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首页> 外文期刊>Molecules and cells >Icariside II Promotes the Differentiation of Adipose Tissue-Derived Stem Cells to Schwann Cells to Preserve Erectile Function after Cavernous Nerve Injury
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Icariside II Promotes the Differentiation of Adipose Tissue-Derived Stem Cells to Schwann Cells to Preserve Erectile Function after Cavernous Nerve Injury

机译:伊卡甙II促进海绵组织损伤后脂肪组织干细胞向雪旺细胞的分化,以保持勃起功能。

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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.
机译:伊卡甙II(ICA II)用于勃起功能障碍的治疗。脂肪组织干细胞(ADSC)可有效改善勃起功能。本研究旨在探讨ADSCs改善勃起功能的作用机制。从大鼠的脂肪组织中分离出ADSC。使用细胞计数试剂盒8(CCK-8)分析确定细胞增殖。通过qRT-PCR和western blot分别测定mRNA和蛋白质的表达。使用重组质粒和细胞转染来调节相关基因的内源表达。进行了双重荧光素酶报告基因测定以确定miR-34a和STAT3之间的相互作用。使用具有双侧海绵状神经损伤(BCNI)的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向雪旺细胞(SCs)的增殖和分化。抑制的miR-34a通过上调STAT3促进ADSC向SC的分化。 ICA II通过miR-34a / STAT3途径促进了ADSC向SC的分化。 ICA II和ADSCs的结合保留了BCNI模型大鼠的勃起功能。 ICA II处理的ADSCs明显保留BCNI模型大鼠的勃起功能,而miR-34a过表达可逆转勃起功能。 ICA II通过miR-34a / STAT3途径促进ADSCs向SCs的分化,有助于在发生海绵状神经损伤后保持勃起功能。

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