| 吴 岩,侍立峰,王延洲,张峥程,毛静月,李彩云.LncRNA-NEAT1对妊娠期高血压大鼠JAK2/STAT3信号通路、炎症反应和妊娠结局的影响[J].,2023,(6):1022-1026 |
| LncRNA-NEAT1对妊娠期高血压大鼠JAK2/STAT3信号通路、炎症反应和妊娠结局的影响 |
| Effects of LncRNA-NEAT1 on JAK2/STAT3 Signaling Pathway, Inflammatory Response and Pregnancy Outcome in Hypertensive Rats during Pregnancy |
| 投稿时间：2022-09-11 修订日期：2022-10-05 |
| DOI：10.13241/j.cnki.pmb.2023.06.005 |
| 中文关键词: LncRNA-NEAT1 妊娠期高血压 JAK2/STAT3信号通路 炎症反应 妊娠结局 |
| 英文关键词: LncRNA-NEAT1 Hypertension during pregnancy JAK2/STAT3 signaling pathway An inflammatory response Pregnancy outcomes |
| 基金项目:国家自然科学基金面上项目（81471443） |
|
| 摘要点击次数: 718 |
| 全文下载次数: 498 |
| 中文摘要: |
| 摘要 目的：探讨LncRNA-NEAT1对妊娠期高血压大鼠JAK2/STAT3信号通路、炎症反应和妊娠结局的影响。方法：采用注射L-精氨酸甲酯的方法构建妊娠期高血压大鼠模型。采用Western blot检测JAK2/STAT3信号通路蛋白表达；采用ELISA法检测炎症因子和血管内皮损伤因子。观察并记录大鼠24 h蛋白尿、尾静脉压和死胎率。结果：与空白组相比，模型组、LncRNA-NEAT1过表达组、LncRNA-NEAT1抑制组JAK2、STAT3的蛋白表达水平明显更高（P＜0.05）；与模型组相比，LncRNA-NEAT1抑制组JAK2、STAT3的蛋白表达水平明显更低（P＜0.05），而LncRNA-NEAT1过表达组JAK2、STAT3的蛋白表达水平明显更高（P＜0.05）；与空白组相比，模型组、LncRNA-NEAT1过表达组、LncRNA-NEAT1抑制组ET-1和sICAM-1水平明显更高，而NO水平明显更低（P＜0.05）；与模型组相比，LncRNA-NEAT1过表达组、LncRNA-NEAT1抑制组ET-1和sICAM-1水平明显更高（P＜0.05），而NO水平明显更低（P＜0.05），而LncRNA-NEAT1过表达组ET-1和sICAM-1表达水平明显更高，而NO明显更低（P＜0.05）；与空白组相比，模型组、LncRNA-NEAT1过表达组、LncRNA-NEAT1抑制组TNF-α、IL-1β、IL-18表达水平明显更高（P＜0.05）；与模型组相比，LncRNA-NEAT1抑制组TNF-α、IL-1β、IL-18表达水平明显更低（P＜0.05），而LncRNA-NEAT1过表达组TNF-α、IL-1β、IL-18表达水平明显更高（P＜0.05）；与空白组相比，模型组、LncRNA-NEAT1过表达组、LncRNA-NEAT1抑制组尾静脉压和24h蛋白尿水平明显更高（P＜0.05）；与模型组相比，LncRNA-NEAT1抑制组尾静脉压和24 h蛋白尿表达水平明显更低（P＜0.05），而LncRNA-NEAT1过表达组尾静脉压和24 h蛋白尿表达水平明显更高（P＜0.05）；LncRNA-NEAT1过表达组（21.56%）死胎率显著高于模型组（16.72%）和LncRNA-NEAT1抑制组（5.65%）。结论：妊娠期糖尿病大鼠LncRNA-NEAT1的表达下调可抑制JAK2/STAT3信号通路的表达并下调下游促炎因子的表达，进而缓解血管内皮损伤降低死胎率。 |
| 英文摘要: |
| ABSTRACT Objective: To investigate the effects of LncRNA-NEAT1 on JAK2/STAT3 signaling pathway, inflammatory response and pregnancy outcome in hypertensive rats during pregnancy. Methods: The hypertensive rat model of pregnancy was established by injecting L-arginine methyl ester. The protein expression of JAK2/STAT3 signaling pathway was detected by Western blot. Inflammatory factors and vascular endothelial injury factors were detected by ELISA. Proteinuria, caudal venous pressure and stillbirth rate were observed and recorded. Results: Compared with blank group, the protein expression levels of JAK2 and STAT3 in model group, LncRNA-NEAT1 overexpression group and LncRNA-NEAT1 inhibition group were significantly higher (P<0.05). Compared with model group, the protein expression levels of JAK2 and STAT3 in LncRNA-NEAT1 inhibition group were significantly lower (P<0.05), while the protein expression levels of JAK2 and STAT3 in LncRNA-NEAT1 overexpression group were significantly higher (P<0.05). Compared with blank group, the levels of ET-1 and sICAM-1 in model group, LncRNA-NEAT1 overexpression group and LncRNA-NEAT1 inhibition group were significantly higher, while the level of NO was significantly lower (P<0.05). Compared with model group, the levels of ET-1 and sICAM-1 in LncRNA-NEAT1 overexpression group and LncRNA-NEAT1 inhibition group were significantly higher (P<0.05), while the level of NO was significantly lower (P<0.05). The expression levels of ET-1 and sICAM-1 in LncRNA-NEAT1 overexpression group were significantly higher, but NO was significantly lower (P<0.05). Compared with blank group, the expression levels of TNF-α, IL-1β and IL-18 in model group, LncRNA-NEAT1 overexpression group and LncRNA-NEAT1 inhibition group were significantly higher (P<0.05). Compared with model group, the expression levels of TNF-α, IL-1β and IL-18 in LncRNA-NEAT1 inhibition group were significantly lower (P<0.05), while the expression levels of TNF-α, IL-1β and IL-18 in LncRNA-NEAT1 overexpression group were significantly higher (P<0.05). Compared with blank group, caudal venous pressure and 24 h proteinuria levels in model group, LncRNA-NEAT1 overexpression group and LncRNA-NEAT1 inhibition group were significantly higher (P<0.05). Compared with model group, the caudal venous pressure and 24 h proteinuria expression levels in LncRNA-NEAT1 inhibited group were significantly lower (P<0.05), while the caudal venous pressure and 24 h proteinuria expression levels in LncRNA-NEAT1 overexpression group were significantly higher (P<0.05). The stillbirth rate of LncRNA-NEAT1 overexpression group (21.56%) was higher than that of model group (16.72%) and LncRNA-NEAT1 inhibition group (5.65%). Conclusion: Down-regulation of LncRNA-NEAT1 in gestational diabetes rats can inhibit the expression of JAK2/STAT3 signaling pathway and down-regulate the expression of downstream pro-inflammatory factors, so as to alleviate vascular endothelial injury and reduce the stillbirth rate. |
|
查看全文
查看/发表评论 下载PDF阅读器 |
| 关闭 |
|
|
|
