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The role of somatostatin and its receptors (sstr2, sstr5) in the contractility of gilt inflamed uterus
Research in Veterinary Science ( IF 2.2 ) Pub Date : 2020-09-19 , DOI: 10.1016/j.rvsc.2020.09.016
Barbara Jana , Jarosław Całka , Marta Czajkowska

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.



中文翻译:

生长抑素及其受体(sstr2,sstr5)在烫发性子宫炎症中的作用

我们研究了对子宫肌瘤中生长抑素受体亚型2(sstr2)和5(sstr5)表达的炎症作用,生长抑素单独或与sstr2和sstr5拮抗剂对烫发性子宫炎的收缩性的影响。在发情周期的第3天,将大肠杆菌悬液(大肠杆菌组)或生理盐水(SAL组)注射入子宫角。在对照猪(CON组)中,仅进行剖腹手术。八天后,在大肠杆菌中本组发展为严重的急性子宫内膜炎。与其他组相比,该组的子宫肌层sstr2 mRNA表达降低,蛋白表达升高。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,CON和SAL组的幅度和频率降低,大肠杆菌的幅度和频率降低。组。与其他组相比,生长抑素使该组的振幅增加。在CON和SAL组中,sstr2消除了生长抑素对振幅的抑制作用,而sstr5拮抗剂则逆转了生长抑素对振幅的抑制作用。在大肠杆菌组中,与单独的生长抑素作用相比,sstr2拮抗剂逆转了促生长素抑制素对振幅的作用,而在sstr5拮抗剂存在下,刺激生长抑素的作用更加加深。使用sstr2拮抗剂后,生长抑素对CON和E.coli频率的抑制作用进一步加深组被发现。在SAL组中,Sstr5拮抗剂部分消除了生长抑素对频率的抑制作用。综上所述,子宫炎症会增加子宫肌层sstr2蛋白的表达。生长抑素会增加由sstr2作用的发炎子宫的幅度,而由sstr5降低该参数。

更新日期:2020-09-28
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