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JNK在海绵体神经损伤急性期海绵体组织凋亡中的作用。

Role of Jun amino-terminal kinase (JNK) in apoptosis of cavernosal tissue during acute phase after cavernosal nerve injury.

作者信息

Song Won Hoon, Son Hwancheol, Kim Soo Woong, Paick Jae-Seung, Cho Min Chul

机构信息

Department of Urology, Seoul National University, College of Medicine, Seoul 03080, Korea.

Department of Urology, Seoul National University, Boramae Medical Center, Seoul 07061, Korea.

出版信息

Asian J Androl. 2018 Jan-Feb;20(1):50-55. doi: 10.4103/aja.aja_10_17.

Abstract

The present study aimed to identify which mitogen-activated protein kinase (p38 or Jun amino-terminal kinase [JNK]) was involved in cavernosal apoptosis during the acute phase after cavernosal nerve crush injury (CNCI) in rats to ameliorate apoptosis of cavernosal tissue, such as smooth muscle (SM). A total of twenty 10-week-old male Sprague-Dawley rats were divided equally into two groups: sham surgery (S) and CNCI (I). The I group approximated the clinical situation of men undergoing radical prostatectomy using two 60-second compressions of both CNs with a microsurgical vascular clamp. At 2-week postinjury, erectile response was assessed using electrostimulation. Penile tissues were harvested for immunohistochemistry analysis of alpha-SM actin (α-SMA), western blot analysis, and double immunofluorescence analysis of α-SMA and phosphorylated p38 or JNK, as well as double immunofluorescent of TUNEL and phosphorylated p38 or JNK. At 2-week postinjury, the I group had a significantly lower intracavernous pressure (ICP)/mean arterial pressure (MAP) and a lower area under the curve (AUC)/MAP than the S group. The I group also exhibited decreased immunohistochemical staining of α-SMA, an increase in the number of SM cells positive for phosphorylated JNK, an increased number of apoptotic cells positive for phosphorylated JNK, and increased JNK phosphorylation compared with the S group. However, there was no significant difference in p38 phosphorylation expression or the number of SM cells positive for phosphorylated p38 between the two groups. In conclusion, our data suggest that JNK, not p38, is involved in cavernosal apoptosis during the acute phase after partial CN damage.

摘要

本研究旨在确定在大鼠海绵体神经挤压伤(CNCI)急性期,哪种丝裂原活化蛋白激酶(p38或c-Jun氨基末端激酶[JNK])参与海绵体凋亡,以改善海绵体组织(如平滑肌[SM])的凋亡。总共20只10周龄雄性Sprague-Dawley大鼠被平均分为两组:假手术组(S)和CNCI组(I)。I组模拟接受根治性前列腺切除术男性的临床情况,用显微外科血管夹对双侧海绵体神经进行两次60秒的压迫。在损伤后2周,使用电刺激评估勃起反应。采集阴茎组织用于α-平滑肌肌动蛋白(α-SMA)的免疫组织化学分析、蛋白质印迹分析,以及α-SMA与磷酸化p38或JNK的双重免疫荧光分析,还有TUNEL与磷酸化p38或JNK的双重免疫荧光分析。在损伤后2周,I组的海绵体内压(ICP)/平均动脉压(MAP)以及曲线下面积(AUC)/MAP均显著低于S组。与S组相比I组还表现出α-SMA免疫组织化学染色减少、磷酸化JNK阳性的平滑肌细胞数量增加、磷酸化JNK阳性的凋亡细胞数量增加以及JNK磷酸化增加。然而,两组之间p38磷酸化表达或磷酸化p38阳性的平滑肌细胞数量没有显著差异。总之,我们的数据表明,在部分海绵体神经损伤后的急性期,参与海绵体凋亡的是JNK而非p38。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c273/5753554/88922812c909/AJA-20-50-g001.jpg

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