The purpose of this study was to evaluate the effect of female sexual hormones on intestinal and serum cytokines following traumatic brain injury (TBI). Adult female rats were ovariectomized and distributed among the following 9 groups: (i) sham trauma, (ii) TBI (Marmarou's method), (iii) vehicle (dimethylsulfoxide) treated, (iv) estrogen (E2) treated, (v) progesterone (P) treated, (vi) treated with E2+P, (vii) propylpyrazole triol (PPT) treated, (viii) diarylpropionitrile (DPN) treated, and (ix) control. PPT and DPN are estrogen receptor αand β agonists, respectively. Serum and intestinal levels of interleukin (IL)-1β were increased by TBI (P < 0.001). The level of intestinal IL-1β was increased in the group treated with E2 (P < 0.001). There was a reduction in serum IL-1β (P < 0.01) and an increase in intestinal IL-1β level (P < 0.001) in the PPT-treated group compared with the vehicle-treated group. TBI reduced serum IL-6 (P < 0.01) and increased intestinal IL-6 (P < 0.001). Serum IL-6 was increased in the group treated with E2 (P < 0.001), P (P < 0.001), E2+P (P < 0.01), and DPN (P < 0.001) after TBI; however, intestinal IL-6 was higher in the E2-treated group compared with the vehicle-treated group (P < 0.01). Intestinal tumor necrosis factor α (TNF-α) was increased by TBI (P < 0.001). Progesterone decreased serum TNF-α (P < 0.01). Intestinal TNF-α in the E2 (P < 0.01), E2+P (P < 0.001), and PPT (P < 0.001) treatment groups was less than in the vehicle-treated group. In conclusion, estrogen influences the intestinal levels of proinflammatory cytokines, in particular TNF-α, mediated through estrogen receptor α.
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【The effect of female sexual hormones on the intestinal and serum cytokine response after traumatic brain injury: different roles for estrogen receptor subtypes.].
【女性性激素对脑外伤后肠道和血清细胞因子反应的影响：雌激素受体亚型的不同作用。】
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DOI：10.1139/cjpp-2012-0359文章类型：杂志文章
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：这项研究的目的是评估女性性激素对脑外伤（TBI）后肠道和血清细胞因子的影响。将成年雌性大鼠切除卵巢，并分布在以下9组中：（i）假创伤，（ii）TBI（Marmarou方法），（iii）媒介物（二甲亚砜）治疗，（iv）雌激素（E2）治疗，（v）孕激素（P）处理，（vi）用E2 P处理，（vii）丙基吡唑三醇（PPT）处理，（viii）二芳基丙腈（DPN）处理，以及（ix）对照。 PPT和DPN分别是雌激素受体α和β激动剂。 TBI可提高血清和肠道白细胞介素（IL）-1β的水平（P <0.001）。 E2治疗组肠道IL-1β水平升高（P <0.001）。与溶媒治疗组相比，PPT治疗组的血清IL-1β降低（P <0.01），肠内IL-1β水平升高（P <0.001）。 TBI降低血清IL-6（P <0.01），增加肠道IL-6（P <0.001）。 TBI后E2组（P <0.001），P组（P <0.001），E2P组（P <0.01）和DPN组（P <0.001），血清IL-6水平升高。然而，E2治疗组的肠道IL-6高于媒介物治疗组（P <0.01）。 TBI可增加肠道肿瘤坏死因子α（TNF-α）（P <0.001）。孕酮降低血清TNF-α（P <0.01）。 E2（P <0.01），E2 P（P <0.001）和PPT（P <0.001）治疗组的肠道TNF-α低于赋形剂治疗组。总之，雌激素影响通过雌激素受体α介导的促炎细胞因子，特别是TNF-α的肠道水平。
