Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.24.3 (collagenase)
 18,340 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The release of cytokine by Kupffer cells during hypoxia/reoxygenation was studied in vitro in male Wistar rats with obstructive jaundice to investigate the kinetics of interleukin-8 (IL-8) release by Kupffer cells during hypoxia/reoxygenation, and to study the influence of endotoxin during the reoxygenation period. The rats were divided into two groups: one that underwent bile duct ligation (group OJ), and one that underwent a sham operation (group C). Kupffer cells were isolated by collagenase digestion and centrifugal elutriation. The cells were first subjected to hypoxia as 95% nitrogen, after which they were given reoxygenation as 95% oxygen. In addition, they were stimulated with lipopolysaccharide (LPS) 0, 1, and 10 ng/ml. In both groups, the levels of IL-8 became increased during the period of hypoxia/reoxygenation, and reoxygenation after hypoxia further intensified IL-8 production. During the period of hypoxia, the IL-8 levels in group OJ were significantly increased compared with those in group C. With the LPS challenge, there was no significant difference in IL-8 levels in either group. In conclusion, obstructive jaundice induces the activation of Kupffer cells, resulting in increased IL-8 production during hypoxia/reoxygenation.
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PMID:Cytokine release during hypoxia reoxygenation by Kupffer cells in rats with obstructive jaundice. 1048 47

The modulatory role of bcl-2 gene in hepatocellular apoptosis of rats with glycochenodeoxycholate (GCDC)-induced obstructive jaundice was investigated. The hepatocytes in normal rats and those with bile duct-ligation for 7 days, 14 days and 21 days were isolated and obtained by in situ collagenase perfusion and primary culture. The expression of bcl-2 mRNA in the hepatocytes was detected by RT-PCR. Primary culture was performed on the hepatocytes from normal rats and those with bile duct-ligation for 14 days. 100 mumol/L GCDC was added to the hepatocytes for incubation for 24 h. The hepatocellular apoptotic ratio was measured by using FCM and hepatocellular apoptosis detected in situ by using TUNEL technique. Results showed that the expression of bcl-2 mRNA was not detectable in the hepatocytes of normal rats by RT-PCR technique, while detectable in the hepatocytes of those with bile duct ligation (BDL) for 7, 14 and 21 days. Hepatocellular apoptosis in the BDL group was obviously decreased as compared with normal control group after addition of 100 mumol/L GCDC to the cells for 24 h. It was concluded that the hepatocytes in the BDL rats expressed bcl-2. During obstructive jaundice, expression of bcl-2 from the hepatocytes can inhibit the bile salt-induced hepatocellular apoptosis.
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PMID:The bcl-2 mRNA expression in GCDC-induced obstructive jaundice in rats and its implication in hepatocellular apoptosis. 1265 78

The regulating mechanism in hepatic injury caused by obstructive jaundice (OJ) was examined in this study. Rat hepatocytes were harvested by in situ collagenase perfusion and subjected to primary culture. The heptocytes were pre-treated with various concentrations of protein kinase C (PKC) agonist PMA and its inhibitor chelerythrine and cultured for 20 min. After the treatment, 50 micromol/L glycochenodeoxycholate (GCDC) was added and the cells were cultured for an additional 24 h. Cells were then detected by flow cytometry (FCM) and TUNEL. After hepatocytes were treated with different concentrations of fructose and 100 microM GCDC, the cells were examined by FCM and TUNEL. Experimental obstructive jaundice (BDL) was induced by double ligation of the bile duct. After BDL, the rats were fed with or without fructos and sacrificed 3, 7, 14 and 21 days after the ligation. The apoptotic status was observed in liver of all rats with TUNEL and PKC protein in liver of OJ was studied by immunohistochemical method. Our results showed that PMA increased GCDC-induced apoptosis and chelerythrine decreased GCDC-induced apoptosis in a concentration-dependent manner. After the treatment with fructose of different concentrations, 100 microM GCDC decreased the apoptotic rate and the apoptotic rate decreased with the increase of fructose concentration. The apoptotic rate of liver was related to the time of OJ. Without the treatment of fructose, PKC and apoptosis index (AI) were highest 14 days after the bile duct ligation. With the treatment of fructose, apoptosis index (AI) and PKC were decreased from the 14th day after the bile duct ligation. It is concluded that PKC is involved in the regulation of apoptosis in the liver cells with OJ and plays important roles in the development and progression of liver injury caused by OJ. Fructose can protect hepatocytes in the bile salt-induced apoptosis by regulating PKC.
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PMID:Roles of protein kinase C and fructose in hepatic injury caused by obstructive jaundice. 1619 96