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二氢淫羊藿素促进脂肪组织源性干细胞向施万细胞分化以保留海绵体神经损伤后的勃起功能。

Icariside II Promotes the Differentiation of Adipose Tissue-Derived Stem Cells to Schwann Cells to Preserve Erectile Function after Cavernous Nerve Injury.

机构信息

Department of Andrology, Institute of Andrology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, 450052, China.

出版信息

Mol Cells. 2018 Jun;41(6):553-561. doi: 10.14348/molcells.2018.2236. Epub 2018 Jun 14.

Abstract

Icariside II (ICA II) is used in erectile dysfunction treatment. Adipose tissue-derived stem cells (ADSCs) are efficient at improving erectile function. This study aimed to explore the action mechanism of ADSCs in improving erectile function. ADSCs were isolated from the adipose tissues of rats. Cell proliferation was determined using the Cell Counting Kit-8 (CCK-8) assay. The expressions of mRNA and protein were determined separately through qRT-PCR and western blot. The endogenous expressions of related genes were regulated using recombinant plasmids and cell transfection. A Dual-Luciferase Reporter Assay was performed to determine the interaction between miR-34a and STAT3. Rat models with bilateral cavernous nerve injuries (BCNIs) were used to assess erectile function through the detection of mean arterial pressure (MAP) and intracavernosal pressure (ICP). ICA II promoted ADSCs' proliferation and differentiation to Schwann cells (SCs) through the inhibition of miR-34a. Suppressed miR-34a promoted the differentiation of ADSCs to SCs by upregulating STAT3. ICA II promoted the differentiation of ADSCs to SCs through the miR-34a/STAT3 pathway. The combination of ICA II and ADSCs preserved the erectile function of the BCNI model rats. ADSCs treated with ICA II markedly preserved the erectile function of the BCNI model rats, which was reversed through miR-34a overexpression. ICA II promotes the differentiation of ADSCs to SCs through the miR-34a/STAT3 pathway, contributing to erectile function preservation after the occurrence of a cavernous nerve injury.

摘要

二氢杨梅素(ICA II)用于治疗勃起功能障碍。脂肪组织来源的干细胞(ADSCs)在改善勃起功能方面效果显著。本研究旨在探讨 ADSCs 改善勃起功能的作用机制。从大鼠脂肪组织中分离 ADSCs。使用细胞计数试剂盒(CCK-8)测定细胞增殖。分别通过 qRT-PCR 和 Western blot 测定 mRNA 和蛋白的表达。使用重组质粒和细胞转染调节相关基因的内源性表达。双荧光素酶报告基因检测法确定 miR-34a 和 STAT3 之间的相互作用。使用双侧海绵体神经损伤(BCNI)大鼠模型通过检测平均动脉压(MAP)和海绵体内压(ICP)来评估勃起功能。ICA II 通过抑制 miR-34a 促进 ADSCs 的增殖和向施万细胞(SCs)的分化。抑制 miR-34a 通过上调 STAT3 促进 ADSCs 向 SCs 的分化。ICA II 通过 miR-34a/STAT3 通路促进 ADSCs 向 SCs 的分化。ICA II 和 ADSCs 的联合使用保留了 BCNI 模型大鼠的勃起功能。用 ICA II 处理的 ADSCs 显著保留了 BCNI 模型大鼠的勃起功能,而通过 miR-34a 过表达则逆转了这一作用。ICA II 通过 miR-34a/STAT3 通路促进 ADSCs 向 SCs 的分化,有助于在发生海绵体神经损伤后保留勃起功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4eb8/6030246/227237109888/molce-41-6-553f1.jpg

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