PMID- 31799680
OWN - NLM
STAT- MEDLINE
DCOM- 20201015
LR  - 20201015
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 22
DP  - 2019 Nov
TI  - Influence of lncRNA ANRIL on neuronal apoptosis in rats with cerebral infarction 
      by regulating the NF-kappaB signaling pathway.
PG  - 10092-10100
LID - 19577 [pii]
LID - 10.26355/eurrev_201911_19577 [doi]
AB  - OBJECTIVE: The aim of this study was to evaluate the influence of long non-coding 
      ribonucleic acid (lncRNA) antisense non-coding RNA in the INK4 locus (ANRIL) on 
      neuronal apoptosis in rats with cerebral infarction (CI), and to further explore 
      the underlying mechanism of lncRNA ANRIL in the occurrence and development of CI. 
      MATERIALS AND METHODS: A total of 60 adult male Wistar rats were randomly divided 
      into three groups using a random number table, including sham group (n=20), CI 
      group (n=20) and CI + lncRNA ANRIL knockdown group [CI + lncRNA ANRIL 
      small-interfering RNA (siRNA) group, n=20]. Focal CI was constructed by suture 
      occlusion. After successful modeling, lncRNA ANRIL siRNA was stereotactically 
      injected into the lateral ventricle of the rats. 24 h after operation, the 
      neurological function of the rats in each group was evaluated by the modified 
      neurological severity score (mNSS). Meanwhile, the infarction area of brain 
      tissues was evaluated using the triphenyl tetrazolium chloride (TTC) method. The 
      protein expression levels of apoptosis-related genes, including B-cell lymphoma-2 
      (Bcl-2) and Bcl-2 associated X protein (Bax), were detected via Western blotting. 
      Subsequently, immunofluorescence staining was performed to detect the expression 
      and location of Caspase-3 in brain tissues. Moreover, the apoptosis level of rats 
      in each group was detected by terminal deoxynucleotidyl transferase-mediated dUTP 
      nick end labeling (TUNEL) assay. Furthermore, the expressions of nuclear 
      factor-kappaB (NF-kappaB) signaling pathway-related proteins were detected via Western 
      blotting. RESULTS: Polymerase Chain Reaction (PCR) results revealed that the 
      expression level of lncRNA ANRIL in the CI group was significantly increased when 
      compared with that of the sham group (p<0.05). The results of mNSS and TTC 
      staining manifested that knockdown of lncRNA ANRIL could significantly reduce 
      CI-induced neurological deficits and CI area (p<0.05). At the same time, 
      knockdown of lncRNA ANRIL markedly decreased the level of Bax, whereas increased 
      the expression of Bcl-2 (p<0.05). Besides, the number of apoptotic cells in the 
      CI + lncRNA ANRIL siRNA group was remarkably decreased (p<0.05). In addition, 
      lncRNA ANRIL down-regulation remarkably inhibited the phosphorylation of p65 
      (p<0.05). CONCLUSIONS: The inhibitory effect of lncRNA ANRIL knockdown on 
      neuronal apoptosis in CI rats may be probably related to its inhibition of the 
      NF-kappaB signaling pathway. Furthermore, lncRNA ANRIL inhibitor is expected to 
      become a targeted drug in the clinical treatment of CI.
FAU - Zhao, J-H
AU  - Zhao JH
AD  - Department of Neurology, First Affiliated Hospital of China Medical University, 
      Shenyang, China. miller78127@163.com.
FAU - Wang, B
AU  - Wang B
FAU - Wang, X-H
AU  - Wang XH
FAU - Wang, J-R
AU  - Wang JR
FAU - Xu, C-W
AU  - Xu CW
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 (ANRIL long non-coding RNA, rat)
RN  - 0 (NF-kappa B)
RN  - 0 (RNA, Long Noncoding)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - Cerebral Infarction/etiology/*genetics/metabolism
MH  - Disease Models, Animal
MH  - Male
MH  - NF-kappa B/metabolism
MH  - Neurons/cytology/*metabolism
MH  - RNA, Long Noncoding/*genetics
MH  - Random Allocation
MH  - Rats
MH  - Rats, Wistar
MH  - *Signal Transduction
MH  - *Up-Regulation
EDAT- 2019/12/05 06:00
MHDA- 2020/10/21 06:00
CRDT- 2019/12/05 06:00
PHST- 2019/12/05 06:00 [entrez]
PHST- 2019/12/05 06:00 [pubmed]
PHST- 2020/10/21 06:00 [medline]
AID - 19577 [pii]
AID - 10.26355/eurrev_201911_19577 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Nov;23(22):10092-10100. doi: 
      10.26355/eurrev_201911_19577.