scholarly journals Cardioprotective effect of 5-lipoxygenase gene (ALOX5) silencing in ischemia-reperfusion.

2009 ◽  
Vol 56 (4) ◽  
Author(s):  
Oleksandr O Lisovyy ◽  
Victor E Dosenko ◽  
Vasyl S Nagibin ◽  
Lesya V Tumanovska ◽  
Maria O Korol ◽  
...  
Keyword(s):  
Rat Model ◽  
Cardiac Tissue ◽  
Ischemia Reperfusion ◽  
Myocardial Cell ◽  
Heart Cells ◽  
Gene Encoding ◽  
Heart Ischemia ◽  
Fold Reduction ◽  
Lipoxygenase Gene

It is well known that 5-lipoxygenase derivates of arachidonic acid play an important pathogenic role during myocardial infarction. Therefore, the gene encoding arachidonate 5-lipoxygenase (ALOX5) appears to be an attractive target for RNA interference (RNAi) application. In experiments on cultivated cardiomyocytes with anoxia-reoxygenation (AR) and in vivo using rat model of heart ischemia-reperfusion (IR) we determined influence of ALOX5 silencing on myocardial cell death. ALOX5 silencing was quantified using real-time PCR, semi-quantitative PCR, and evaluation of LTC(4) concentration in cardiac tissue. A 4.7-fold decrease of ALOX5 expression (P < 0.05) was observed in isolated cardiomyocytes together with a reduced number of necrotic cardiomyocytes (P < 0.05), increased number live (P < 0.05) and unchanged number of apoptotic cells during AR of cardiomyocytes. Downregulation of ALOX5 expression in myocardial tissue by 19% (P < 0.05) resulted in a 3.8-fold reduction of infarct size in an open chest rat model of heart IR (P < 0.05). Thus, RNAi targeting of ALOX5 protects heart cells against IR injury both in culture and in vivo.

scholarly journals Efficacy Evaluation and Tracking of Bone Marrow Stromal Stem Cells in a Rat Model of Renal Ischemia-Reperfusion Injury

2019 ◽  
Vol 2019 ◽  
pp. 1-11
Author(s):  
Ling-Jie Wang ◽  
Chang-Ping Yan ◽  
Dan Chen ◽  
Ting Xu ◽  
Sheng He ◽  
...  
Keyword(s):  
Renal Artery ◽  
Rat Model ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Therapeutic Effects ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Renal Tubular ◽  
Stromal Stem Cells

Objectives. The aim of this study was to evaluate the effects of bone marrow stromal stem cells (BMSCs) on renal ischemia-reperfusion injury (RIRI) and dynamically monitor engrafted BMSCs in vivo for the early prediction of their therapeutic effects in a rat model. Methods. A rat model of RIRI was prepared by clamping the left renal artery for 45 min. One week after renal artery clamping, 2 × 106 superparamagnetic iron oxide- (SPIO-) labeled BMSCs were injected into the renal artery. Next, MR imaging of the kidneys was performed on days 1, 7, 14, and 21 after cell transplantation. On day 21, after transplantation, serum creatinine (Scr) and urea nitrogen (BUN) levels were assessed, and HE staining and TUNEL assay were also performed. Results. The body weight growth rates in the SPIO-BMSC group were significantly higher than those in the PBS group (P < 0.05), and the Scr and BUN levels were also significantly lower than those in the PBS group (P < 0.05). HE staining showed that the degree of degeneration and vacuole-like changes in the renal tubular epithelial cells in the SPIO-BMSC group was significantly better than that observed in the PBS group. The TUNEL assay showed that the number of apoptotic renal tubular epithelial cells in the SPIO-BMSC group was significantly lower than that in the PBS group. The T2 value of the renal lesion was the highest on day 1 after cell transplantation, and it gradually decreased with time in both the PBS and SPIO-BMSC groups but was always the lowest in the SPIO-BMSC group. Conclusion. SPIO-labeled BMSC transplantation can significantly promote the recovery of RIRI and noninvasive dynamic monitoring of engrafted cells and can also be performed simultaneously with MRI in vivo for the early prediction of therapeutic effects.

scholarly journals New insights into application of cardiac monophasic action potential

2010 ◽  
pp. 645-650
Author(s):  
S-G Yang ◽  
O Kittnar
Keyword(s):  
Action Potential ◽  
Time Course ◽  
Cardiac Tissue ◽  
Femoral Vein ◽  
Myocardial Cell ◽  
Monophasic Action Potential ◽  
Seldinger Technique ◽  
Accurate Information ◽  
Length Changes

Monophasic action potential (MAP) recording plays an important role in a more direct view of human myocardial electrophysiology under both physiological and pathological conditions. The procedure of MAP measuring can be simply performed using the Seldinger technique, when MAP catheter is inserted through femoral vein into the right ventricle or through femoral artery to the left ventricle. The MAP method represents a very useful tool for electrophysiological research in cardiology. Its crucial importance is based upon the fact that it enables the study of the action potential (AP) of myocardial cell in vivo and, therefore, the study of the dynamic relation of this potential with all the organism variables. This can be particularly helpful in the case of arrhythmias. There are no doubts that physiological MAP recording accuracy is almost the same as transmembrane AP as was recently confirmed by anisotropic bidomain model of the cardiac tissue. MAP recording devices provide precise information not only on the local activation time but also on the entire local repolarization time course. Although the MAP does not reflect the absolute amplitude or upstroke velocity of transmembrane APs, it delivers highly accurate information on AP duration and configuration, including early afterdepolarizations as well as relative changes in transmembrane diastolic and systolic potential changes. Based on available data, the MAP probably reflects the transmembrane voltage of cells within a few millimeters of the exploring electrode. Thus MAP recordings offer the opportunity to study a variety of electrophysiological phenomena in the in situ heart (including effects of cycle length changes and antiarrhythmic drugs on AP duration).

scholarly journals QKI 6 ameliorates CIRI through promoting synthesis of triglyceride in neuron and inhibiting neuronal apoptosis associated with SIRT1-PPARγ-PGC-1α axis

2020 ◽  
Author(s):  
Rui Liu ◽  
Hongzeng Li ◽  
Jingyuan Deng ◽  
Qunqiang Wu ◽  
Chunhua Liao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Rat Model ◽  
Neuronal Apoptosis ◽  
Rna Binding ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Artery Occlusion ◽  
Post Transcriptional Regulation

AbstractThe stroke induced by ischemia of brain remains high incidence and death rate. The study wanted to confirm the effects of QKI 6 on the protection role in neurons of rat model of cerebral ischemia/reperfusion injury (CIRI). The rat model with CIRI induced by MCAO (middle cerebral artery occlusion) was well established and rat neurons were isolated to characterize the effects of QKI 6 mediated by SIRT1 on synthesis of triglyceride in neuron and neuronal apoptosis via activation of SIRT1-PPARγ-PGC-1α signaling pathway. The expression levels of SIRT1 or QKI 6, and acetylation level of QKI 6 was decreased in neurons of rat model with CIRI. QKI 6 deacetylated and mediated by SIRT1 that contributed to suppressing the progression of neuronal apoptosis in rat through promoting synthesis of triglyceride in vivo and in vitro via SIRT1-PPARγ-PGC-1α signaling pathway, then inhibiting CIRI. In conclusion, our results demonstrated SIRT1 deacetylates QKI 6, the RNA-binding protein, that affects significantly the synthesis of triglyceride in neurons of CIRI rat model. Moreover, it activated transcription factor PGC-1α through post-transcriptional regulation of the expression of PPARγ, and further enhanced synthesis of triglyceride, thereby restrained the progression of neural apoptosis and CIRI.

Blood pressure and cardiac tissue responses to prostacyclin (PGI2) in various species

1982 ◽  
Vol 60 (2) ◽  
pp. 134-139 ◽  
Author(s):  
G. A. Collins ◽  
B. A. MacLeod ◽  
M. J. A. Walker
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Tissue ◽  
Isolated Heart ◽  
Heart Tissue ◽  
Neonatal Rat ◽  
Heart Cells ◽  
Camp Content ◽  
Rat Atria

The effect of prostacyclin (PGI2) on blood pressure and heart rate (in vivo) and on isolated heart tissue has been investigated in different species. Isolated cardiac tissue had limited resposes to PGI2 tested at 10−13 to 10−5 M. Cultured neonatal rat heart cells did not respond to PGI2, neither did intact rat hearts or rabbit cardiac tissue. Guinea pig and rat atria showed limited dose-dependent responses to PGI2 at concentrations greater than 10−7 M. In rat atria, 10−5 M PGI2 produced a limited elevation of tissue cAMP content. When given by intravenous injection or infusion, PGI2 produced hypotension in anaesthetized primates (three species), rat, rabbit, pig, and dog. As a vasodepressor in all species, PGI2 (on a weight basis) was more active than prostaglandins of the B or E type and, in most species tested, it was approximately five times more active than PGE2. Heart responses in intact animals were often paradoxical in that decreases in heart rate often accompanied blood pressure falls.

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