, middle and low dose of Danggui-beimu-kushen Pill respectively, while the positive control group was fed Qianliekang liquid, 600 mg/kg. All mice were executed on the 21 day. Such values were observed as the prostate index changes, pathological changes of prostate by HE staining light microscopy and the expression changes of PCNA,bcl-2 and bax by immunohistochemistry. Results The prostate index of the treatment group was lower than the model group; the PCNA and bcl-2 expression were lower than the model group, while the bax expression was higher than the model group. Meanwhile; there is no significant difference among the treatment groups.Moreover, the difference between the treatment groups and the positive control group has no statistic meaning.Conclusion Danggui-beimu-kushen Pill can suppress BPH in mice. The mechanism may be related to the reduction expression of cell-proliferation protein PCNA and apoptosis profilin bcl-2, and the increase of bax expression.