ABSTRACT
Objective@#To probe into the mechanism and interventional effects of silybin-phospholipid complex on amiodarone-induced steatosis in mice.@*Methods@#Eight-week-old male C57BL/6 mice were divided into three groups (5 mice in each group): a control group (WT) with normal diet, a model group with amiodarone 150mg/kg/d by oral gavage (AM), and an intervention group on amiodarone 150mg/kg/d combined with silybin-phospholipid complex(AM+SILIPHOS. All mice were fed their assigned diet for one week. Then, one week later, serum alanine aminotransferase, aspartate aminotransferase, triglyceride, total cholesterol and high-density lipoprotein were detected of each group. A liver pathological change was observed by oil red O and H&E staining. Ultrastructural pathological changes of hepatocytes were observed to evaluate the intervention effect by transmission electron microscopy. RT-q PCR was used to detect the expression of peroxisome proliferator-activated receptor alpha and its regulated lipid metabolism genes CPTI, CPTII, Acot1, Acot2, ACOX, Cyp4a10 and Cyp4a14 in liver tissues. Intra-group comparison was done by paired t-test. One-way ANOVA was used for comparison between groups and semi-quantitative data were tested using Mann-Whitney U test.@*Results@#Oil Red O and H&E staining results of liver tissue in the intervention group showed that intrahepatic steatosis was significantly reduced when compared to model group. Transmission electron microscopy showed that the model group had pyknotic nuclei, mitochondrial swelling, structural damage, and lysosomal degradation whereas the intervention group had hepatic nucleus without pyknosis, reduced mitochondrial swelling and slight structural damage than that of model group. RT-q PCR results showed that the expression of peroxisome proliferator-activated receptor alpha, CPTI, CPTII, Acot1, Acot2, ACOX, Cyp4a10 and Cyp4a14 were increased in the model group but the expression of CPTI, Cyp4a14, Acot1 and peroxisome proliferator-activated receptor alpha were decreased in the intervention group (P < 0.05).@*Conclusion@#Silybin-phospholipid complex can alleviate amiodarone-induced steatosis, and its mechanism may play a role in protecting mitochondrial function and regulating fatty acid metabolism. Thus, silybin-phospholipid complex has potential intervention effect on amiodarone-induced fatty liver.
ABSTRACT
Objective To investigate the relationship between Helicobacter pylori(H. pylori)infection and gastric metaplasia in the duodenal bulb and to pursue whether they play critical roles in pathogenesis of duodenitis and ulcer.Methods Eighty-two archive paraffin blocks of duodenal biopsy were obtained. All sections were stained with H-E, AB/PAS and Giemsa stains for histology, gastric metaplasia and H. pyloriassessment. There were 10 patients with normal duodenum, 47 with duodenitis and 25 with ulcer confirmed by endoscopy. Results There was a discrepancy in diagosis of the normal duodenal bulb mucosa between endoscopy and histopathology. Mild to moderate infiltration of inflammatory cell without gastric metaplasia were detected in 60% of cases with the normal duodenal bulb mucosa judged by endoscopy. Gastric metaplasia in duodenal bulb was the major phenomena in the patients with duodenitis and ulcer (37/82, 45%). H. pyloriinfection in the duodenal bulb always appeared in areas of gastric metaplasia. H. pyloriwas identified in 28 out of 37 (76%) cases in the gastric metaplasia mucosa. The prevalence of gastric metaplasia in the duodenal bulb between the patients with ulcer (72%) and duodenitis (40%) was significantly different (P=0.0078). The frequency of H. pyloricolonization was higher in the patients with duodenal ulcer (89%) than the patients with duodenitis (63%), but did not reach statistical significance(P=0.062). H. pyloriinfection was also higher in the ulcer patients with active, healed or scar stage, being 9/10, 5/6 and 2/2, respectively. Conclusions There is a difference in the frequency of H. pyloricolonization in the gastric metaplasia mucosa in the patients with ulcer and duodenitis, which suggests that infection with H. pylorimay play an important role in ulcer recurrence.