ABSTRACT
Objective:To explore the regulatory effect of glutathione S-transferase P1(GSTP1) on the radiosensitivity of mouse Lewis lung cancer (LLC) cells.Methods:GSTP1-shRNA lentivirus and negative control lentivirus were used to respectively infect the LLC cells, and stable transgenic strains were selected. Real-time PCR and Western blot were conducted to quantitatively measure the expression levels of GSTP1 mRNA and protein in the LLC cells to verify the knockdown effect. The cell counting kit-8(CCK-8) assay was used to detect cell viability after irradiation. The colony formation assay was utilized to assess the cell proliferation ability after irradiation. Flow cytometry was performed to assess the level of cell apoptosis after irradiation. The tumor-bearing mice were established and irradiated to detect the changes in the tumor volume after irradiation. TUNEL staining was employed to detect the level of tumor apoptosis after irradiation. Immunofluorescence was used to detect the number of CD 4+ CD 8+ T cells in the tumor after irradiation. Results:Real-time PCR and Western blot showed that after shRNA lentivirus interference, the expression levels of GSTP1 mRNA and protein were significantly down-regulated. Down-regulation of GSTP1 reduced cell viability and proliferation, and increased the rate of cell apoptosis after irradiation. The tumor volume of the tumor-bearing mice after irradiation in the GSTP1 knockdown group was significantly smaller than that in the NC group, whereas the tumor apoptosis rate was significantly higher and the number of infiltrating CD 4+ CD 8+ T cells in the tumor was remarkably higher compared with those in the control group. Conclusion:Knockdown of GSTP1 can significantly increase the radiosensitivity of LLC cells and enhance the infiltration of lymphocytes in tumor tissues.
ABSTRACT
In order to investigate the change in and relationship between endothelin 1(ET 1) and nitric oxide(NO) in hypoxic pulmonary hypertension(HPH),the content of ET 1 and NO in plasma and lung tissue homogenate, the expression and localization of ET 1, constitutive and inducible nitric oxide synthase(cNOS,iNOS) using immunohistochemistry in HPH of rats were assayed. The effect of NOS inhibitor nitro L arginine methyl ester(L NAME) on the content of ET 1 was also studied. The results showed that the content of ET 1 and NO in plasma of the HPH rats were significantly higher than that of controls; positive expression of ET 1 and iNOS were enhanced in the endothelium of vessels, the epithelium of bronchi and the smooth muscle of vessels and bronchi,but the expression of cNOS weakened The content of ET 1 in plasma and lung tissue homogenate were increased after administration of L NAME. The results indicate that in the normal animals, NO may suppress the secretion of ET 1. The increased ET 1 may play an important role in the development of HPH, and the induced iNOS may be the result of functional adaptation to chronic hypoxia.
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Objective To observe the changes in gut mucosal barrier and gut-origin bacteria-endotoxin translocation in acute necrotizing pancreatitis (ANP) rats. Methods Wistar rats were divided randomly into normal group (n=6), sham operation group (n=30) and ANP group (n=39). ANP was introduced by infusion of artificial bile into biliopancreatic duct. Morphology of pancreas and intestine were observed and tight junction on ileum epithelia were assessed by cryofracture replicas electroscopy. Plasma levels of D-lactic acid and endotoxin were examined at various time points. The rates of bacterial translocation to abdominal organs were also calculated. Results Mucosal and tight junction damages of the gut were found during early stage of ANP. Simultaneously, plasma D-lactate levels increased and endotoxemia occurred. The rate of bacterial translocation to organs was 59.5% 72h after ANP occurred. Conclusions Gut barrier function can be injured in the early stage of ANP, and resulting in gut origin bacteria-endotoxin translocation, which may be the originator of systemic inflammatory reaction and secondary infection of the pancreas.
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An animal model of encephalitis B was successfully established with Jin Wei Yan I strain virus in mice,which made it possible to study the ultrastructural pathology as well as the morphogenesis and release of encephalitis B exerimentally.The ultrapathological changes occurring to the brain tissues especially in the neuron cells were described systematically.A preliminary hypothesis about the morphogenesis and release of encephalitis B virus (Jin Wei Yah I strain) was proposed on the basis of these changes.Replication of the virus was also found to occur in the oligodendroglia but not in the microglia,which maintained its phagocytic function.This fact evidently shows that the micrioglia is not controlled by the mRNA of the virus.According to the literature available to the authors,it seems that the ultrastructural pathological changes of encephalitis B with typical histological lesions in animals had not been reported previously.
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The changes of the pulmonary ultrastructures of 15 dogs of respiratory distress syndrome (RDS)induced with intravenous injections of different doses of oleic acid under different methods of management (nontreated and treated with scopolamine) were observed after the animals were killed 6 hours and 24 hours after injection. The changes were similar on all the specimens except that those of the dogs killed at the earlier interval were less severe. The nontreated dogs and the dogs treated with scopolamine slso showed similar changes, which indicates that scopolamine is useless in treating the RDS produced by oleic acid.Correlating to the accumulation of neutrophils in the capillaries, the authors suggested that the injury induced by oleic acid to the capillary endothelium, besides the chemical toxic action of the drug, was also due to the complement and the toxic oxygen radicals produced by neutrophils.It was found that the hyaline membrane consisted of plasma protein granules in some cases and fibrin in others but no necrosis of the epithelial cells underneath the hyaline membrane was seen. Some authers suggested that the different constituents of the hyaline membrane were resulted from the precipitation of the edema-tous fluid protein on the surface of alveoli, but this suggestion could not be confirmed either by the electron microscopic study of othrs or by ours.There was a large amount of surfactant found in the intraalveolar space and vacuolation was seen, which indicates that no reduction of surfactant occurred in RDS but there was some alteration of its nature resulting in the loss of its activity.