PMID- 31210322
OWN - NLM
STAT- MEDLINE
DCOM- 20200925
LR  - 20200925
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 11
DP  - 2019 Jun
TI  - Association of the TLR4-MyD88-JNK signaling pathway with inflammatory response in 
      intracranial hemorrhage rats and its effect on neuronal apoptosis.
PG  - 4882-4889
LID - 18076 [pii]
LID - 10.26355/eurrev_201906_18076 [doi]
AB  - OBJECTIVE: 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. PATIENTS AND METHODS: 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-1beta and tumor necrosis factor-alpha (TNF-alpha) 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. RESULTS: 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. CONCLUSIONS: The 
      TLR4-MyD88-JNK signaling pathway can facilitate the inflammatory response in ICH 
      rats, thereby promoting the neuronal apoptosis.
FAU - Huang, D-J
AU  - Huang DJ
AD  - Department of Neurosurgery and Neurointerventional, General Hospital of Ningxia 
      Medical University, Yinchuan, China. 2099371057@qq.com.
FAU - Li, Y
AU  - Li Y
FAU - Yang, Z-X
AU  - Yang ZX
FAU - Sun, Y-N
AU  - Sun YN
FAU - Wan, D
AU  - Wan D
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Myd88 protein, rat)
RN  - 0 (Myeloid Differentiation Factor 88)
RN  - 0 (Tlr4 protein, rat)
RN  - 0 (Toll-Like Receptor 4)
SB  - IM
MH  - Animals
MH  - Apoptosis/*immunology
MH  - Cell Proliferation
MH  - Cerebral Hemorrhage/*immunology/pathology
MH  - Disease Models, Animal
MH  - Down-Regulation
MH  - Humans
MH  - MAP Kinase Signaling System/genetics/*immunology
MH  - Male
MH  - Myeloid Differentiation Factor 88/metabolism
MH  - Neurons/immunology/*pathology
MH  - Rats
MH  - Toll-Like Receptor 4/metabolism
EDAT- 2019/06/19 06:00
MHDA- 2020/09/26 06:00
CRDT- 2019/06/19 06:00
PHST- 2019/06/19 06:00 [entrez]
PHST- 2019/06/19 06:00 [pubmed]
PHST- 2020/09/26 06:00 [medline]
AID - 18076 [pii]
AID - 10.26355/eurrev_201906_18076 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Jun;23(11):4882-4889. doi: 
      10.26355/eurrev_201906_18076.