Tunçel N, Gürer F, Aral E, Uzuner K, Aydin Y, Bayçu C
Department of Physiology, University of Osmangazi, Faculty of Medicine, Eskişehir, Türkiye.
Peptides. 1996;17(5):817-24.
The effect of VIP on mast cell invasion/degranulation in testicular interstitium of stressed (immobilization and cold) and beta-endorphin-treated rats were investigated. Fifty-three Wistar male rats were used in four series of experiments. Initially, the effect of immobilization and cold stress on mast cell invasion and degranulation in testicular interstitium was examined in three age group of rats: 15 (n = 6), 30 (n = 6), and 45 (n = 7) days of age. Five animals per age group were used as controls. Because the most obvious effect of the stress on mast cell invasion/degranulation in testicular interstitium was observed in 45-day-old rats, the action of VIP in stressed and beta-endorphin-treated rats was only investigated at this age group. Mast cells and Leydig cells were evaluated by using histochemical and light microscopic protocols. Stress caused mast cell accumulation and degranulation in the testicular interstitium. Stress decreased heparin synthesis and possibly increased histamine content of mast cells. The effect of beta-endorphin was not as high as seen with stress. In some areas of testicular interstitium of stressed rats, there were aplasic and/or inactive Leydig cells. VIP inhibited proliferation and degranulation of mast cells, increased heparin content of the cells, and protected Leydig cells. By way of mast cell accumulation and degranulation in the testicular interstitium, exposure to stress may lead to Leydig cell damage and infertility. VIP may be involved in the protection of normal testicular function under stress conditions.
研究了血管活性肠肽(VIP)对处于应激状态(固定和寒冷)的大鼠以及经β-内啡肽处理的大鼠睾丸间质中肥大细胞浸润/脱颗粒的影响。在四组系列实验中使用了53只Wistar雄性大鼠。最初,在三个年龄组的大鼠中检测了固定和寒冷应激对睾丸间质中肥大细胞浸润和脱颗粒的影响,这三个年龄组分别为15日龄(n = 6)、30日龄(n = 6)和45日龄(n = 7)。每个年龄组中有五只动物用作对照。由于在45日龄大鼠中观察到应激对睾丸间质中肥大细胞浸润/脱颗粒的影响最为明显,因此仅在该年龄组研究了VIP在应激和经β-内啡肽处理的大鼠中的作用。通过组织化学和光学显微镜方法评估肥大细胞和睾丸间质细胞。应激导致睾丸间质中肥大细胞积聚和脱颗粒。应激降低了肥大细胞中肝素的合成,并可能增加了组胺含量。β-内啡肽的作用不如应激明显。在应激大鼠的睾丸间质某些区域,存在发育不全和/或无活性的睾丸间质细胞。VIP抑制肥大细胞的增殖和脱颗粒,增加细胞中的肝素含量,并保护睾丸间质细胞。通过睾丸间质中肥大细胞的积聚和脱颗粒,应激可能导致睾丸间质细胞损伤和不育。VIP可能参与在应激条件下保护正常的睾丸功能。