Division of Reproductive Biology, Institute of Animal Reproduction and Food Research of the Polish Academy of Sciences, Tuwima 10, 10-078 Olsztyn, Poland.
Division of Clinical Physiology, Faculty of Veterinary Medicine, University of Warmia and Mazury, Oczapowskiego 13 Str., 10-718 Olsztyn, Poland.
Res Vet Sci. 2020 Dec;133:163-173. doi: 10.1016/j.rvsc.2020.09.016. Epub 2020 Sep 19.
We studied the inflammation effect on somatostatin receptors subtypes 2 (sstr2) and 5 (sstr5) expression in myometrium and somatostatin influence alone or with sstr2 and sstr5 antagonists on the contractility of gilt inflamed uterus. On day 3 of the estrous cycle, either E.coli suspension (E.coli group) or saline (SAL group) were injected into uterine horns. In the control pigs (CON group), only laparotomy was performed. Eight days later, in the E.coli group developed severe acute endometritis. In this group, myometrial sstr2 mRNA expression lowered and protein expression increased compared to other groups. Compared to period before somatostatin administration, somatostatin did not change tension in myometrium and endometrium/myometrium of three groups, reduced amplitude and frequency in the CON and SAL groups, and increased amplitude and decreased frequency in the E.coli group. In this group, amplitude was increased by somatostatin compared to other groups. In the CON and SAL groups, sstr2 eliminated inhibitory somatostatin effect on amplitude, while sstr5 antagonist reversed inhibitory somatostatin effect on amplitude. In the E.coli group, sstr2 antagonist reversed stimulatory somatostatin effect on amplitude, while in sstr5 antagonist presence stimulatory somatostatin effect was more deepened compared to somatostatin action alone. After using sstr2 antagonist more deepened inhibitory somatostatin effect on frequency in the CON and E.coli groups was found. Sstr5 antagonist partly eliminated inhibitory somatostatin effect on frequency in the SAL group. Summarizing, the uterine inflammation increases the myometrial sstr2 protein expression; somatostatin raises amplitude of the inflamed uterus acting by sstr2, while drops this parameter by sstr5.
我们研究了炎症对生长抑素受体亚型 2（sstr2）和 5（sstr5）在子宫肌层表达的影响，以及生长抑素单独或与 sstr2 和 sstr5 拮抗剂对发炎子宫收缩性的影响。在发情周期的第 3 天，将大肠杆菌悬浮液（大肠杆菌组）或生理盐水（SAL 组）注入子宫角。在对照组猪（CON 组）中，仅进行剖腹手术。8 天后，大肠杆菌组发生严重急性子宫内膜炎。在该组中，与其他组相比，子宫肌层 sstr2 mRNA 表达降低，蛋白表达增加。与生长抑素给药前相比，生长抑素未改变三组子宫肌层和子宫内膜/子宫肌层的张力，降低了 CON 和 SAL 组的幅度和频率，增加了大肠杆菌组的幅度和降低了频率。在该组中，与其他组相比，生长抑素增加了幅度。在 CON 和 SAL 组中，sstr2 消除了生长抑素对幅度的抑制作用，而 sstr5 拮抗剂逆转了生长抑素对幅度的抑制作用。在大肠杆菌组中，sstr2 拮抗剂逆转了生长抑素对幅度的刺激作用，而在 sstr5 拮抗剂存在的情况下，与生长抑素单独作用相比，刺激生长抑素的作用更加深入。使用 sstr2 拮抗剂后，在 CON 和大肠杆菌组中发现对频率的抑制性生长抑素作用进一步加深。sstr5 拮抗剂部分消除了 SAL 组中生长抑素对频率的抑制作用。总之，子宫炎症增加了子宫肌层 sstr2 蛋白表达；生长抑素通过 sstr2 增加发炎子宫的幅度，而通过 sstr5 降低该参数。
