Chen Zhen-Hua, Xiao Ling, Chen Ji-Hong, Luo He-Shen, Wang Gao-Hua, Huang Yong-Lan, Wang Xiao-Ping
Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China.
World J Gastroenterol. 2008 Dec 7;14(45):6993-8. doi: 10.3748/wjg.14.6993.
To investigate the effects of fluoxetine on depression-induced changes of mast cell morphology and protease-1 (rMCP-1) expression in rats.
A Sprague-Dawley rat model of chronic stress-induced depression was established. Fifty experimental rats were randomly divided into the following groups: normal control group, fluoxetine+normal control group, depressed model group, saline+depressed model group, and fluoxetine+depressed model group. Laser scanning confocal microscopy (LSCM) immunofluorecence and RT-PCR techniques were used to investigate rMCP-1 expression in gastric antrum. Mast cell morphology was observed under transmission electron microscopy. ANOVA was used for statistical analysis among groups.
Morphologic observation indicated that depression induced mast cell proliferation, activation, and granule hyperplasia. Compared with the normal control group, the average immunofluorescence intensity of gastric antrum rMCP-1 significantly increased in depressed model group (37.4+/-7.7 vs 24.5+/-5.6, P<0.01) or saline+depressed model group (39.9+/-5.0 vs 24.5+/-5.6, P<0.01), while there was no significant difference between fluoxetine + normal control group (23.1+/-3.4) or fluoxetine+depressed model group (26.1+/-3.6) and normal control group. The average level of rMCP-1mRNA of gastric antrum significantly increased in depressed model group (0.759+/-0.357 vs 0.476+/-0.029, P<0.01) or saline+depressed model group (0.781+/-0.451 vs 0.476+/-0.029, P<0.01), while no significant difference was found between fluoxetine+normal control group (0.460+/-0.027) or fluoxetine+depressed model group (0.488+/-0.030) and normal control group. Fluoxetine showed partial inhibitive effects on mast cell ultrastructural alterations and de-regulated rMCP-1 expression in gastric antrum of the depressed rat model.
Chronic stress can induce mast cell proliferation, activation, and granule hyperplasia in gastric antrum. Fluoxetine counteracts such changes in the depressed rat model.
研究氟西汀对大鼠抑郁诱导的肥大细胞形态变化及蛋白酶-1（rMCP-1）表达的影响。
建立慢性应激诱导抑郁的Sprague-Dawley大鼠模型。50只实验大鼠随机分为以下几组：正常对照组、氟西汀+正常对照组、抑郁模型组、生理盐水+抑郁模型组、氟西汀+抑郁模型组。采用激光扫描共聚焦显微镜（LSCM）免疫荧光和RT-PCR技术检测胃窦中rMCP-1的表达。在透射电子显微镜下观察肥大细胞形态。采用方差分析进行组间统计学分析。
形态学观察表明，抑郁诱导肥大细胞增殖、活化和颗粒增生。与正常对照组相比，抑郁模型组（37.4±7.7 vs 24.5±5.6，P<0.01）或生理盐水+抑郁模型组（39.9±5.0 vs 24.5±5.6，P<0.01）胃窦rMCP-1的平均免疫荧光强度显著增加，而氟西汀+正常对照组（23.1±3.4）或氟西汀+抑郁模型组（26.1±3.6）与正常对照组之间无显著差异。抑郁模型组（0.759±0.357 vs 0.476±0.029，P<0.01）或生理盐水+抑郁模型组（0.781±0.451 vs 0.476±0.029，P<0.01）胃窦rMCP-1mRNA的平均水平显著增加，而氟西汀+正常对照组（0.460±0.027）或氟西汀+抑郁模型组（0.488±0.030）与正常对照组之间无显著差异。氟西汀对抑郁大鼠模型胃窦肥大细胞超微结构改变和rMCP-1表达失调有部分抑制作用。
慢性应激可诱导胃窦肥大细胞增殖、活化和颗粒增生。氟西汀可抵消抑郁大鼠模型中的此类变化。
