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鞘内给予罗哌卡因通过糖萼/α7 烟碱型乙酰胆碱受体通路缓解子痫前期诱导的肾损伤。

Ropivacaine with intraspinal administration alleviates preeclampsia-induced kidney injury via glycocalyx /alpha 7 nicotinic acetylcholine receptor pathway.

机构信息

Department of Anaesthesiology, Obstetrics and Gynaecology Hospital of Fudan University, Shanghai, China.

出版信息

Bioengineered. 2022 May;13(5):13131-13140. doi: 10.1080/21655979.2022.2080365.

DOI:10.1080/21655979.2022.2080365
PMID:35635041
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9275932/
Abstract

Preeclampsia is characterized by hypertension and proteinuria, which is associated with kidney injury. Glycocalyx (GCX) degradation mediated endothelial injury can result in proteinuria and kidney damage. alpha 7 nicotinic acetylcholine receptor (α7nAChR) connects nervous and immune systems to respond to stress or injury. We aimed to explore the protective effect and mechanism of intraspinal analgesia on maternal kidney injury in preeclampsia. Endotoxin-induced preeclampsia rats treated with ropivacaine via intraspinal administration. Renal histopathological examination was performed, cell apoptosis in the kidney, the levels of Glycocalyx markers of Syndecan-1 and heparin sulfate (HS) in maternal serum, Syndecan-1 along with α7nAChR in the kidney were measured. Our results showed that kidney injury was obviously in preeclampsia rats with proteinuria, endothelial damage, higher apoptosis rate, increasing levels of Syndecan-1 and HS in serum, upregulated Syndecan-1 expression but downregulated α7nAChR expression in kidney. Preeclampsia rats treated with intraspinal injected ropivacaine attenuated preeclampsia-induced kidney injury as Syndecan-1 and HS were decreased in serum, Syndecan-1 expression was suppressed as well as α7nAChR was activated in the kidney. Our results suggested that Ropivacaine administered through the spinal canal may protect preeclampsia-induced renal injury by decreasing GCX and α7nAChR activation.

摘要

子痫前期的特征是高血压和蛋白尿,这与肾脏损伤有关。糖萼(GCX)降解介导的内皮损伤可导致蛋白尿和肾脏损害。α7 烟碱型乙酰胆碱受体(α7nAChR)连接神经系统和免疫系统,以应对应激或损伤。我们旨在探讨椎管内镇痛对子痫前期母鼠肾脏损伤的保护作用及其机制。通过椎管内给予罗哌卡因治疗内毒素诱导的子痫前期大鼠。进行肾组织病理学检查,检测肾脏细胞凋亡、母血清中糖萼标志物硫酸乙酰肝素(HS)和硫酸皮肤素(HS)水平、肾脏中硫酸乙酰肝素(HS)和α7nAChR 的水平。结果表明,子痫前期大鼠蛋白尿、内皮损伤、细胞凋亡率升高、血清中硫酸乙酰肝素(HS)和硫酸皮肤素(HS)水平升高、肾脏中硫酸乙酰肝素(HS)和α7nAChR 表达上调,表明肾脏损伤明显。椎管内注射罗哌卡因治疗子痫前期大鼠可减轻子痫前期引起的肾脏损伤,降低血清中硫酸乙酰肝素(HS)和硫酸皮肤素(HS)水平,抑制肾脏中硫酸乙酰肝素(HS)表达,激活α7nAChR。我们的结果表明,椎管内注射罗哌卡因可能通过减少 GCX 和 α7nAChR 的激活来保护子痫前期引起的肾脏损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9167/9275932/851e70df0053/KBIE_A_2080365_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9167/9275932/3a1c2a67365e/KBIE_A_2080365_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9167/9275932/d3bf96938893/KBIE_A_2080365_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9167/9275932/fa9747b54b76/KBIE_A_2080365_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9167/9275932/11f744d68725/KBIE_A_2080365_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9167/9275932/851e70df0053/KBIE_A_2080365_F0004_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9167/9275932/3a1c2a67365e/KBIE_A_2080365_UF0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9167/9275932/d3bf96938893/KBIE_A_2080365_F0001_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9167/9275932/fa9747b54b76/KBIE_A_2080365_F0002_OC.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9167/9275932/11f744d68725/KBIE_A_2080365_F0003_B.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9167/9275932/851e70df0053/KBIE_A_2080365_F0004_OC.jpg

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