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ABSTRACT: To investigate the effect of Chai Qin Cheng Qi decoction (CQCQD) on serum cholecystokinin-8 (CCK-8) and calcium overload of pancreatic acinar cells in acute pancreatitis (AP) mice.
Twenty four mice were randomly divided into control group, AP group, CQCQD group and siRNA group, each comprising 6 mice. AP mouse model was induced by intraperitoneal injection of 8% L-arginine in a dose of 4 g/kg. The AP mice in the CQCQD group were fed with 0.4 mL/100 g of Chai Qin Cheng Qi solution once every two hours. The AP mice in the siRNA group were injected intraperitoneally with CCK-siRNA in a dose of 0.88 mg/kg. The changes of serum CCK-8 and calcium concentrations in the pancreatic acinar cells and pancreatic pathology were observed 6 hours after the interventions.
The serum CCK-8 [(3764.3 +/- 369.2) ng/mL], calcium fluorescence intensity (34.8 +/- 27.1) of pancreatic acinar cells and pancreas pathology scores (6.2 +/- 1.1) of the AP mice were significantly greater (P < 0.05) than those in the control group [(1253.5 +/- 39.5) ng/mL, 5.2 +/- 2.3, 2.8 +/- 0.4], CQCQD group [(1230.5 +/- 46.1) ng/mL, 9.6 +/- 1.6, 3.8 +/- 0.8, 4.1 +/- 0.5] and siRNA group[(1702.3 +/- 598.3) ng/mL, 7.6 +/- 2.0]. Serum CCK-8 was positively correlated with intracellular calcium concentrations (r = 0.793, P = 0.021) in pancreatic acinar cells and pancreas pathology scores (r = 0.847, P = 0.000).
Acute pancreatitis in mice induced by L-arginine is associated with calcium overload in pancreatic acinar cells induced by increased serum CCK-8. CQCQD can reduce serum levels of CCK-8, alleviate calcium overload in pancreatic acinar cells, and reduce pancreas pathological changes in AP mice.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 09/2011; 42(5):704-6.
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ABSTRACT: To investigate clinical characteristics of fulminant pancreatitis (FP) died at early and late stage, analyze the difference in death causes of FP at these two stage.
Ninety-two (92) patients with FP were admitted in our center from January 2000 to June 2010, and 55 patients of them died of FP. These dead FP patients were divided into two groups according to the death time: within 7 d (early death group) or after 7 d (late death group). The 24 h Acute Physiology and Chronic Heath Evaluation II (APACHE II) score, the occurrence of complications were compared between these two groups.
The mortality of FP was 59.8% (55/92), in which 20.6% (19 cases) died within 3 d and 29.3% (27 cases) died after 14 d. Compared with the late death group, the early death group showed higher 24 h APACHE II score and serum triglyceride level (P < 0.05), and also had higher occurring time of renal failure, shock, hepatic failure, encephalopathy, gastrointestinal hemorrhage and infection (P < 0.05). However, the incidences of encephalopathy, gastrointestinal hemorrhage and pancreatic necrosis infection in the late death group were higher than those in the early group (P < 0.05). In addition, the major pathogenesis of infection was Gram-negative bacterium.
The most important and common cause of death for the patients with FP is multiple organ dysfunction syndrome, which usually was the consequence of systemic inflammation response syndrome in the early stage, and the severe infection in the later stage, respectively.
Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition 09/2011; 42(5):686-90.
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