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Meng G.-X.,Tianjin Hepatobiliary Research Institute | Yuan Q.,Tianjin Hepatobiliary Research Institute | Wei L.-P.,Tianjin Union Medicine Center | Meng H.,Capital Medical University | Wang Y.-J.,Tianjin Hepatobiliary Research Institute
Experimental and Therapeutic Medicine | Year: 2016

Hepatic ischemia and reperfusion (I/R) injury plays an active role in hepatic resection and transplantation. While the effects of protein kinase C (PKC)-βII activation and the role of PKC-β inhibitors are well understood in myocardial I/R in diabetes, they remain unclear in liver I/R. The aim of this study was to explore the effect of PKC-β inhibition and the potential mechanism by which PKC-β inhibitor treatment protects against hepatic I/R injury in diabetic rats. Diabetic rats were established and randomized into two groups. These were an untreated group (n=10), which did not receive any treatment, and a treatment group (n=10), orally treated with ruboxistaurin at a dose of 5 mg/kg/day for 2 weeks. The rats from the two groups were subjected to hepatic I/R. Aspartate transaminase (AST) and lactate dehydrogenase (LDH) levels were measured by enzymatic methods at 1, 3 and 5 h after I/R. Tumor necrosis factor-α (TNF-α) and intercellular adhesion molecule 1 (ICAM-1) were examined by enzyme-linked immunosorbent assay at the same time-points. Nuclear factor-κB (NF-κB) p65 expression was analyzed by immunofluorescence and western blotting. Apoptosis of hepatic cells was examined by the western blot analysis of caspase 3 expression and by DNA ladder analysis. Pathological changes were examined using light and electron microscopy. Serum AST and LDH levels in the PKC-β inhibitor treatment group were diminished compared with those in the untreated group (P<0.01). Serum TNF-α and ICAM-1 (P<0.01) levels were also decreased at different time-points in the PKC-β inhibitor treatment group. The relative expression of NF-κB p65 and caspase 3 in the hepatic tissue was weakened in the PKC-β inhibitor treatment group compared with that in the untreated group (P<0.01). Pathological changes in hepatic tissue were attenuated by the PKC-β inhibitor. In conclusion, PKC-β inhibitor treatment protected against liver I/R injury in diabetic rats. The mechanisms probably involved the attenuation of microvascular injury, reduced transport of injury-associated factors and diminishment of the activation of NF-κB p65. © 2016, Spandidos Publications. All rights reserved. Source


Meng G.,Tianjin Hepatobiliary Research Institute | Xing Q.,Tianjin Hepatobiliary Research Institute | Yuan Q.,Tianjin Hepatobiliary Research Institute | Du Z.,Tianjin Hepatobiliary Research Institute | And 2 more authors.
Chinese Journal of Cancer Research | Year: 2014

Objective: To compare internal with external drainage of the pancreatic duct during pancreaticoduodenectomy with regard to the incidence of postoperative pancreatic fistula (POPF) and other complications. Methods: We retrospectively analyzed 316 patients who underwent pancreaticoduodenectomy with a placed drainage tube (external, n=128; internal, n=188) in the pancreatic duct from 1 January 1999 to 31 December 2011 in Tianjin Third Central Hospital of China. The incidence of POPF and some other complications were compared. Results: There was no difference in the incidence rates of POPF between those given an internal or external drainage tube (P=0.788), but POPF was more severe in the former (P=0.014). Intraperitoneal bleeding rate was also higher in the patients with internal drainage (P=0.040), but operative time and postoperative hospitalization were longer in those with external drainage (P=0.002 and P=0.007, respectively). There was no difference between the groups with regard to the incidence rates of gastrointestinal bleeding, delayed gastric emptying, pulmonary infection, or incision infection and in-hospital mortality. Conclusions: External drainage of the pancreatic duct during pancreaticoduodenectomy can decrease the severity of POPF, but operative time and postoperative hospitalization will be extended. © Chinese Journal of Cancer Research. All rights reserved. Source

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