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Objective To compare the effect of autologous bone marrow stem cells transplantation on liver function between first and second transplantation in decompensated liver cirrhosis patients.MethodsA total of 45 decompensated liver cirrhosis patients were enrolled, and 23patients in first transplantation group were transplanted with autologous bone marrow stem cells through femoral artery when condition was stable after medical treatment.In second transplantation group, 22 patients were accepted second transplantation in 4-12 month after the first transplantation.All the patients undergone routine blood test, congulation test and liver function examination at the fourth week and eighth week after transplantation.ResultsEight weeks after transplantation, the liver function was improved obviously in both first and second autologous bone marrow stem cells transplantation.The level of albumin in patients of second transplantation group increased from (37.26± 5.90) g/L before transplantation to (42.49 ± 4.80) g/L (P＜0.01), alanine aminotransferase (ALT) decreased from (57.05±45.51) U/L to (44.86±29.19) U/L (P＜0.05),aspartate aminotransferase (AST) decreased from (39.14-±-15.07) U/L to (53.73 ± 24.98) U/L(P＞0.05).Congulation parameters were also improved, prothrombin time (PT) decreased from (16.15±3.01) s to (14.63±2.32) s (P＜0.01), fibrinofen (Fib) increased from (2.44±0.61) g/L to (3.00±0.81) g/L (P＜0.01).Compared with first transplantation group, the albumin level was higher in second autologous bone marrow stem cells transplantation group, which increased from (38.00±6.33) g/L to (42.49±4.80) g/L (P＜0.05), AST and ALT also improved obviously, and there was significant difference between two groups.Meanwhile, Child-Pugh scores decreased from (7.22±0.67) to (6.67±[0.71) (P＜0.05).But there was no significant difference in bilirubin, FIB and PT.ConclusionThe second transplantation of autologous bone marrow stem cells could further improve liver function and maintain symptoms remission of liver cirrhosis.
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Objective To analyze the effect of autologous bone marrow stem cells transplantation in treatment of patients with decompensated cirrhosis. Methodls Seventy-eight patients (aged from 26 to 67) with decompensated cirrhosis, including 56 with hepatitis B, 21 with alcoholic cirrhosis and 1 with schistosomial cirrhosis, were included. Bone marrow was aspirated from poster superior spine. After isolation and purification, the stem cells were transplanted into liver via hepatic artery. The liver function, laboratory parameters and Child-Tureotte-Pugh scores were evaluated in 2,4 and 8 weeks after transplantation. Results At the 4th week after transplantation, the level of albumin was increased obviously from (32.9±5.58) g/L to (38.32±6.45) g/L,whereas the alanine aminotransferase was decreased from (96.92±83.91) U/L to (73.48±18.46)U/L. It was revealed that the prothrombin time was decreased from (16.66±3.91) s to (15.52±3.35) s and fibronegen increased from (2. 22 ± 0. 88) g/L to (2. 58±0. 88) g/L. After transplantation, appetite was improved in 72 cases (92.3%), ascites was decreased in 70 cases (89.7%) and abdomen distention was ameliorated in 68 cases (87.2%). There was no complications related to the transplantation. Conclusion Transplantation of autologous bone marrow stem cells is a safe and effective method in treatment of patients with decompensated cirrhosis.
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Objective To investigate the underlying mechnisms of Kangai-1(KAI1)gene,a tumor metastasis suppressor gene,on metastasis and prolification of pancreatic cancer cells.Methods The plasmin containing Ad-KAI1 was established and transfected into pancreatic cancer cell line PCNA Ⅰ.The PCNA Ⅰ cells were then divided into different groups according to the times induced by vascular endothelial growth factor(VEGF)and epidermal growth factor(EGF).The morphology and migrational ability of PANC Ⅰ cells were compared before and after transfection by microscopy and transwell method,respectively.The expressions of intercellular adhesion molecule-1(ICAM-1)and matrix metalloproteinases-9(MMP-9)in PANC Ⅰ cells were examined by immunocytochemistry before and after transfection.Results The migrational ability of PCNA Ⅰ cells transfected with Ad-KAI1 was siginificantly decreased compared with untransfected PCNA Ⅰ cells(P＜0.05).Immunocytochemistry study revealed that the expressions of ICAM-1 and MMP-9 were both positive in untransfected PCNA Ⅰcells,but were both negative in transfected PCNA Ⅰ cells.Conclusion The inhibitory mechanism of KAI1 gene on metastasis of pancreatic cancer is associated with down-regulation of ICAM-1 and MMP-9expressions.
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Objective To observe the inhibitory effect on metastasis and growth of pancreatic cancer in mice by injection of KAI1 gene in vivo. Methods Pancreatic cancer cell line MiaPaCa Ⅱ was used to construct the nude mice models bearing tumors, then the mice were divided into normal saline group, Ad group and Ad-KAI1 group. Since the 10th days of model construction, the Ad-KAI1 was injected every 7 d and repeated twice, then the tumor size, the weight of liver, lung and their pathologic changes were evaluated. Results The tumor sizes were not significantly different between the three groups. The weight of lung and liver of Ad-KAI1 group was (0.366±0.041) g and (1. 35±0.21) g, respectively; the weight of lung and liver of Ad group was (0.57±0.065) g and (1.58±1.828) g, respectively; the weight of lung and liver of control group was (0.66±0.13)g and (1.95±0.344)g, respectively. The difference between Ad-KAI1 group and control group was significantly different (t = 5.984, P < 0. 05), and there was no significant difference between Ad group and control group (t=1.089, P > 0.05). The number of pulmonary, liver and lymph node metastasis in Ad-KAI1 group was (1±1), (2±1) and (2±2), respectively; in Ad group was (6±2), (5 ±1), (10±2), respectively; in control group was (7±2), (6±2), (11±3), respectively. The difference between Ad-KAI1 group and control group was significantly different (t = 7.44, 4.34, 8. 16, P < 0.05), while the difference between Ad group and control group was not significantly different (t=0.92, 0.64, 0.42, P >0.05). Conclusions KAI1 gene directly injected into tumors of nude mice may inhibit the growth and metastasis of pancreatic cancer.
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Objective To determine the role of endogenous NO in gastric mucosal tolerant cytoprotection under stress and its possible mechanism. Methods SD rats were exposed to WRS repeatedly during which L NAME, a non selective NOs inhibitor, and L Arg, a substrate for NO synthesis, were administered to inhibit or promote the synthesis of NO, GMBF was measured using LDF 3 flowmeter, NO levels in gastric mucosa were tested by Griess reaction and gastric mucosal lesions were evaluated by ulcer index (UI). Results Gastric tolerant cytoprotection was accompanied by increased GMBF and NO levels in gastric mucosa. Inhibition of endogenous NO synthesis by L NAME worsened mucosal lesions induced by WRS. After repeated WRS, adaptive increase of GMBF was abolished and NO content in gastric mucosa significantly reduced. In contrast, enhancement of endogenous NO synthesis by L Arg attenuated mucosal erosions caused by WRS. GMBF and NO content in mucosa increased. After 4th WRS, mucosal lesions could be negligible. Conclusion By regulating GMBF, endogenous NO might play an important role in the gastric mucosal tolerant cytoprotection under stress. Inhibition of NO synthesis delayed the induction of tolerant cytoprotection, while increase NO synthesis will ptomote the induction of tolerant cytoprotection.
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Objective To determine the changes of caspase 3 and 8 genes and protein expressions during indomethacin (IND) induced gastric mucosal cell apoptosis in vivo . Methods Healthy male SD rats were treated intragastrically with four different doses of IND. The rats were killed 3 hours after IND administration and the TUNEL technique was applied to detect mucosal cell apoptosis. The change of caspase 3 mRNA expression was detected by in situ hybridization and RT PCR techniques and the changes of caspase 3, 8 protein expression were monitored immunohistochemically. Results In the rats of control group, TUNEL assay revealed that only a few apoptotic cells. Oral administration of IND resulted in the appearance of massive TUNEL positive cells. Computer aided image analysis showed that the mean pixels in 30~120mg/kg groups were 6 3 , 8 0 , 12 6 and 17 1 fold that in control group ( P
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To determine the role of GMBF in gastric mucosal tolerant cytoprotection under stress and its possible regulator, SD rats were exposed to repeated WRS, during which L NAME , a non selective NOS inhibitor, or L Arg, a substrate for NO synthesis, was administered to inhibit or promote the synthesis of NO, GMBF was measured using LDF 3 Flowmeter, NO level in gastric mucosa was monitored by Griess reaction, and gastric mucosal lesions were evaluated by UI. The results showed that gastric tolerant cytoprotection was accompanied by increased GMBF and NO level in gastric mucosa. Inhibition of endogenous NO synthesis by L NAME worsened mucosal lesions induced by WRS. After repeated WRS, adaptive increase of GMBF was abolished and NO content in gastric mucosa significantly reduced. In contrast, enhancement of endogenous NO synthesis by L Arg attenuated mucosal erosions produced by WRS and GMBF, NO content in mucosa increased. Good relationships between the changes in GMBF, UI, NO content in mucosa were found. It suggested that GMBF might play an important role in gastric mucosal tolerant cytoprotection. Endogenous NO might be one of its regulators. Inhibition of its synthesis delayed the induction of tolerant cytoprotection, while enhancementpromoted it.
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SD rats were exposed to single or repeated water immersion restraint stress (WRS) for 4 h every other day for up to 6 days, during which the extent of gastric mucosal lesions was evaluated grossly and histologically. The expressions of EGF and EGFR in gastric mucosa were assayed by immunohistochemistry. The results showed that single exposure to WRS led to haemorrhagic lesions, but tolerance developed following repeated exposures to WRS. Histological evaluations showed that single exposure to stress conditions led to crater like haemorrhagic necrosis almost extending to the muscularis mucosae. The submucosa was apparently congestive and edematous. Following repeated WRS, however, mucosal haemorrhagic necrosis was significantly attenuated and submucosal edema and congestion apparently lessened. Active regeneration and proliferation of mucosal cells were observed at the same time. The expressions of EGF and EGFR could be detected in normal gastric mucosa. EGF was expressed in cytoplasma mainly in the regenerative zone with weaker expression at the basal portions of the gastric glands. EGFR was mainly distributed on the membrane of cells in the regenerative zone. Single WRS led to significant decreased in the expressions of EGF and EGFR. their expressions were absent in the necrotic region. After repeated WRS, enhanced expression of EGF and its receptors could be observed not only in mucosal cells of regenterative zone but also in other areas including the lumen of gastric glands. The results suggested that single WRS could cause severe gastric mucosal lesions, but gastric mucosa became tolerant to repeated WRS by way of toleration cytoprotection. Gastric adaptation was accompanied by active regeneration of mucosal cells mediated by EGF binding with its receptor, EGFR.