CAJ | 학술논문

目的：探讨β-细辛醚对抑郁模型大鼠海马组织及Bax、Bcl-2蛋白表达的影响。方法：经过敞箱实验选取得分相近的2~3个月龄SD大鼠80只，按随机数字表法分为四组，每组20只，结合孤养并给予慢性轻度不可预见刺激，复制抑郁模型，于造模成功第2天开始，分别给予氟西汀组和β-细辛醚组1.2 mg/（kg·d）氟西汀和25 mg/（kg·d）β-细辛醚灌胃，模型组与正常组给予等体积生理盐水。于第21天对大鼠处死取脑，免疫组织化学法检测Bax、Bcl-2蛋白相对含量。结果：模型组大鼠海马组织神经元数目减少，散在排列，细胞核发生固缩变形，CA1区，CA3区变化显著。与模型组比较，β-细辛醚组、氟西汀组Bax蛋白表达均显著降低（P<0.01）。结论：β-细辛醚可以降低大鼠海马组织Bax蛋白表达，促进Bcl-2蛋白表达。
목적：탐토β-세신미대억욱모형대서해마조직급Bax、Bcl-2단백표체적영향。방법：경과창상실험선취득분상근적2~3개월령SD대서80지，안수궤수자표법분위사조，매조20지，결합고양병급여만성경도불가예견자격，복제억욱모형，우조모성공제2천개시，분별급여불서정조화β-세신미조1.2 mg/（kg·d）불서정화25 mg/（kg·d）β-세신미관위，모형조여정상조급여등체적생리염수。우제21천대대서처사취뇌，면역조직화학법검측Bax、Bcl-2단백상대함량。결과：모형조대서해마조직신경원수목감소，산재배렬，세포핵발생고축변형，CA1구，CA3구변화현저。여모형조비교，β-세신미조、불서정조Bax단백표체균현저강저（P<0.01）。결론：β-세신미가이강저대서해마조직Bax단백표체，촉진Bcl-2단백표체。
To investigate the effect ofβ-assrone on the hippocampus and the expressions of protein Bax and Bcl-2 in the hippocampus of depression model rats.Method:According to the open field test,adult Sprague-Dawley rates with similar scores were randomly divided into 4 groups,each group had 20 cases. Solitary and chronic mild unpredictability stimulation on each one except the normal control group,copy the model of depression. On the second day of a successful model replication,the fluoxetine control group and theβ-asarone group were given 1.2 mg/(kg·d)the fluoxetine and 25 mg/(kg·d)theβ-asarone. The model control group and the normal control group were given equal volumes of normal saline. On the 21th day,rats were to be put to death and take brain tissue. The protein expression of Bax and Bcl-2 in the hippocampus were tested by immunohistochemical staining method.Result:The numbers of neurons were reduced in the hippocampus of model group,scattered in the arrangement,the nucleus of neurons were pycnosis deformation,especially on the region of CA1 and CA3. Compared with model group,the protein expression of Bax reduced and Bcl-2 increased with statistical significance in the hippocampus in fluoxetine control group andβ-asarone group (P<0.01).Conclusion:β-asarone can reduce the protein expression of Bax,while promote the protein expression of Bcl-2 in the hippocampus of depression model rats.