The mechanism related to ovarian follicular is complex, which has not been fully elucidated. Abundant reports have confirmed that the ovarian function development is closely related to sympathetic innervation. As one of the major neurotransmitters, norepinephrine (NE) is considered an effective regulator of ovarian functions like granulosa cell (GC) apoptosis. However, the mechanism between NE and GC apoptosis in rat is still unclear. In our study, GCs were isolated and cultured in vitro with NE treatment. The apoptosis of GCs was facilitated by NE. Wilms tumor 1 (WT1) was found to be significantly downregulated in GCs after NE treatment, and overexpression of WT1 repressed apoptosis in rat GCs induced by NE. rno-miR-128-3p was found to be significantly enhanced by NE in GCs, and inhibition of rno-miR-128-3p repressed apoptosis in rat GCs induced by NE. Mechanistically, rno-miR-128-3p interacted with WT1 and repressed its expression. In summary, inhibition of rno-miR-128-3p may enhance WT1 expression, and then repress NE-induced apoptosis in rat GCs. Our research may provide a new insight for the improvement of ovarian follicular development.

与卵泡相关的机制复杂，尚未完全阐明。大量报道证实，卵巢功能发育与交感神经支配密切相关。作为主要的神经递质之一，去甲肾上腺素 (NE) 被认为是卵巢功能如颗粒细胞 (GC) 凋亡的有效调节剂。然而，大鼠 NE 与 GC 细胞凋亡之间的机制尚不清楚。在我们的研究中，用 NE 处理在体外分离和培养 GC。NE促进GCs的凋亡。发现 NE 治疗后，Wilms 肿瘤 1（WT1）在 GC 中显着下调，并且 WT1 的过表达抑制了 NE 诱导的大鼠 GC 中的细胞凋亡。发现 rno-miR-128-3p 在 GC 中被 NE 显着增强，和抑制 rno-miR-128-3p 抑制了 NE 诱导的大鼠 GCs 的细胞凋亡。从机制上讲，rno-miR-128-3p 与 WT1 相互作用并抑制其表达。总之，rno-miR-128-3p 的抑制可能会增强 WT1 的表达，然后抑制 NE 诱导的大鼠 GC 细胞凋亡。我们的研究可能为改善卵巢卵泡发育提供新的见解。