ObjectiveTo explore the protective mechanism and effect of the resveratrol for kidney injury of obstructive jaundice. MethodsThe rats were randomly divided into three groups: sham operation group receiving laparotomy without bile duct ligation (BDL), the obstructive jaundice group with BDL, and the obstructive jaundice + resveratrol group given resveratrol following BDL. The levels of total bilirubin (TBIL), direct bilirubin (DBIL), blood urea nitrogen (BUN), and creatinine (Cr) in the serum were tested. The superoxide dismutase (SOD) activity, malondialdehyde (MDA) content, glutathione (GSH) level in the renal tissues were detected. The expressions of the silent information regulator 1 (SIRT1) and nuclear factor-κB (NF-κB) proteins were tested by Western blot. The expression of SIRT1 mRNA was detected by RT-PCR and the renal cell apoptosis was examined by TUNEL staining. Results①Compared with the sham operation group, the levels of serum TBIL, DBIL, BUN and Cr were significantly higher (P < 0.05); the activity of SOD and level of GSH, and the expressions of SIRT1 mRNA and SIRT1 protein in the renal tissues were signi-ficantly lower (P < 0.05); the content of MDA, the expression of NF-κB protein, and the rate of cell apoptosis in the renal tissues were significantly higher (P < 0.05) in the obstructive jaundice group.②Compared with the obstructive jaundice group, the levels of serum TBIL, DBIL, BUN and Cr were significantly lower (P < 0.05); the activity of SOD and level of GSH, and the expressions of SIRT1 mRNA and SIRT1 protein in the renal tissues were significantly higher (P < 0.05); the content of MDA, the expression of NF-κB protein, and the rate of cell apoptosis in the renal tissues were significantly lower (P < 0.05) in the obstructive jaundice+resveratrol group. ConclusionThe resveratrol could alleviate renal damage and play a beneficial role to resist inflammation, oxidation, and apoptosis by activating the SIRT1 which probably inhibits the expression of NF-κB protein and promotes the activity of SOD in cholestatic kidney injury.
ObjectivesTo provide a reference for the evaluation procedures of genetic testing technology applicable to China by combining the existing evaluation frameworks and procedures for genetic testing techniques globally, and also put forward design suggestions for the construction of evaluation procedures in China.MethodsThe literature research method was primarily used to summarize different evaluation progress, as well as put forward design suggestions.ResultsAt present, numerous developed countries have organized genetic testing technology evaluation projects. The various evaluation frameworks developed were based on the ACCE or HTA framework. The evaluation and decision-making procedures were similar in general, including topic selection, evaluation implementation, results reporting and making recommendations. However, there still remained difficulties such as limited evidence and uncertainty in decision-making.ConclusionsTo establish the procedures of genetic testing technology applicable in China, the following specific procedures are recommended: selecting target genetic testing technology topics; analyzing necessity and feasibility of target testing technology evaluation; evaluating and reviewing the evidence; applying results and decision-making transformation; developing regular review and revision mechanisms.
Objective To compare two ways of establishing hyperlipidemia model in rats with fat emulsion.Methods Thirty male SD rats were randomly divided into three groups， which fed with normal diet （normal control group）， low concentration fat emulsion （low concentration fat emulsion group）， and high concentration fat emulsion （high concentration fat emulsion group）， respectively. All the rats were sacrificed and tested for serum total cholesterol （TC）， triglyceride （TG）， high density lipoprotein-cholesterol （HDL-C）， and low density lipoprotein-cholesterol （LDL-C）in two weeks after establishment. Results The levels of TC， TG， HDL-C， and LDL-C in the high concentration fat emulsion group were significantly higher than those in the normal control group and the low concentration fat emulsion group （P＜0.05）；the levels of TC， TG， and HDL-C in the low concentration fat emulsion group didn’t significantly differ from normal control group （P＞0.05）. Conclusions High concentration fat emulsion can be used to establish hyperlipidemia model in SD rats， low concentration fat emulsion is not suitable for establishing hyperlipidemia model in SD rats.
ObjectiveTo explore the change of expression of oxygen-regulated protein 150 (ORP150) in pancreatic injury of rats with severe acute pancreatitis. MethodsForty male Wistar rats were randomly allocated into two groups: sham operation group (SO group， n=10) and severe acute pancreatitis model group （SAP group， 3 h, 6 h， and 12 h after modeling, each time n=10）. SO group rats were only turned over the pancreas, and the SAP group rats were induced by retrogradely infusing 5% sodium taurocholate into the biliopancreatic duct. SO group rats were killed at 12 h after sham operation, and the SAP group rats were killed at 3 h, 6 h, and 12 h after modeling. Blood samples were obtained for detecting the amylase (AMY) and alanine transarninase (ALT) levels. The quantity of ascites were collected and measured. Pancreatic tissue samples were stained with hematoxylin and eosin for histopathological evaluation. Pancreatic tissue was collected to detect the expressive quantity of ORP150 mRNA by RT-PCR. ResultsThe quantity of ascites, AMY and ALT levels, and histopathological evaluation were significantly higher in SAP group than those in SO group (Plt;0.05). AMY and ALT levels, histopathological detection, and expression of ORP150 mRNA in pancreatic rats among 3 h, 6 h, and 12 h after modeling were significantly different from each other (Plt;0.05), except for ascites. The ascites were not significantly different between 3 h and 6 h after modeling (Pgt;0.05), while 12 h were significantly higher than those at 3 h and 6 h (Plt;0.05). The expression of ORP150 mRNA was low in SO group, and were rise in subgroup SAP 12 h, 6 h, and 3 h gradually. Subgroup was statistical difference (Plt;0.05). ConclusionThe expressive quantity of ORP150 mRNA is high in pancreatic tissues with SAP rats, prompting that ORP150 may play a role in pancreatic injury with SAP.
Objective Observing the expressions of inducible nitric oxide synthase （iNOS） and endothelial nitric oxide synthase （eNOS） mRNA in lung tissues of rats with acute necrotizing pancreatitis （ANP） to explore the role of NOS in ANP associated-lung injury. Methods Forty Wistar rats were assigned into ANP group (n=30) and sham-operation group (SO group, n=10). ANP model was induced by retrograde injection of 5% sodium taurocholate into the bili-pancreatic duct. Pathological changes of the lung tissue were observed under light microscope at 3 h, 6 h and 12 h after the ANP-model operation, and the expressions of iNOS mRNA and eNOS mRNA in lung tissue were assayed by RT-PCR. Results Different degrees of pathological changes of the lung tissue, such as hyperemia, edema, inflammatory cells infiltration, hemorrhage and necrosis, were found in the ANP group. The pathologic injury scores of lung tissue in ANP group were higher than that in SO group (Plt;0.05), and gradually increased with the duration extension of ANP (Plt;0.05). Compared with the SO group, the expressions of iNOS and eNOS mRNA in ANP group were all higher at 3 h, 6 h, and 12 h (Plt;0.05). Conclusions The overexpressions of iNOS and eNOS mRNA may play important roles in lung injury of ANP. This provides us a theory basis that lung injury of ANP could be relieved by inhibiting the expressions of iNOS and eNOS mRNA.
Objective To investigate the protective effect of castanospermine (CS) on renal injury induced by severe acute pancreatitis (SAP) in rats and its possible mechanism. Methods Twenty-four SPF adult male Sprague Dawley rats were randomly divided into three groups: shame operation group (SO group, n=8), SAP group (n=8), and CS group (n=8). SAP models were induced by retrograde injection of 5% sodium taurocholate (1 mL/kg) in biliopancreatic duct in the SAP group and the CS group. CS solution (200 mg/kg) was immediately administered via intraperitoneal injection after the induction of pancreatitis in the CS group. Rats in the SO group were subjected to a sham surgery that the pancreas and duodenum were flipped a number of times. All rats were sacrificed at 12 h after modeling. Blood samples were collected by inferior vena cava puncture, and serum activities of amylase (AMY), levels of blood urea nitrogen (BUN) and creatinine (Cr) were measured by using a fully automatic chemistry analyzer. The head of pancreas and renal tissues were harvested and pathological change was observed under the light microscope. Expressions of nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α), intercellular adhesion molecule-1 (ICAM-1), and Caspase-3 in renal tissues were evaluated by immunohistochemistry assay. Results ① Compared with the SO group, the damages of the pancreas and kidney tissues were significantly worse in the SAP group, and the above damages in the CS group were significantly decreased when comparing with the SAP group. ② Compared with the SO group, the serum activities of AMY, levels of BUN and Cr were significantly increased in the SAP group (P<0.05). The serum activities of AMY, levels of BUN and Cr in the CS group were significantly lower than those of the SAP group (P<0.05). ③ Compared with the SO group, the integrated optical density (IOD) of NF-κB, TNF-α, ICAM-1, and Caspase-3 in renal tissues were significantly increased in the SAP group (P<0.05), and the above indicators in kidney tissues of the CS group were significantly decreased when comparing with the SAP group (P<0.05). Conclusions CS can mitigate severe acute pancreatitis-induced renal injuries in rats, it ameliorates renal injury and improves renal function. The mechanism for the above improvements is that CS can widely inhibit the activation of NF-κB, and then downregulate the expressions of TNF-α, ICAM-1, and Caspase-3.
ObjectiveTo investigate The role of tumor necrosis factor-α (TNF-α) in pancreatitis-associated adrenal cells' apoptosis of severe acute pancreatitis (SAP). MethodsForty Wistar rats were randomly divided into sham operation group (SO group) and SAP group by random number method, the SAP group was divided into 3, 6, 12, and 24 h 4 subgroups, 8 rats in each group. SAP model was induced by retrograde injection of 5% sodium taurocholate into the bilipancreatic duct. At 3, 6, 12, and 24 h after operation, serum amylase and lipase was measured, adrenal injury was evaluated by histological examination, apoptosis of the adrenal cells was observed by TUNEL method, and expressions of TNF-α and Caspase-3 protein were detected by Western blot. ResultsThe levels of serum AMY and LIP, histopathological scores of pancreatic tissues and adrenal tissues at each time point after operation in SAP group increased significantly than SO group (P < 0.05). With the duration extension of SAP, the apoptosis index of adrenal cells in SAP group progressively heightened, and were higher than those in the SO group (P < 0.05). And the expressions of TNF-α and Caspase-3 protein in adrenal tissues of SAP group gradually increased, at 24 h this data slightly decreased, but still higher than SO group (P < 0.05). ConclusionTNF-α may be involved in the pathogenesis of adrenal injury in SAP rats by activate the protein expression of Caspase-3.