OBJECTIVETo investigate the protect effects of sodium ferulate (SF) on the daunormbicin(DNR-induced cardiotoxicity in juvenile rats.

METHODSForty male juvenile SD rats were randomly divided into control group (Control), daunorubicin group (DNR), sodium ferudate treatment group (DNR + SF), sodium ferudate group (SF) (n = 10) . Juvenile rats were intraperitoneally treated with DNR (2.5 mg/kg every week for a cumulative dose of 10 mg/kg) preparation immature myocardial injury model in presence with SF (60 mg/kg) oral treat- ment for 25 days. The left ventricular pressure and its response to isoproterenol were measured using left ventricular catheter. Rat myocardium myocardial pathology specimens and ultrastructure changes were also observed. The expression of cardiac Troponin I (cTNI) was detected by Western blot and RT-PCR. Results: SF treatment could inhibit the decreasing of heart rates induced by DNR damage (P < 0.05); it could increase the left ventrivular end diastolic pressure(LVEDP), heart rate, the maximal left ventrivular systolic speed(LVP + dp/dtmax) and the maximal left ventrivular diastolic speed (LVP-dp/dtmax) responding to isoproterenol stimulation(P < 0.01); SF also could improve the myocardial ultrastructure injuries and inhibit the decreasing of cTNI expression caused by DNR damages (P < 0.05).

CONCLUSIONSF treatment could alleviate the decreasing of cardiac reservation induced by DNR damages in juvenile rats, which might be related to its reversing the effects on the cardiac systolic and diastolic function injuries and its inhibiting effects on the decreasing of cTNI expression caused by DNR. The mechanism of SF preventing daunorubicin-induced cardiotoxicity in juvenile rats is relevant to inhabited cardiac Troponin I expression.

Animals ; Blood Pressure ; Cardiotoxicity ; drug therapy ; Coumaric Acids ; pharmacology ; Daunorubicin ; toxicity ; Heart ; physiopathology ; Heart Rate ; Isoproterenol ; Male ; Myocardium ; pathology ; Protective Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Troponin I ; metabolism

Animals ; Animals, Newborn ; Chronic Disease ; Daunorubicin ; adverse effects ; Disease Models, Animal ; Heart Failure ; chemically induced ; Rats ; Rats, Sprague-Dawley

There is increasing evidence that long non-coding RNA (lncRNA) plays critical roles in cancer progression. However, the role of long non-coding RNA 00665 (LINC00665) in most cancers is poorly understood. The purpose of the present study was to reveal the functional role of LINC00665 in cervical cancer cells. HeLa cells were subjected to LINC00665 short hairpin RNA (shRNA) or control shRNA treatment to investigate the metastasis and proliferation phenotype of cervical cancer cells in vitro and in vivo. Transcriptome sequencing experiments of HeLa cells in LINC00665 silencing or control group were conducted, and the differentially expressed genes (DEGs) were screened. The DEGs were subjected to Metascape database functional analysis and gene set enrichment analysis. Epithelial-mesenchymal transition (EMT) related markers and a key element of WNT/β‑catenin pathway, CTNNB1 (catenin beta 1), were detected by Western blot and immunofluorescence assay. The results showed that silencing LINC00665 reduced cell viability of Hela cells, up-regulated protein expression level of E-cadherin, down-regulated protein expression levels of N-cadherin, Vimentin and CTNNB1, and inhibited cell migration and invasion of HeLa cells. Bioinformatics analysis results showed that LINC00665 might promote EMT by activating WNT-CTNNB1/β‑catenin signaling pathway. These results indicate that LINC00665 has functions in transcriptional EMT regulation via WNT-CTNNB1/β‑catenin signaling pathway and therefore can be developed as a therapeutic target for cervical cancer.
Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Epithelial-Mesenchymal Transition ; Female ; Gene Expression Regulation, Neoplastic ; HeLa Cells ; Humans ; Wnt Signaling Pathway ; beta Catenin/metabolism*