ABSTRACT
The effect of the complement C1q expression on total hepatic ischemia-reperfusion (I/R) injury in rats was investigated. Sixty healthy male Sprague Dawley (SD) rats weighing 180-200 g were randomly divided into 5 groups: sham-operation group (S group, n=12); group of I/R for 1 h (I/R 1 h group, n=12); group of I/R for 3 h (I/R 3 h group, n=12); group of I/R for 6 h (I/R 6 h group, n=12); group of I/R for 24 h (I/R 24 h group, n=12). The hepatic I/R model of rats was established, and liver tissues were obtained 1 h, 3 h, 6 h and 24 h after hepatic I/R, respectively. Furthermore, the tissues were stained using hematoxylin-eosin, and the liver injuries of rats were observed using a microscope. The malondialdehyde (MDA) level and superoxide dismutase (SOD) activity in liver tissue were determined. Real-time polymerase chain reaction (PCR) and Western blotting were used to detect the expression levels of C1q mRNA and protein, respectively. As compared with the S group, the histopathological changes in I/R 1 h-24 h groups were gradually aggravated with the extension of I/R time. As compared with the S group, SOD activity and MDA content in the I/R groups were reduced and increased respectively with the extension of I/R time (P<0.01). Furthermore, the C1q expression at mRNA and protein levels in the I/R groups (especially in the I/R 3 h group) was significantly higher than that in the S group (P<0.05). It is suggested that C1q expression may play a principal role in hepatic I/R injury, particularly at the early stage of perfusion.
ABSTRACT
The effect of the complement C1q expression on total hepatic ischemia-reperfusion (I/R) injury in rats was investigated. Sixty healthy male Sprague Dawley (SD) rats weighing 180-200 g were randomly divided into 5 groups: sham-operation group (S group, n=12); group of I/R for 1 h (I/R 1 h group, n=12); group of I/R for 3 h (I/R 3 h group, n=12); group of I/R for 6 h (I/R 6 h group, n=12); group of I/R for 24 h (I/R 24 h group, n=12). The hepatic I/R model of rats was established, and liver tissues were obtained 1 h, 3 h, 6 h and 24 h after hepatic I/R, respectively. Furthermore, the tissues were stained using hematoxylin-eosin, and the liver injuries of rats were observed using a microscope. The malondialdehyde (MDA) level and superoxide dismutase (SOD) activity in liver tissue were determined. Real-time polymerase chain reaction (PCR) and Western blotting were used to detect the expression levels of C1q mRNA and protein, respectively. As compared with the S group, the histopathological changes in I/R 1 h-24 h groups were gradually aggravated with the extension of I/R time. As compared with the S group, SOD activity and MDA content in the I/R groups were reduced and increased respectively with the extension of I/R time (P<0.01). Furthermore, the C1q expression at mRNA and protein levels in the I/R groups (especially in the I/R 3 h group) was significantly higher than that in the S group (P<0.05). It is suggested that C1q expression may play a principal role in hepatic I/R injury, particularly at the early stage of perfusion.
Subject(s)
Animals , Male , Rats , Blotting, Western , Complement C1q , Genetics , Metabolism , Gene Expression , Liver , Metabolism , Malondialdehyde , Metabolism , Random Allocation , Rats, Sprague-Dawley , Reperfusion Injury , Reverse Transcriptase Polymerase Chain Reaction , Superoxide Dismutase , Metabolism , Time FactorsABSTRACT
<p><b>OBJECTIVE</b>To study the pretreatment effect of adenosine on NF-kappaB nuclear activity in ischemia/reperfusion myocardium in rats.</p><p><b>METHODS</b>Eighteen healthy male S-D rats were randomly divided into three groups. Group I was the control group. The other two groups were subjected to 30 minutes of ischemia, followed by 2 hours of reperfusion. In group III, adenosine was given 40 microg.kg(-1).min(-1) 30 minutes before coronary artery occlusion. The NF-kappaB in nuclear was extracted and measured with western blot analysis. TNF-alpha levels in myocardium were measured with enzyme-linked immunosorbent assay (ELISA) system. All the data were recorded with mean +/- SEM, differences at the 95% confidence level were considered significant.</p><p><b>RESULTS</b>NF-kappaB activity in the nucleus significantly increased after ischemia/reperfusion and TNF-alpha levels changed. Adenosine significantly inhibited NF-kappaB activity in nucleus, and concomitantly decreased the level of TNF-alpha in myocardium.</p><p><b>CONCLUSIONS</b>Adenosine modulation of NF-kappaB activation may be the cellular molecular mechanism of decreasing of TNF-alpha. The cardioprotective action of adenosine may be involved in the differential modulation of NF-kappaB activation during myocardial ischemia/reperfusion.</p>