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PubMed1991

[Inhibition of hepatic DNA synthesis after partial hepatectomy in the rats with obstructive jaundice with special reference to the enhancement of hepatic protein synthesis].

We studied the liver regeneration after partial (68%) hepatectomy in rats with obstructive jaundice followed by the relief of obstruction. Rats received bile duct ligation, then 5 or 14 days later choledocho-duodenostomy was performed. Partial hepatectomy was done at various intervals after the relief of obstruction. DNA synthesis of the regenerating liver, hepatic protein synthesis and mitochondrial swelling induced by exogenous phospholipase A2 (PLA2) were determined. Hepatic DNA synthesis was significantly inhibited in obstructive jaundiced rats compared to controls. While the inhibition disappeared 5 days after the relief of obstruction in 5-day-obstructed group, it was still detectable as late as 21 days after the drainage in 14-day-obstructed group. Hepatic protein synthesis was markedly increased by obstructive jaundice, and this increase continued until 10 days after drainage in 14-day-obstructed group. Partial hepatectomy also increased the hepatic protein synthesis significantly in normal rats, but failed to show any significant changes in obstructive jaundiced rats. Any difference could not be found in PLA2-induced hepatic mitochondrial swelling between obstructive jaundiced rats and normal rats. We concluded the preceding energy-requiring responses in obstructive jaundiced liver resulted in the reduction of hepatic DNA synthesis and in the lack of additional increase of hepatic protein synthesis as the responses to a further insult of partial hepatectomy.

Animals↗
PubMed2003

Obstructive jaundice alters proliferating cell nuclear antigen expression in rat small intestine.

Translocation of bacteria and endotoxin has long been documented in obstructive jaundice, and altered intestinal barrier function is considered to be one of the important mechanisms for this phenomenon. Proliferating cell nuclear antigen (PCNA), also known as cyclin, is an auxiliary protein of DNA polymerase-delta, and the level of synthesis correlates directly with rates of cellular proliferation and DNA synthesis. This study was designed with the aim of evaluating the effect of obstructive jaundice on PCNA expression in small bowel epithelium. Male Sprague-Dawley rats were randomized to four groups. Group A (n = 10, control group) underwent a sham operation. Group B (n = 9, obstructive jaundice group for 1 week) underwent common bile duct ligation. Group C (n = 8, obstructive jaundice group for 2 weeks) underwent common bile duct ligation. Group D (n = 8, obstructive jaundice group for 2 weeks) underwent common bile duct ligation with oral glutamine intake. After periods of 7 days and 2 weeks, segments of small bowel were harvested from groups A & B and groups C & D, respectively. Nuclear immunohistochemical expression of PCNA in small bowel was evaluated. The PCNA-labeling index [(PCNA-positive cells/500 cells) x 100] was quantified. Comparisons among the four groups were performed. The PCNA-labeling index in small bowel of group B was significantly higher than that of group A (29.0% vs 21.2%, p = 0.001). After 2 weeks of common bile duct ligation, the PCNA-labeling index in small bowel of group C was significantly lower than that of group A (19.4% vs 21.2%, p = 0.045). With oral glutamine intake daily, the PCNA-labeling index in small bowel of Group D was restored and was significantly higher than that of group A (24.5% vs 21.2%, p = 0.002). Obstructive jaundice for 1 week upgraded PCNA expression in rat small intestine. PCNA expression in rat small intestine later became depressed after obstructive jaundice for 2 weeks. Oral glutamine intake daily could effectively restore the PCNA expression in small bowel of rats subjected to obstructive jaundice for 2 weeks.

Animals↗
PubMed1993

[Changes in gastric mucosal glycosidases and thiobarbituric acid reactants induced by burn stress in obstructive jaundice rats].

To elucidate the pathogenesis of acute gastric mucosal lesion (AGML), burn stress was loaded in rats with and without obstructive jaundice. The activation of gastric mucosal glycosidases (beta-N-acetyl-D-glucosaminidase (NAG), beta-glucuronidase (BG)), which were released into the cytoplasm as a results of instability of the lysosomal membrane, was studied biochemically, enzymatically and histochemically after burn stress with and without obstructive jaundice. The latent enzyme activity calculated by NAG or BG, which represented the stability of lysosomal membrane, was lowest at 2-3 hour after burn stress in both groups. In other words, the degree of activation of the glycosidases was highest at 2-3 hour after burn stress. The latent enzyme activity calculated by NAG decreased significantly (p < 0.05) at 1 hour after burn stress in obstructive jaundice group compared with the non-obstructive jaundice group. The staining of NAG before burn stress was observed in mucus neck cell and surface epithelial cell in granular shape and it was observed diffusely after burn stress, especially in obstructive jaundice group. The changes in staining of BG was similar to NAG. Before activation of glycosidases, the thiobarbituric acid reactants, which are considered products of lipid peroxidation, increased promptly at 30 min after burn stress in both groups. Ulcer index increased gradually after burn stress and the significance was found between in the obstructive jaundice group and in non-obstructive jaundice group at 3 hour after burn stress. It's concluded that obstructive jaundice accelerated the fragility of lysosomal membrane after burn stress and these change were considered to be the reasons of frequent occurrence of AGML.

Acetylglucosaminidase↗