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首页> 外文期刊>Cytokine >Androstenediol ameliorates alterations in immune cells cytokine production capacity in a two-hit model of trauma-hemorrhage and sepsis.
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Androstenediol ameliorates alterations in immune cells cytokine production capacity in a two-hit model of trauma-hemorrhage and sepsis.

机译：在创伤性出血和败血症的两次打击模型中，雄烯二醇改善了免疫细胞细胞因子产生能力的改变。

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Although administration of androstenediol (a metabolite of dehydroepiandrosterone) following trauma-hemorrhage (T-H) produces beneficial effects on inflammatory cytokines and organ function, it remains unknown whether this metabolite has any salutary effects in preventing alterations in immune cell cytokine production following a combined insult of T-H and sepsis. To examine this, male rats underwent laparotomy, hemorrhagic shock (mean BP 40 mmHg for 90 min) and resuscitation or sham operation. Androstenediol (1 mg/kg BW i.v.) or vehicle was administered at the end of resuscitation. Twenty hrs after T-H or sham operation, sepsis was induced by cecal ligation and puncture (CLP). Five hours thereafter, plasma cytokine levels and cytokine production of various immune cells were determined. In a separate set of experiments, survival was monitored for 10 days after the induction of sepsis. Administration of androstenediol markedly decreased plasma IL-6 and TNF-alpha levels following T-H and CLP. Furthermore, it prevented the increased production of IL-6 and TNF-alpha by Kupffer cells and alveolar macrophages and attenuated the decrease in IL-6 and TNF-alpha production by splenic macrophages; however, it had no significant effects on the depressed IL-6 and TNF-alpha production by PBMC following T-H and CLP. The depressed IL-2 and IFN-gamma production by splenocytes under those conditions was attenuated by the administration of androstenediol. Furthermore, survival rate following T-H and subsequent sepsis was improved by androstenediol treatment. Since androstenediol administration following T-H attenuated cytokine production and reduced mortality in a double-hit model of T-H and sepsis, this agent appears to be a novel and useful adjunct for maintaining the immune cell functions following T-H and for decreasing the mortality rate from subsequent susceptibility to sepsis.
机译：尽管在创伤性出血（TH）后服用雄烯二醇（脱氢表雄酮的代谢物）对炎性细胞因子和器官功能产生了有益的作用，但仍不清楚这种代谢物是否具有任何有益的作用，可以防止由于以下原因共同造成的免疫细胞因子的改变TH和败血症。为了对此进行检查，对雄性大鼠进行剖腹手术，失血性休克（平均BP 40 mmHg，持续90分钟）并进行复苏或假手术。在复苏结束时给予雄烯二醇（1 mg / kg BW i.v.）或赋形剂。 T-H或假手术20小时后，盲肠结扎和穿刺（CLP）诱发败血症。此后五个小时，测定各种免疫细胞的血浆细胞因子水平和细胞因子产生。在另一组实验中，在诱发败血症后监测存活10天。 T-H和CLP后，给予雄烯二醇显着降低血浆IL-6和TNF-α水平。此外，它阻止了枯否细胞和肺泡巨噬细胞产生IL-6和TNF-α的增加，并减弱了脾巨噬细胞引起的IL-6和TNF-α的减少。然而，它对T-H和CLP后PBMC抑制IL-6和TNF-α的产生没有明显影响。在这些条件下脾细胞抑制的IL-2和IFN-γ的产生通过雄烯二醇的给药而减弱。此外，通过雄烯二醇治疗可提高T-H继发败血症的存活率。由于在TH和败血症的双重打击模型中，TH后施用雄烯二醇降低了细胞因子的产生并降低了死亡率，因此该药物似乎是一种新型且有用的辅助剂，可用于维持TH继发后的免疫细胞功能并降低随后的易感性至败血症。

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