Sixteen patients who received TPN treatment after abdominal surgery were studied. The group of phosphorus supplement (9 cases) and the control group (7 cases) were divided at random. After serially phosphorus in 24 hours, we found that the levels of serum phosphorus decreased on the fouth day (2.57?0.48mg/dl) and remained unchanged until the seventh day (2.60?0.27mg/dl) of TPN (P

ObjectiveTo investigate the relationship between the severity of acute pancreatitis and apoptosis of acinar cells. MethodsThe apoptotic ratio of acinar cells was measured in rat acute pancreatitis model by methods of in situ end labeling.ResultsThere was almost no apoptotic acinar cells in the model of acute edematous pancreatitis. With the increase in the severity of the pancreatitis apoptotic cells were more and more common until to the late stage of hemorrhagic and necrotic pancreatitis when the apoptotic ratio of acinar cells dwindled, meanwhile the necrotic acinar cell increased continuously.ConclusionsIn acute simple edematous pancreatitis apoptotic acinar cells is infrequently seen. In acute moderate hemorrhagic and necrotic pancreatitis the ratio is correlated positively with the severity of pancreatitis.In the late stage the ratio was correlated negatively with the severity of pancreatitis.

Objective To investigate the mechanism by which taxol induces apoptosis of pancreatic acinar cells during experimental acute pancreatitis in rats. Methods Intrapancreatobiliary duct injection of sodium deoxycholate was carried out to establish acute pancreatitis model in Wistar rats. Taxol was injected intraperitonealy to induce pancreatic acinar cell apoptosis. The expression of apoptosis associated protein Bcl-2,Bax,Fas,FasL and p53 was detected by immunohistochemistry. Results The expression of Bax(2 506?942),Fas(279?150) and p53(180?56) increased,while Bcl-2(79?42) remained unchanged in pancreatic acinar cells during acute pancreatitis,and the expression of FasL could only be detected in infiltrative inflammatory cells. Conclusions During acute pancreatitis,the acinar cell apoptosis induced by taxol is associated with activity regulation of Bax,Fas/FasL system and p53.

Objective To observe the apoptosis of interstitial cells of Cajal in deep muscular layer ( ICC-DMP ) of small intestine in rats with multiple organ dysfunction syndrome ( MODS ) as a result of bacterial peritonitis, and the expression of c-kit ( an ICC phenotype marker ) and Bax/Bcl-2, in order to investigate the mechanism of gastrointestinal motility dysfunction in MODS. Methods According to the random number table, 40 Wistar rats were randomly divided into two groups:control group ( n=20 ) and MODS group ( n=20 ). The MODS model in rats was reproduced by intraperitoneal injection of 8×108 cfu/mL Escherichia coli suspension 1 mL, and the control group was given the same amount of normal saline. After 24 hours, the upper small intestine was harvested for examination. Ultrastructure of ICC-DMP was observed using electron microscope. The network structure of ICC-DMP and the expression of c-kit and Bax/Bcl-2 were observed and determined with immunofluorescence and laser scanning confocal microscope. Results Macroscopic observation revealed that the gastrointestinal motility of rats was normal in the control group. Compared with the control group, gastro intestine was significantly expanded with parulytic ileus in MODS group. It was shown by transmission electron microscopy that intermediate filament structure of ICC-DMP was clear without swelling of mitochondria; chromatin distributed uniformly with small amounts of heterochromatin aggregated in perinuclear. Compared with the control group, intermediate filament structure of ICC-DMP was fuzzy, and mitochondria were swollen obviously in MODS group;chromatin was assembled in nucleus centre. It was shown by laser scanning confocal microscope that the network structure of ICC-DMP was clear, the expression of c-kit and Bcl-2 was strongly and overlapping;the expression of Bax was weak and scatter distributed. Compared with control group, ICC-DMP quantity in MODS group was significantly reduced ( cells/HP: 15.80±2.30 vs. 25.70±3.97, t = 6.819, P = 0.000 ), and ICC network was incomplete. The expression of c-kit and Bcl-2 was significantly decreased as compared with control group [ c-kit ( fluorescence intensity ):129.56±36.90 vs. 307.23±40.07, t=10.314, P=0.000;Bcl-2 ( fluorescence intensity ):103.23±25.19 vs. 378.92±43.79, t=17.259, P=0.000 ], whereas, the expression of Bax was significantly increased ( fluorescence intensity:270.94±36.98 vs. 92.57±20.92, t=-13.277, P=0.000 ). Conclusion The mechanism of gastrointestinal motility dysfunction in MODS maybe closely related to ultrastructural damage of ICC-DMP, changes of c-kit phenotypic and activation of mitochondrial apoptosis pathway.

Objective To explore the effect of icariin on stimulating Smad4 mRNA level in MC3T3-E1 cells. Methods MC3T3-E1 cells were treated by 0 ng/ml, 10 ng/ml, 20 ng/ml, 40 ng/ml icariin respectively. MTT method and population diploid time were applied to observe the cell proliferation. The cell ALP level was measured by atomic absorptiometry and the type Ⅰ collagen was observed by immunohisto-chemistry. RT-PCR was used to find the Smad4 mRNA level in the MC3T3-E1 cells. Results Under the inversion phase contrast microscopy, MC3T3-E1 cells were oligodendrocytes-shaped rich with cell organs. The cells density in 10 ng/ml, 20 ng/ml were higher than those in 0 ng/ml,40 ng/ml. Cell growth curve in 10 ng/ml was higher than other 3 groups and the 20ng/ml was higher than 0 ng/ml, 40 ng/ml groups( P

Objective To explore the changes of colon motility of the rats in multiple organ dysfunction syndrome (MODS) induced bacterial peritonitis and the effects of IL-6, TNF-? and induce nitricoxide synthase (iNOS) on colon motility. Methods Wistar rats were divided into two groups, which were the control group and the MODS group. The number of stool, the amplitude changes of circular smooth muscle strip, the length of smooth muscle cell, and the changes of serum NO in two groups were observed. The expressions of IL-6, TNF-? and iNOS protein and IL-6 mRNA, TNF-? mRNA and iNOS mRNA in distal colon were investigated by using immunohistochemical methods and RT-PCR. Results The numbers of stool and the amplitude in the MODS group were lower than those of the control group (P

Objective　To study the efficiency of the treatment of experimental hepatocellular carcinoma in rats with arsenic trioxide and to elucidate the possible mechanism.Methods　Wistar rats were fed with diethylnitrosamine (DEN) to induce HCC, then treated with As2O3. The histological changes in liver tissue were observed under microscope, and the cellular dynamic parameters were studied by flow cytometry. Results　Treatment with As2O3 caused HCC cells death via both apoptotic and non-apoptotic mechanisms when the dose was high (5 mg/kg), the necrosis was seldom and apoptosis was common when the dose was appropriate (1 mg/kg). Proliferation index (PI) decreased sharply in high-dose (5 mg/kg) group (P＜0.01), but not in other two (1 mg/kg, 0.2 mg/jg) groups (P＞0.05). However, S phase fraction (SPF) decreased dramatically in all three groups (P＜0.01). Although apoptosis of HCC cells was common in all three groups, it reached the top only when the dose (1 mg/kg) was appropriate (P＜0.001), and it was obviously accompanied with accumulation of cells in G2/M (G2/M restriction). Conclusion　These date demonstrate that arsenic trioxide induces apoptosis of rat HCC cells, and it is closely associated with G2/M restriction when apoptosis reaches the top. The data also suggest that arsenic trioxide can inhibit cell proliferation, which is dose-dependent and time-dependent. The fact that continuous intermittent i.p. injection of arsenic trioxide can also be effective may afford a novel way to use the drug more safely.

ObjectiveTo observe the morphological changes of enteric nerve-interstitial cells of Cajal (ICC) network in rats with the bacterial peritonitis, and to investigate the main cause of gastrointestinal dysfunction and gastrointestinal failure with the bacterial peritonitis. Methods Sixty Wistar rats of both sexes were randomly divided into two groups. The model of the bacterial peritonitis was established.To record the frequency and amplitude of slow wave in myoelectricity of intestine in vivo to assess the function of the intestine motility. The proximal 10.0 cm segment of jejunum beginning 2 cm distal to the pylorus from each group was studied using c-Kit and vesicular acetylcholine transporter (VAChT)/ neuronal nitric oxide synthase (nNOS) immunohistochemical double-staining with whole-mount preparation technique and laser scanning confocal microscopy(CLSM). Results Compared the result of the bacterial peritonitis group with the normal group, it was found that the frequency and amplitude of slow wave in myoelectricity of intestine of the bacterial peritonitis group were slower and lower than the normal group, CLSM scanned ICC network showed that compared with the control group, the distributions and densities of ICC of intestine in the bacterial peritonitis group decreased significantly(P<0.01), the number of ICC synapse decreased, the cell junction between ICC and the ICC network was disrupted, and the fluorescence intension of cell decreased. CLSM scanned enteric nerve-ICC network indicated that compared with the control group, in the bacterial peritonitis group, the distributions and densities of cholinergic nerves (P<0.01)/ nitrergic nerves(P<0.01)and ICC(P<0.01)of intestine significantly decreased respectively, the cell junction between enteric nerve and enteric nerve -ICC network was disrupted, and the fluorescence intension of enteric nerve -ICC network decreased. The network of cholinergic/nitrergic nerve-ICC was disrupted. Conclusion The number of cholinergic nerves and nitrergic nerves were reduced, and the enteric nerve-ICC network was damaged in rats with bacterial peritonitis. Gastrointestinal motility dysfunction can be caused by the bacterial peritonitis.

ObjectiveTo discuss the mechanism of promotion of gastrointestinal motility during multiple organ dysfunction syndrome ( MODS ) by Dachengqi decoction, by examining the expression of Bcl-2, Bax of mitochondrial pathway, and nuclear factor-κB (NF-κB) in smooth muscle of the small intestinal in rats.Methods According to the random number table, 100 healthy adult Wistar rats were divided into three groups: control group with 20 rats, model group with 40 rats, and Dachengqi decoction group with 40 rats. Rat model of MODS was reproduced by bacterial peritonitis induced by an injection of 1 mLEscherichia coli suspension (8×108 cfu/mL) into peritoneal cavity. The rats in control group were given 1 mL normal saline intraperitoneally. The rats in Dachengqi decoction group were given 10 mL/kg Dachengqi decoction by gavage, twice a day, before inoculation of the bacterial suspension. Twenty-four hours after modelling, rats in all groups were sacrificed by cervical vertebra luxation, and the upper small intestine was harvested to detect the protein expressions of Bcl-2, Bax, and NF-κB in smooth muscle tissue using immunohistochemical staining.Results In the control group, a large amount of Bcl-2 protein was expressed and it was distributed uniformly in small intestinal smooth muscle. On the other hand, a small amount of Bax and NF-κB protein was expressed, and they were also distributed uniformly. Compared with the control group, Bcl-2 protein was distributed only sparsely, and it was scattered in intestinal smooth muscle in blocks in the model group. The expression of Bcl-2 protein was obviously down-regulated [integral optical density (A) value: 7 115.3±1 797.2 vs. 22 085.5±4 892.2, P< 0.05], and this phenomenon was more prominent in circular muscle layer. Bax and NF-κB were densely distributed, and their expressions were upgraded obviously [Bax (A value): 33 802.6±5 778.0 vs. 7 984.4±1 804.5, NF-κB (A value): 2 465.9±664.8 vs. 1 572.6±256.0, bothP< 0.05]. This phenomenon was more outstanding in circular muscle layer. Compared with that of the model group, the expression of Bcl-2 protein was stronger obviously in intestinal smooth muscle in Dachengqi decoction group (A value: 12 458.6±2 491.1 vs. 7 115.3±1 797.2,P<0.05). The expressions of Bax and NF-κB were down-regulated obviously [Bax (A value): 12 529.2±2 018.5 vs. 33 802.6±5 778.0, NF-κB (A value): 1 843.1±373.6 vs. 2 465.9±664.8, bothP< 0.05], and the change was more obvious in circular muscle layer.Conclusions Dachengqi decoction may promote recovery of gastrointestinal motility through an increase of Bcl-2 expression in nuclear membrane, thus preventing translocation of Bax to mitochondrion, thereby reduces mitochondrial damage in MODS.

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