PDF(Pubmed)
Abstract：
UNASSIGNED: Erectile dysfunction (ED) occurs in an increasing number of patients after radical prostatectomy and cystectomy, and the phenotypic modulation of corpus cavernosum smooth muscle cells is closely related to ED.
UNASSIGNED: To determine whether endoplasmic reticulum stress (ERS) is implicated in the phenotypic modulation of ED induced by bilateral cavernous nerve injury (BCNI).
UNASSIGNED: In total, 36 Sprague-Dawley rats were randomly divided into 3 groups: sham, in which rats received sham surgery with bilateral cavernous nerve exposure plus phosphate-buffered saline; control, in which rats received BCNI plus phosphate-buffered saline; and experimental, in which rats received BCNI plus 4-phenylbutyric acid. Analysis of variance and a Bonferroni multiple-comparison test were utilized to evaluate differences among groups.
UNASSIGNED: Erectile function, smooth muscle/collagen ratios, and the expression levels of phenotypic modulation and ERS were measured.
UNASSIGNED: Two ratios-maximum intracavernosal pressure/mean arterial pressure and smooth muscle/collagen-were decreased in the control group as compared with the sham group. In penile tissue, there was increased expression of GRP78 (78-kDa glucose-regulated protein), p-PERK/PERK (phosphorylated protein kinase R-like endoplasmic reticulum kinase/protein kinase R-like endoplasmic reticulum kinase), caspase 3, CHOP (C/EBP homologous protein), and OPN (osteopontin) but decreased expression of nNOS (neuronal nitric oxide synthase) and α-SMA (α-smooth muscle actin). As compared with the control group, erectile function was improved and pathologic changes were partially recovered in the experimental group.
UNASSIGNED: The present study demonstrated that ERS is involved in ED caused by cavernous nerve injury, thereby providing a new target and theoretical basis for clinical treatment.
UNASSIGNED: The present study demonstrated for the first time that ERS is related to ED caused by cavernous nerve injury. Inhibition of ERS reverses phenotypic modulation and improves erectile function in rats with BCNI. Additional in vitro studies should be performed to verify these conclusions and explore the specific mechanism of phenotypic modulation.
UNASSIGNED: The present study demonstrated that inhibiting ERS reverses phenotypic modulation and enhances erectile function in rats with BCNI.
UNASSIGNED: To determine whether endoplasmic reticulum stress (ERS) is implicated in the phenotypic modulation of ED induced by bilateral cavernous nerve injury (BCNI).
UNASSIGNED: In total, 36 Sprague-Dawley rats were randomly divided into 3 groups: sham, in which rats received sham surgery with bilateral cavernous nerve exposure plus phosphate-buffered saline; control, in which rats received BCNI plus phosphate-buffered saline; and experimental, in which rats received BCNI plus 4-phenylbutyric acid. Analysis of variance and a Bonferroni multiple-comparison test were utilized to evaluate differences among groups.
UNASSIGNED: Erectile function, smooth muscle/collagen ratios, and the expression levels of phenotypic modulation and ERS were measured.
UNASSIGNED: Two ratios-maximum intracavernosal pressure/mean arterial pressure and smooth muscle/collagen-were decreased in the control group as compared with the sham group. In penile tissue, there was increased expression of GRP78 (78-kDa glucose-regulated protein), p-PERK/PERK (phosphorylated protein kinase R-like endoplasmic reticulum kinase/protein kinase R-like endoplasmic reticulum kinase), caspase 3, CHOP (C/EBP homologous protein), and OPN (osteopontin) but decreased expression of nNOS (neuronal nitric oxide synthase) and α-SMA (α-smooth muscle actin). As compared with the control group, erectile function was improved and pathologic changes were partially recovered in the experimental group.
UNASSIGNED: The present study demonstrated that ERS is involved in ED caused by cavernous nerve injury, thereby providing a new target and theoretical basis for clinical treatment.
UNASSIGNED: The present study demonstrated for the first time that ERS is related to ED caused by cavernous nerve injury. Inhibition of ERS reverses phenotypic modulation and improves erectile function in rats with BCNI. Additional in vitro studies should be performed to verify these conclusions and explore the specific mechanism of phenotypic modulation.
UNASSIGNED: The present study demonstrated that inhibiting ERS reverses phenotypic modulation and enhances erectile function in rats with BCNI.
摘要：
■在根治性前列腺切除术和膀胱切除术后，勃起功能障碍（ED）发生在越来越多的患者中，阴茎海绵体平滑肌细胞的表型调节与ED密切相关。
■确定内质网应激（ERS）是否与双侧海绵状神经损伤（BCNI）引起的ED的表型调节有关。
■总共，36只Sprague-Dawley大鼠随机分为3组：假，其中大鼠接受假手术，双侧海绵体神经暴露加磷酸盐缓冲盐水；对照组，其中大鼠接受BCNI加磷酸盐缓冲盐水；和实验，其中大鼠接受BCNI加4-苯基丁酸。方差分析和Bonferroni多重比较检验用于评估组间差异。
■勃起功能，平滑肌/胶原蛋白比例，测量表型调节和ERS的表达水平。
■与假手术组相比，对照组的两个比率-最大海绵体内压/平均动脉压和平滑肌/胶原-降低。在阴茎组织中，GRP78（78kDa葡萄糖调节蛋白）的表达增加，p-PERK/PERK(磷酸化蛋白激酶R样内质网激酶/蛋白激酶R样内质网激酶),caspase3,CHOP(C/EBP同源蛋白),和OPN（骨桥蛋白），但nNOS（神经元一氧化氮合酶）和α-SMA（α-平滑肌肌动蛋白）的表达降低。与对照组相比,实验组勃起功能得到改善，病理变化部分恢复。
■本研究表明ERS与海绵状神经损伤引起的ED有关，从而为临床治疗提供新的靶点和理论依据。
■本研究首次证明ERS与海绵状神经损伤引起的ED有关。ERS的抑制逆转了BCNI大鼠的表型调节并改善了勃起功能。应进行其他体外研究以验证这些结论并探索表型调节的具体机制。
■本研究表明，抑制ERS可以逆转BCNI大鼠的表型调节并增强勃起功能。
■确定内质网应激（ERS）是否与双侧海绵状神经损伤（BCNI）引起的ED的表型调节有关。
■总共，36只Sprague-Dawley大鼠随机分为3组：假，其中大鼠接受假手术，双侧海绵体神经暴露加磷酸盐缓冲盐水；对照组，其中大鼠接受BCNI加磷酸盐缓冲盐水；和实验，其中大鼠接受BCNI加4-苯基丁酸。方差分析和Bonferroni多重比较检验用于评估组间差异。
■勃起功能，平滑肌/胶原蛋白比例，测量表型调节和ERS的表达水平。
■与假手术组相比，对照组的两个比率-最大海绵体内压/平均动脉压和平滑肌/胶原-降低。在阴茎组织中，GRP78（78kDa葡萄糖调节蛋白）的表达增加，p-PERK/PERK(磷酸化蛋白激酶R样内质网激酶/蛋白激酶R样内质网激酶),caspase3,CHOP(C/EBP同源蛋白),和OPN（骨桥蛋白），但nNOS（神经元一氧化氮合酶）和α-SMA（α-平滑肌肌动蛋白）的表达降低。与对照组相比,实验组勃起功能得到改善，病理变化部分恢复。
■本研究表明ERS与海绵状神经损伤引起的ED有关，从而为临床治疗提供新的靶点和理论依据。
■本研究首次证明ERS与海绵状神经损伤引起的ED有关。ERS的抑制逆转了BCNI大鼠的表型调节并改善了勃起功能。应进行其他体外研究以验证这些结论并探索表型调节的具体机制。
■本研究表明，抑制ERS可以逆转BCNI大鼠的表型调节并增强勃起功能。
