Department of Neurosurgery and Neurointerventional, General Hospital of Ningxia Medical University, Yinchuan, China.
Eur Rev Med Pharmacol Sci. 2019 Jun;23(11):4882-4889. doi: 10.26355/eurrev_201906_18076.
To investigate the association of Toll-like receptor 4-myeloid differential protein-88- c-Jun N-terminal kinase (TLR4-MyD88-JNK) signaling pathway with inflammatory response in intracranial hemorrhage (ICH) rats and its effect on neuronal apoptosis.
The autologous blood was drawn and injected into the brain to establish the rat model of ICH (model group), and the control group was set up. The neurological behavior Longa score was given. The blood and brain tissues of rats were then collected to detect the serum indexes, including glucose (GLU), creatinine (CR), K+ and Na+, and the content of interleukin-6 (IL-6), IL-1β and tumor necrosis factor-α (TNF-α) in each group. The neuronal apoptosis of brain tissues was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Moreover, the expressions of apoptosis- and TLR4-MyD88-JNK pathway-related genes and proteins were detected via Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blotting. Finally, the association of TLR4-MyD88-JNK signaling pathway with the inflammatory response in ICH rats and its effect on neuronal apoptosis were completely observed.
MiR-23b was dramatically down-regulated in CC and the low miR-23b expressions were associated with the poor prognosis and worse OS of CC patients. Additionally, the functional assays demonstrated that miR-23b overexpression obviously repressed CC cell proliferation, invasion and migration abilities through the regulation of the AKT/mTOR pathway and the epithelial-to-mesenchymal transition (EMT) progress. Moreover, the luciferase reporter assay indicated that six1 was one functional target for miR-23b in CC cells, indicating that the inhibitory functions of miR-23b in CC cells were partially regulated by six1. Moreover, miR-23b restoration could prominently repress tumor growth in vivo.
The TLR4-MyD88-JNK signaling pathway can facilitate the inflammatory response in ICH rats, thereby promoting the neuronal apoptosis.
探讨 Toll 样受体 4-髓样分化蛋白 88- c-Jun N 端激酶（TLR4-MyD88-JNK）信号通路与脑出血（ICH）大鼠炎症反应的关系及其对神经元凋亡的影响。
抽取自体血注入脑内建立 ICH 大鼠模型（模型组），并设立对照组。采用 Longa 神经行为学评分法进行评分。采集各组大鼠的血液和脑组织，检测血清指标，包括葡萄糖（GLU）、肌酐（CR）、K+和 Na+，以及白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）的含量。采用末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记法（TUNEL）染色检测脑组织神经元凋亡情况。此外，采用逆转录-聚合酶链反应（RT-PCR）和 Western blot 检测凋亡及 TLR4-MyD88-JNK 通路相关基因和蛋白的表达。最后，观察 TLR4-MyD88-JNK 信号通路与 ICH 大鼠炎症反应的关系及其对神经元凋亡的影响。
CC 中 miR-23b 明显下调，低 miR-23b 表达与 CC 患者的不良预后和更差的总生存期（OS）相关。此外，功能测定表明，通过调节 AKT/mTOR 通路和上皮间质转化（EMT）进程，miR-23b 过表达可明显抑制 CC 细胞的增殖、侵袭和迁移能力。此外，荧光素酶报告基因检测表明，six1 是 CC 细胞中 miR-23b 的一个功能靶标，表明 miR-23b 在 CC 细胞中的抑制作用部分受 six1 调节。此外，miR-23b 恢复可明显抑制体内肿瘤生长。
TLR4-MyD88-JNK 信号通路可促进 ICH 大鼠炎症反应，从而促进神经元凋亡。
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