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首页> 外文期刊>Journal of cellular physiology. >PRR34-AS1 overexpression promotes protection of propofol pretreatment against ischemia/reperfusion injury in a mouse model after total knee arthroplasty via blockade of the JAK1-dependent JAK-STAT signaling pathway
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PRR34-AS1 overexpression promotes protection of propofol pretreatment against ischemia/reperfusion injury in a mouse model after total knee arthroplasty via blockade of the JAK1-dependent JAK-STAT signaling pathway

机译：PRR34-AS1超表达促进保护异丙酚预处理对缺血/再灌注损伤的小鼠模型全膝关节置换术后通过封锁的JAK1-dependent JAK-STAT信号通路

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摘要

Long noncoding RNAs have been documented to be protective against ischemia/ reperfusion (I/R) injury. However, few research works have focused on the protective effects of PRR34-AS1 on I/R injury after total knee arthroplasty (TKA). The objective of the present study was to investigate the possible effect of PRR34-AS1 on I/R injury after TKA. A mouse model with I/R injury after TKA was established. The interaction between PRR34-AS1 and Janus kinase 1 (JAK1) was examined and thoroughly investigated. Next, the effects of PRR34-AS1 on the expression of apoptosis-related proteins, JAS-signal transducer and activator of transcription (STAT) signaling pathways, and inflammation-related genes, chon-drocyte proliferation, and apoptosis were analyzed after gain- and loss-of-function experiments. Attenuated symptoms were observed in mice pretreated with propofol, which was evidenced by decreased positive expression rate of JAK1 protein and superoxide dismutase content along with increased malondialdehyde content and IL-10 levels. PRR34-AS1 was poorly expressed in mice with I/R injury after TKA. JAK1 was a target of PRR34-AS1. Upregulated PRR34-AS1 diminished expression of JAK1, STAT1, JAK2, and STAT3 as well as cell apoptosis, while enhancing cell proliferation in vitro. Furthermore, JAK1 silencing could reverse the suppressed cell proliferation and enhanced cell apoptosis of chondrocytes imposed by silencing PRR34-AS1. Upregulation of PRR34-AS1 can potentially relieve I/R injury after TKA in mice pretreated with propofol through inhibition of the JAS-STAT signaling pathway by targeting JAK1.
机译：长非编码rna已经记录预防缺血/再灌注(I / R)受伤。的保护作用PRR34-AS1对I / R损伤后全膝关节置换术(TKA)。本研究的目的是调查可能PRR34-AS1对I / R损伤的影响TKA之后。TKA成立。PRR34-AS1和Janus激酶1 (JAK1)检查和彻底调查。PRR34-AS1 apoptosis-related的表达蛋白质,JAS-signal传感器和催化剂转录(STAT)信号通路炎症相关的基因,chon-drocyte增殖和细胞凋亡进行了分析获得和功能丧失的实验。减毒症状观察老鼠用异丙酚预处理,证明了这一点JAK1的阳性表达率下降蛋白质和超氧化物歧化酶含量丙二醛含量增加和il - 10的水平。TKA后与I / R损伤。PRR34-AS1。表达JAK1、STAT1 JAK2和STAT3细胞凋亡,同时提高细胞体外增殖。沉默可以反向抑制细胞扩散和增强细胞的凋亡软骨细胞由沉默PRR34-AS1。Upregulation PRR34-AS1可能会减轻I / R损伤在老鼠TKA后使用通过抑制JAS-STAT的异丙酚针对JAK1信号通路。

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