Search

Objective: The aim of this study was to detect the relationship between long-chain non-coding RNA (lncRNA) NEAT1 and microRNA-1224 (miR-1224) in lung cancer and to explore its underlying mechanism., Materials and Methods: The expression levels of lncRNA NEAT1 and miR-1224 in lung cancer tissues and cells were detected by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The interaction between lncRNA NEAT1 with miR-1224, miR-1224, and KLF3 was detected by Dual-Luciferase Reporter Gene Assay. MTT 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide and flow cytometry were used to detect the changes in the proliferative and apoptosis abilities of lung cancer cells after silencing lncRNA NEAT1 or up-regulating miR-1224, respectively., Results: Compared with adjacent normal tissues, lncRNA NEAT1 was significantly up-regulated, while miR-1224 was significantly down-regulated in lung cancer tissues. LncRNA NEAT1 could specifically bind to the 3'UTR of miR-1224 and regulate its expression. The inhibition of lncRNA NEAT1 remarkably reduced the proliferation and enhanced the apoptosis of lung cancer cells. However, the upregulation of the expression of miR-1224 level could significantly inhibit proliferation and promote the apoptosis rate of lung cancer cells. Furthermore, miR-1224 could downregulate KLF3 expression by directly binding to its 3'UTR., Conclusions: LncRNA NEAT1 can sponge the expression of miR-1224, thereby affecting the proliferation and apoptosis of lung cancer.

Objective: To investigate the effect of micro ribonucleic acid (miR)-101a on myocardial cell apoptosis in the rat model of acute myocardial infarction (AMI) and its regulatory mechanism., Materials and Methods: A total of 30 Sprague-Dawley (SD) rats were randomly divided into the Sham group, Model group, and miR-101a mimic group, with 10 rats in each group. The rat model of AMI was established by the ligation of the anterior descending coronary artery. The rat left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) were detected using a color Doppler ultrasonic apparatus. Subsequently, the miRNA online database (TargetScan) was adopted to predict miRNAs that could be able to regulate TGF-β1. Hematoxylin and eosin (H&E) staining was conducted to reveal the histopathological morphology changes in the rat heart. The serum levels of cysteinyl aspartate specific proteinase-3 (Caspase-3) and Bcl-2-associated X protein (Bax) in rats were detected via enzyme-linked immunosorbent assay (ELISA). Moreover, the expression levels of the transforming growth factor-beta l (TGF-β1) and c-Jun N-terminal kinase (JNK) in rat heart were measured via Western blotting., Results: Through searching miRNA database, miR-101a and TGF-β1 messenger RNAs (mRNAs) had binding sites in the 3' untranslated region (3'UTR). Compared with those in Sham group, the rat LVEDV and LVESV were notably elevated, the histopathological morphology of the heart was seriously damaged, the apoptotic rate of myocardial cells and the levels of TGF-β1 and JNK proteins significantly increased in the Model group. Additionally, compared with those in the Model group, the LVEDV and LVESV of rats in miR-101a mimic group were significantly reduced, the histopathological morphology of the heart was markedly improved, and the apoptotic rate and the levels of TGF-β1 and JNK in rat heart were remarkably decreased., Conclusions: The myocardial cell apoptosis in AMI rats can be suppressed by overexpression of miR-101a by inhibiting the TGF-β1/JNK signaling pathway.

OBJECTIVE: To study the effect of promethazine on neuronal apoptosis in rats with cerebral infarction (CI) through the phosphatidylinositol 3-hydroxy kinase/protein kinase B (PI3K/Akt) signaling pathway. MATERIALS AND METHODS: A total of 36 Sprague-Dawley rats were randomly divided into the sham group (n=12), model group (n=12), and promethazine group (n=12). The external carotid artery was only exposed in the model group, and the ischemia-reperfusion model after CI was established using the suture method in the other two groups. After modeling, the normal saline was intraperitoneally injected in the sham group and model group, while promethazine was intraperitoneally injected in the promethazine group. The rats were sampled after 1 week of intervention. The neurological deficits of rats were evaluated using the Zea-Longa score, and the cognitive function, the spatial learning, and memory of rats were detected via the water maze test. Moreover, the expressions of B-cell lymphoma-2 (Bcl-2) and Bcl-2 associated X protein (Bax) in brain tissues were detected via immunohistochemistry, and the relative protein expressions of PI3K p85, PI3K p110, and p-Akt were detected via Western blotting. The mRNA expressions of Bax and Bcl-2 were detected via quantitative Polymerase Chain Reaction (qPCR), and the apoptosis was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay. RESULTS: The Zea-Longa score was significantly increased in the model group and promethazine group compared with that in the sham group (p<0.05), while it significantly declined in the promethazine group compared with that in the model group (p<0.05). The escape latency was significantly prolonged and the times of crossing platform were significantly reduced in the model group and promethazine group compared with those in the sham group (p<0.05), while the escape latency was significantly shortened and the times of crossing platform were significantly increased in the promethazine group compared with those in the model group (p<0.05). Compared with those in the sham group, the positive expression of Bax was significantly increased, while the positive expression of Bcl-2 was remarkably decreased in the model group and promethazine group (p<0.05). Compared with those in the model group, the positive expression of Bax was significantly decreased, while the positive expression of Bcl- 2 was remarkably increased in the promethazine group (p<0.05). Besides, the model group and promethazine group had evidently higher relative protein expressions of PI3K p85, PI3K p110, and p-Akt than the sham group (p<0.05), while the promethazine group also had evidently higher relative protein expressions of PI3K p85, PI3K p110, and p-Akt than the model group (p<0.05). Compared with the sham group, model group, and promethazine group had remarkably increased relative mRNA expression of Bax, and remarkably decreased relative mRNA expression of Bcl-2 (p<0.05). Compared with those in the model group, the relative mRNA expression of Bax was remarkably decreased, while the relative mRNA expression of Bcl-2 was remarkably increased in the promethazine group (p<0.05). Finally, the apoptosis rate was significantly higher in the model group and promethazine group than that in the sham group (p<0.05), while it was significantly lower in the promethazine group than that in the model group (p<0.05). CONCLUSIONS: Promethazine inhibits neuronal apoptosis in CI rats by upregulating the PI3K/Akt signaling pathway, thereby exerting a protective effect. [ABSTRACT FROM AUTHOR]