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Objective:To explore the association of miRNA-146a (miR-146a), miRNA-196a2 (miR-196a2), and miRNA-499 (miR-499) single nucleotide polymorphisms with genetic susceptibility in hepatocellular carcinoma.Methods:A case-control study was designed. A total of 175 patients (hepatocellular carcinoma group) in Affiliated Hospital of Yangzhou University from April 2015 to March 2019 and 302 healthy people undergoing physical examination during the same period (the control group) were selected. The genotype distribution of miR-146a, miR-196a2 and miR-499 in the peripheral blood of the two groups were detected by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Logistic regression model was used to analyze the association of 3 genotypes of miRNA, genotypes of hepatitis virus infectors with genetic susceptibility in hepatocellular carcinoma. The relationship between miR-146a gene polymorphism and demography factor as well as the clinical characteristics was also analyzed by using Spearman correlation analysis.Results:In hepatocellular carcinoma group, miR-146a single nucleotide polymorphism of CC, CG, GG site genotypes had 52 (29.7%) cases, 86 (49.1%) cases, 37 (21.1%) cases, respectively; in the control group, the corresponding genotypes had 137 (45.4%) cases, 135 (44.7%) cases and 30 (9.9%) cases, respectively, and the difference in genotype distribution of both groups was statistically significant ( χ2 = 17.23, P < 0.05). There were no statistical differences in genotype distribution of miR-196a2 and miR-499 ( χ2 = 0.51, P = 0.776; χ2 = 0.05, P = 0.976). Single factor logistic regression analysis showed that in the co-dominant model of miR-146a genotype, genotypes of CG ( OR = 1.96, 95% CI 1.13-3.41, P = 0.017) and GG ( OR = 3.30, 95% CI 1.85-5.89, P<0.01) had elevated risk of hepatocellular carcinoma compared with CC genotype. In the dominant model, the risk of hepatocellular carcinoma in CG+GG genotypes was increased compared with that in CC genotype ( OR=1.97, 95% CI 1.33-2.93, P = 0.001); in the recessive model, the risk of hepatocellular carcinoma in GG genotype was increased compared with that in CG+ GG genotype ( OR=2.43, 95% CI 1.44-4.11, P = 0.001). Single factor logistic regression analysis showed that there was no significant difference in the risk of hepatocellular carcinoma in the co-dominant, dominant and recessive models between miR-196a2 and miR-499 genotypes (all P > 0.05). For hepatocellular carcinoma patients with positive hepatitis B virus (HBV), CG genotype had a 2.02-fold (95% CI 1.06-5.07) risk of hepatocellular carcinoma compared with CC genotype, and GG genotype had a 3.12-fold (95% CI 1.66-10.07) risk of hepatocellular carcinoma compared with CC genotype; CG+GG genotype had a 1.91-fold (95% CI 1.85-3.38) compared with CC genotype, GG genotype had a 1.54-fold (95% CI 1.15-6.08) compared with CG+GG genotype. The increasing risk of hepatocellular carcinoma by miR-146a gene polymorphisms was not found in hepatocellular carcinoma patients with hepatitis C virus (HCV) infection or without HBV and HCV infection. Spearman correlation analysis showed that miR-146a gene polymorphisms was not related with age, gender, smoking, drinking, family history of cancer, alanine transaminase and aspartate aminotransferase (all P>0.05). Conclusions:GG and CG genotypes of miR-146a increase the risk of genetic susceptibility in hepatocellular carcinoma, especially for patients with HBV infection. miR-196a2 and miR-499 single nucleotide polymorphisms don't increase the risk of hepatocellular carcinoma.
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Objective To research the effect and autophagy in hepatic ischemia-reperfusion injury based on relevant indicators of the specimens of rat liver which ischemia reperfusion model by salidroside pretreatment. Methods A total of 90 male SD rats were randomly divided into the sham group, the model group, the low, medium and high dose group, 18 rats in each group. The low, medium and high dose group rats were treated with 7.5, 15, 30 mg/kg salidroside solution by gavage, and the sham group and model group and model group were filled with saline in the same volume,one time per day. After 7 days, all the rats were set up with the model of IR except the rats in sham groups. The AST and ALT of serum, contrast between groups liver tissue by Optical microscope with HE dyeing at 4, 8, 16 h after reperfusion. Western Blot was used to detect the expression of protein of LC3 and Beclin-1. The number and morphology of autophagy in each group of liver cells were observed by electron microscopy. Results After reperfusion 4, 8, 16 h, the level of ALT (662.36 ± 5.82 U/L vs. 983.67 ± 8.96 U/L, 436.49 ± 12.93 U/L vs. 1536 ± 10.77 U/L, 168.61 ± 8.34 U/L vs. 280.42 ± 17.37 U/L) of the high dose group weresignificantly lower than the model group, and the AST (513.29 ± 11.74 U/L vs. 656.38 ± 7.67 U/L, 276.29 ± 9.21 U/L vs. 930.19 ± 15.62 U/L, 97.83 ± 4.29 U/L vs. 211.23 ± 7.87 U/L) of the high dose group were significantly lower than the model group. After reperfusion 8, 16 h, the expression of LC3-Ⅱ (1.21 ± 0.16 vs. 1.91 ± 0.12, 2.00 ± 0.14 vs. 1.09 ± 0.11) in the high dose group were significantly lower than the model group, and the results were same to Beclin1 (3.53 ± 0.19 vs. 7.15 ± 0.14, 2.65 ± 0.27 vs. 7.60 ± 0.21) (P<0.05). After reperfusion 8 h, the number of autophagosome (3.24 ± 0.62 vs.7.84 ± 0.45) in the high dose group were significantly lower than the model group (P<0.05). Conclusions The hepatic ischemia-reperfusion injury was serious, and inhibiting autophagy was one of possible mechanisms to protect liver cells by salidroside.
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Objective To explore the role of salidroside in HIRI and its related mechanism. MethodsA total of 90 male SD rats were randomly divided into the sham group, the model group, the low, medium and high dose group, 18 rats in each group. The low, medium and high dose group rats were injected with 7.5, 15, 30 mg/kg salidroside solution, and the sham group and model group were injected with saline in the same volume, one time per day. After 7 days, all the rats were set up with the model of IR except the rats in Sham groups. The AST and ALT of serum, contrast between groups liver tissue by Optical microscope with HE dyeing at 4, 8, 16 h after reperfusion. Western Blot was used to detect the expression of protein of MAPK, JNK, ERK and NF-κB.ResultsFour, 8, 16 h after reperfusion, the level of ALT (540.67 ± 15.91 U/L vs.697.67 ± 5.98 U/L, 307.50 ± 12.97 U/L vs.962.50 ± 17.63 U/L, 103.33 ± 3.95 U/L vs.198.17 ± 9.73 U/L) and AST (651.17 ± 7.39 U/L vs.944.67 ± 11.38 U/L, 415.50 ± 10.97 U/L vs.1561.83 ± 15.76 U/L, 168.33 ± 5.81 U/L vs. 280.33 ± 12.35 U/L) in the high dose group were significantly lower than those in the model group. Eight and 16 hours after reperfusion, the expression of MAPK (1.28 ± 0.19 vs. 2.10 ± 0.12, 1.64 ± 0.14 vs.1.89 ± 0.14), JNK (1.80 ± 0.10 vs. 2.42 ± 0.11, 0.84 ± 0.17 vs. 3.32 ± 0.19), ERK (2.43 ± 0.10 vs.5.95 ± 0.09, 2.07 ± 0.13 vs. 6.61 ± 0.14), NF-κB (2.32 ± 0.16 vs. 3.08 ± 0.10, 2.11 ± 0.13 vs. 2.74 ± 0.17) in the high dose group were significantly lower than the model group (P<0.05).Conclusions The salidroside could reduce the liver ischemia- reperfusion injury, and its mechanisms may rugulate the MAPK/NF-κB signaling pathways.
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Objective To establish a human HepG2 cell growth model under the low oxygen environment induced by cobalt chloride in order to observe the impacts of human HepG2 cell proliferation,cellular cycles and apoptosis,namely cellular growth conditions,under the low oxygen environment induced by cobalt chloride with different concentrations and to study the HepG2 cell growth mechanism under the low oxygen environment induced by cobalt chloride.Methods The human HepG2 cells in the logarithmic phase were randomized grouping as control group and CoCl2 experimental group with different concentrations (50 μm/L,100 μm/L,150 μm/L and 200 μm/L).① HepG2 cell proliferation was tested by MTT assay to calculate cell's suppression rate and draw HepG2 cell growth inhibition curves.② The move ability of HepG2 cells was observed by scratch test.③ The cellular apoptosis and periodic changes were detected using the flow cytometer Annexin-V FITC/PI double-staining and PI single staining methods.④HepG2 cell's Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) and Bcl-2 protein expression were detected by Western Blot.Results ① The test results obtained via MTT assay showed that CoCl2 suppressed the human HepG2 cell proliferation within a certain amount of time and concentration and presented a time-dose dependent relation.② Scratch damage trial suggested that the cobalt chloride suppressed the HepG2 cell migration and wound repair capacity and presented a concentration dependent relation.③ Flow cytometer' s test results revealed that the apoptosis rates (％) in control group and experimental group with different concentrations (50 μm/L,100 μm/L,150 μm/L and 200 μm/L) were 3.42,7.74,13.07,20.56,28.53 and 44.45 (P ＜0.05),respectively.The apoptosis rate of the experimental group was significantly increased compared with the control group,as well as showing a concentration dependency.The results of cellular cycles revealed that the cobalt chloride significantly suppressed the HepG2 cell's periodic changes along with increases of concentration,as well as blocked the cell cycle staying in phase G1,thereby suppressing cell proliferation.④Western Blot test:Compared with the control group,the Bcl-2 protein expression was significantly decreased in the experimental group after treatment of cobalt chloride with different concentrations.Conclusion Within a certain range,CoC12-indiuced low oxygen environment can suppress the human HepG2 cell proliferation and healing migration capacity,induce apoptosis and present a time-dose dependent relation.The mechanism is likely associated with decreases of Bcl-2 protein expression.
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Ischemia-reperfusion injury (IR) refers to the ischemic tissues or organs to regain perfusion on tissue and organ damage.The reactive oxygen species(ROS)generated by the mitochondrial and the change of the mitochondrial permeability can be induced mitophagy.And dysfunction of the mitophagy is closely related to the body a variety of disease.This article aims to introduce the research of progress about mitophagy in recent years,especially the role it play in the ischemia-reperfusion injury.
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Objective To explore the protective effect of astilbin in hepatic ischemia-reperfusion injury (HIRI).Methods SD rats were divided into Sham group (control group),HIRI group (ischemia-reperfusion group),astilbe (low dose group,middle dose group,high dose group),and estabilished the model of rat HIRI.After liver were reperfused with blood (in 4 h,8 h,16 h),collecting the specimens of blood and liver tissues.Detection of serum alanine aminotransferase (ALT),aspertate aminotransferase (AST);Then observed the changes of liver cell microstructure;Western blot analysised the expression of HMGB1,TLR4,NF-kB,TNF-α in liver tissue.Results The serum ALT levels of Sham group in 4 h,8 h,16 h were (58.11 ±4.81) U/L,(57.12 ± 5.33) U/L,(57.63 ±4.54) U/L,the serum ALT levels of HIRI group in 4 h,8 h,16 h were (540.38 ± 21.41) U/L,(831.21 ± 20.11) U/L,(191.95 ± 15.35) U/L.Compared with Sham group,the serum ALT levels of HIRI group were significantly increased(P ＜ 0.01).Compared with HIRI group,The serum ALT levels of three dose groups in 4 h,8 h,16 h were significantly declined,including high dose group lower the most obvious (The serum ALT levels of high dose group in 4 h,8 h,16 h were (223.75 ± 10.53) U/L,(412.14 ±23.59) U/L,(205.25 ± 15.48) U/L (P ＜0.01).The results of light microscope indicated that drug groups significantly reduce the liver cell damage.The results of Western blot displayed that High dose group of HMGB1,TLR4 protein expression in 4 h,8 h,16 h drop significantly than HIRI group(P ＜0.05).High dose group of NFkB,TNF-α protein expression in postoperative 8 h,16 h decrease significantly than HIRI group (P ＜ 0.05),but in postoperative 8 h,there was no statistically significant difference compared with group HIRI (P＞0.05).Conclusion Astilbe pretreatment can reduce HIRI and its mechanism may be associated with downregulating the axis of HMGB1/TLR4/NF-kB/TNF-α,proceed to the next inhibiting the inflammatory response.
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Surgical resection of liver diseases such as liver cancer,traumatic hepatic rupture,it was often faced with ischemia-reperfusion injury of the residual liver,which significantly increased the risk of surgical treatment and impact the postoperative recovery of patients.Autophagy was a way of programmed cell death after hepatic ischemia reperfusion.When researching hepatic ischemia-reperfusion injury simulated by animal experiments,it ofen detected the level change of autophagy marker molecular LC3-Ⅱ representing the activity of cell autophagy.Now the authors write the research progress of LC3-Ⅱ in hepatic ischemia-reperfusion injury.
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Postsurgical gastroparesis syndrome (PGS) is a functional disease,characterized by nauseating,vomiting,and gastric atony without of mechanical gastric outlet obstruction,and is ofen caused by operation at the abdomen,especially gastric and pancreatic operation.In recent years,the incidence rate of PGS presents ascendant tendency,and more and more doctor attach importance to PGS.A better knowledge of the etiology,pathogenesis,clinical manifestation,diagnosis and treatment of PGS can help decrease the incidence rate of PGS and improve the cure rate of PGS.Thus,the authors write this review about these aspects of PGS.
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Colorectal cancer (CRC),a common gastrointestinal malignancy,has been a threat to the health and life of human being.CRC is concealed with no obvious clinical symptoms or signs.Therefore,most of the patients have been in the middle and advanced stage when CRC has been diagnosed.Thus it seriously affects the prognosis and life.Accordingly,early diagnosis is crucial in earlier treating,prognosis improving and survivability increasing.In recent years,the morbidity and mortality of CRC are still on the rise.Hence,how to improve the early diagnosis rate has been a research focus in clinical study.Based on this point,the author makes a literature review on the early diagnosis of CRC.
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Objective To explore the impact and significance of hypoxia preconditioning on the expression of cytochrome C and caspase 3 protein in rats after hepatic resection.Methods A hepatectomy model was used to study the ischemia reperfusion injury in hepatic resection.Sprague-Dawley rats were randomly divided into the following three groups:normal control (NC) group,hepatic resection(HR) group,and hypoxia preconditioning (HP) group,there were twenty four rats in each group.HP Group was given an 10％ oxygen-mixed gas for 90 minutes before the operation.At 1,6,12 and 24 hours after the operation,the rats were killed and the following tests were conducted:(1) Liver tissue was sampled to observe the expression of cytochrome C and caspase 3 protein; (2) blood was drawn to conduct a chemical examination; (3) Liver tissue and morphology was observed by transmission electron microscopy.Results The serum levels of ALT and AST in HP group were significantly lower than that of HR group (P＜0.05) at 1,6,12 and 24 hours after the hepatic resection.In each time,liver function of the HP group was significantly better than the HR group; The expression of cytochrome C and caspase 3 protein was decreased significantly in HP group at each measurement point.Hepatic cells in HR group showed typical apoptosis signs under transmission electron microscopy (TEM),but no apoptosis was found in HP group.Conclusion HP has marked inhibition to apoptosis by down-regulating the expression of Cyt C and Caspase-3protein and protection to chondrosomes after a hepatic resection.
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Objective To investigate the effects of intermittent hypoxic preconditioning on residual liver regeneration after parital hepatectomy in rats.Methods Fifty-four Sprague-Dawley rats were randomly divided into 3 groups (each group contained eighteen animals):sham operation group (SO group),parital hepatectomy group (PH group)and intermittent hypoxic preconditioning group (IHP group).The rats in PH group underwent the left and middle lobectomy of liver(70％ hepatectomy).The rats in IHP group were exposed to hypoxic environment of 10％ oxygen for 1 h/d.And after a week,the rats underwent parital hepatectomy.Six rats in each group were sacrificed respectively on postoperative day 1,3 and 5 (POD 1,3 and 5).The resected liver and the regenerated liver were weighed to calculate liver regeneration degree and regeneration index.The values of alaninea minotransferase (ALT) and aspartate aminotransferase (AST) in the inferior vena venous blood were examined by automatic biochemical analyzer.The positive ratio of hepatocellular proliferating cell nuclear antigen (PCNA) in the residual liver was investigated immunohistochemically.Results The degree and index of liver regeneration in IHP group were respectively higher than those in PH group on POD 1 and 3(P ＜0.05),but there were no statistical differences between the two groups on POD 5.The levels of ALT and AST in PH and IHP group began to decline after surgery,but they remined higher than those in SO group.Moreover,the ALT and AST levels in IHP group were significantly lower than those in PH group on POD 1 (P ＜0.05).The positive ratios of hepatocellular PCNA were respectively higher than those in SO and PH group on POD 1,3 and 5 (P ＜ 0.05).Conclusions To some extent,preoperative intermittent hypoxic preconditioning could prevent hepatocellular damage after parital hepatectomy,what is more,it also could promote the remnant liver regeneration.But the mechanism still needs to be studied furter.
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Objective To observe the effects of intermittent hypoxic preconditioning on the expression of apoptosis-related Bcl-2 and Bax protein after 70％ hepatectomy combined with ischemia-reperfusion injury.Methods A total of fifty-four SD rats were randomly divided into three groups (n =18).Partial hepatectomy hroup (PH Group):Rats underwent the left and middle lobectomy of liver(70％ hepatectomy).Ischemia reperfusion group (IR group):The left and middle lobes of liver were resected during the occlusion of the hepatoduodenal ligament for 20 minutes.Residual liver underwent the process of ischemia-reperfusion.Intermittent hypoxia preconditioning group (IHP group):rats were exposed to hypoxic environment of 10％ oxygen for 1 h/d.After 7 consecutive days,the left and middle lobes of liver were resected under the portal triad clamping.At 12,24 and 48 hours after the operation,the rats were killed and detected.The serum levels of ALT and AST were determined by automatic biochemical analyzer.The expression of Bcl-2 and Bax protein in liver tissue were measured by immunohistochemistry.Results At each time point after surgery,the serum levels of ALT and AST in IR group and IHP group were higher than that of PH group,and IHP group were lower than in IR group.Compared with IR group,the expression of Bcl2 protein significantly increased and Bax protein expression significantly decreased in IHP group.All these differences were statistically significant (P ＜ 0.05).Conclusions Intermittent hypoxic preconditioning might protect residual liver against ischemia reperfusion injury,through increasing the expression of Bcl-2 protein and reducing the expression of Bcl-2 protein to decrease liver cell apoptosis.
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Objective To investigate the effect of Heat shock protein 70 induced by hypoxic precondition on apoptosis of the remnant livers after the hepatectomy of transplanted hepatic cancer models in SD rants and it's possible mechanisms.Methods Sixty SD rats of transplanted hepatic cancer models were divided into group A (sham operation group),group B (IR + hepatectomy group),and group C (hypoxia precondition + IR + hepatectomy group),with 20 rats in each group.C group was given 10％ oxygen atmosphere for 90 minutes before operation,In 15 minutes of hepatic vascular occlusion with pringle method,Left lateral of liver which tumor was located was resected.At 1,8,12,24 hours after operation,Five rats of each group were killed respectively,then the remnant liver tissues were sampled to measured the hepatocytes apoptosis rate with flow cytometry,expression of heat shock protein 70 (HSP70) and Bax were detected by Western blotting.The serum AST and ALT activities were measured by an automatic analyzer.The histological changes of the hepatocytes were also observed by optical microscopy.All the data were statistically analyzed.Results (1) Compared with A and B group,the HSP70 expression increased obviously in C group at each time point (all P ＜ 0.05).The protein showed a weak expression in group A and B group,while the index had no significant differences between two groups (P ＞ 0.05).(2) In B group compared with A group,the expression of Bax and the hepatocytes apoptosis rate were significantly increased (all P ＜ 0.01 or P ＜0.05).However,amplitudes of the above changes in C group were significantly lower than those of B group (all P ＜ 0.05).(3)The liver function was improved in group HP.The pathological examination showed that the liver tissues in A group were general normal and in C group were showed mild changes,but in B group presented evident pathological changes.Conclusions HP can protect against ischemia-reperfusion injury after the hepatectomy of transplanted hepatic cancer models in SD rants,one of possible mechanisms is that HP can induce HSP70 expression at great intensity,which may decrease expression of Bax protein and the apoptosis of hepatocytes.
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Objective To explore the effect of Radix Isatidis( indigowoad root,RI) polysaccharide on NO and ET-1 in orthopotic liver autotransplantation of rats.Methods The rats used in the experiment were randomly divided into three groups:normal control group (NC), autotransplantation group (AT) and RI polysaccharide group (RIPS).At 1, 6, 12 and 24 hours after autotransplantation, the content of NO,ET-1, alanine aminotransferase ( ALT), and aspartate amin-otransferase ( AST) in serum was assayed.Morphological observation of hepatic tissues was also performed.Results The serum level of ET-1 in RIPS group was significantly lower than that of AT group (P<0.05), and NO content in serum of RIPS group was increased significantly compared with AT group ( P<0.05) at 1, 6, 12 and 24 hours after autotransplanta-tion.The serum level of ALT and AST in RIPS group was lower than that of AT group (P<0.05) at each measurement point.The morphology of hepatocytes changed abnormally under light microscopy.The blood stasis and swelling of hepatic tissues, denaturalization and necrosis of hepatocytes in RIPS group were milder than that in AT group.Conclusion RIPS has a protective effect on hepatic ischemia reperfusion injury after orthotopic liver autotransplantation, which may be related to increased NO levels and lower levels of ET-1.
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Gallstone ileus is a rare complication of cholelithiasis,and is common in older gallstones patients.It lacks the typical clinical presentation,so preoperative diagnosis is very difficult.The best diagnostic modality now is abdominal CT scan.Surgery is the most important and useful treatment.According to patient' s own situation,choose individualized surgical approach.Endoscopic,laparoscopic and other minimally invasive treatment are promising.With the development of related technologies,it maybe increased of the gollstone ileus treatment.
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Objective To observe the effects of intermittent hypoxic preconditioning on the expression of apoptosis-related EPO after 70％ hepatectomy combined with ischemia-reperfusion injury.Methods One hundred and twenty healthy SD rats of clean grade,simple random divided into 3 groups:Sham operation group of 40 rats ; Pure major hepatic resection group was 40 (Major hepatectomy,MH),namely in the hepatic portal blocking liver resection of the left and middle lobes,hepatic portal blocking 20 min ; intermittent hypoxia preconditioning group 40 (Intermittent hypoxia preconditioning,IHP group).Results MH group,S group,IHP group,EPO level in three experimental groups in postoperative residual liver tissue in rats with significant difference (P ＜ 0.05),Intermittent hypoxia preconditioning group of residual liver EPO content was significantly higher than that of simple hepatic resection group 40.Conclusion Intermittent hypoxia preconditioning can promote the expression of residual liver after hepatectomy in EPO.
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Children's portal hypertension is a hemodynamic abnormalities syndrome,it refers to children with portal vein pressure exceeds 5 mmHg,or portal vein,hepatic venous pressure gradient exceeds 10 mmHg.Etiology of portal hypertension of children:portal vein obstruction,congenital hepatic fibrosis,biliary atresia.Current treatment methods are:drug treatment,varicose vein ligation or sclerosis,surgical treatment.Although the incidence of children's portal hypertension is relatively low,it can cause various serious complications,such as ascites,gastric variceal bleeding,hepatic encephalopathy and so on.To increase awareness,improve the cure rate and reduce complications,the artical will review the children's portal hypertension etiology,pathogenesis,diagnosis,and treatment progress.
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Objective To investigate the different effects of internal and external biliary drainage on the levels of TNF-α,NO in blood serum and NO,inducible nitric oxide synthase(iNOS) in gastric mucosa with obstructive jaundice and explore the mechanism of gastric mucosa damage and compare the quality of internal and external drainage.Methods To establish the animal model:one hundred male adult Sprague-Dawley rats were randomly assigned to five groups:obstructive jaundice for 7 days group (OJ-7 d group),obstructive jaundice for 14 days (OJ-14 d group),internal biliary drainage group(ID group),external drainage group(ED group)and sham operation group(SH group).The OJ-7 group rats were executed 7 days after the first operation,the rest four groups were executed 7 days after the secondary surgery,leaving serum and gastric mucosa.Tested the levels of INF-α,NO in blood serum and NO,iNOS in gastric mucosa and did pathological biopsy of gastric mucosa.Results The levels of TNF-α,NO in blood serum and NO,iNOS in gastric mucosa significantly increased in OJ-7 group.The levels of TNF-α,NO in blood serum and NO,iNOS in gastric mucosa continued to rise in OJ-14 group,and was significantly higher than OJ-7 group,the gastric mucosa was obviously impaired.The levels of TNF-α,Internal drainage can significantly NO in blood serum and NO,iNOS in gastric mucosa were significantly lower in ID group,gastric mucosal damage significantly reduced.Conclusions After internal drainage,iNOS expression was inhited in gastric mucosal,NO production was significantly reduced,led to protect the gastric mucosa,which provide experimental basis for choice in OJ clinical treatment.
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Caspase proteins play a key role in the process of promoting apoptosis,we can often detect caspase proteins in hepatic ischemia-reperfusion injury and in experimental study on apoptosis.Now studies on caspase proteins in hepatic ischemia-reperfusion injury of experimental field are reviewed.
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Intrahepatic cholangiocarcinomas is a type of biliary epithelial cell carcinoma.Hepatolithiasis,viral hepatitis,primary sclerosing cholangitis,Caroli disease,parasitic infections are its risk factors.In recent years,the incidence of intrahepatic cholangiocarcinomas is gradually increased.Ultrasound,CT,MRI can be used to diagnose.The main way to treat intrahepatic cholangiocarcinomas is comprehensive treatment based on liver resection.There is still some controversy in liver transplantation.Adjuvant therapy will play a more and more important role in patients who unable to accept surgery.