Role of vascular endothelial growth factor in rats with severe acute pancreatitis / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the role of vascular endothelial growth factor (VEGF) in the pathogenesis of severe acute pancreatitis (SAP) in rats.</p><p><b>METHODS</b>Sixty-four male SD rats were randomly divided into control group and SAP group, and in the latter group, SAP was induced by retrograde injection of 5% sodium taurocholate in the pancreaticobiliary duct. The rats were sacrificed at 1, 3, 6 and 12 h after the operation, and the severity of pancreatitis was assessed according to histological scoring. The serum levels of VEGF were examined with enzyme-linked immunosorbent assay, and the expression of VEGF in the pancreatic tissues was measured by SP immunohistochemistry. Another 30 SD rats were randomized into the control group, SAP group and SAP+recombinant rat VEGF injection group, and the vascular permeability of the pancreatic microcirculation was determined by Evans Blue leakage test.</p><p><b>RESULTS</b>At each of the time points for measurement, both the serum VEGF level and scores of pancreatic tissue injury were significantly higher in SAP group than in the control group (P<0.05). Compared with the control group, the expressions of VEGF in the pancreatic tissues of SAP group were significantly up-regulated following the operation (P<0.05). The vascular permeability of the pancreatic microcirculation significantly increased after the onset of SAP, and injection of recombinant rat VEGF significantly increased the leakage rate of Evans Blue.</p><p><b>CONCLUSION</b>VEGF may play an important role in the pathogenesis of pancreatitis and in causing edema and hemorrhage in SAP, and the level of serum VEGF may reflect the severity of pancreatic injury.</p>

Protective effects of captopril against lung injury in rats with severe acute pancreatitis / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the protective effects of captopril against lung injury in a rat model of severe acute pancreatitis (SAP).</p><p><b>METHODS</b>Seventy-two male SD rats were randomized into sham-operated group (SO group), SAP group and captopril intervention group (CAP group). Serum amylase and myeloperoxidase (MPO) activity in the lung tissue were examined at 1, 6 and 12 h after the operation. TNF-α and AngII in the lung tissue were detected by ELISA, and the histopathological changes of the pancreas and lung were observed microscopically.</p><p><b>RESULTS</b>The MPO activity , which was similar between SAP group and CAP group at 1 h, were significantly lowered in CAP group at 6 and 12 h (P<0.05). Serum amylase level and the levels of TNF-α and AngII in the lung tissue homogenate were all reduced significantly in CAP group as compared to those in SAP group (P<0.01). The pathological injury of the lung was obviously lessened in CAP group in comparison with that in SAP group.</p><p><b>CONCLUSION</b>Captopril can ameliorate SAP-induced lung injury in rats.</p>

Antitumor and immune-modulating effects of Scutellaria barbata extract in mice bearing hepatocarcinoma H22 cells-derived tumor / 南方医科大学学报

<p><b>OBJECTIVE</b>To investigate the effects of Scutellaria barbata extract (ESB) in suppressing tumor growth and modulating the immune functions in mice bearing tumors derived from hepatocarcinoma H22 cells.</p><p><b>METHODS</b>Fifty mice inoculated subcutaneously with H22 cells were equally divided into the model group, high-, moderate-, and low-dose ESB groups, and 5-Fu group, with corresponding treatments for 10 days. Another 10 mice with only saline injection served as the normal control group. The body weight, tumor mass, thymus index and spleen index of the mice were measured, and the lymphocyte proliferation activity, NK cell activity and interleukin-2 (IL-2) production by the splenocytes were detected.</p><p><b>RESULTS</b>Moderate- and high-dose ESB significantly suppressed the tumor growth with tumor inhibition rate of 28.68% and 36.98%, respectively. ESB treatment at moderate and high doses significantly increased the thymus index and spleen index (P < 0.01), which were decreased significantly in 5-Fu group. The lymphocyte proliferation activity, NK cell activity and IL-2 production by the splenocytes were significantly lower in the model group than in the normal group (P < 0.05). Compared with the model group, ESB at the high dose obviously increased the three indexes above mentioned. The NK cell activity was also significantly improved in moderate-dose ESB group (P < 0.05).</p><p><b>CONCLUSION</b>ESB can suppress the growth of H22 implant tumor and enhance the immune function of the tumor-bearing mice.</p>

Apoptotic mechanism of gastric carcinoma cells induced by matrine injection / 中华胃肠外科杂志

<p><b>OBJECTIVE</b>To investigate the mechanism of gastric carcinoma cells apoptosis induced by matrine injection in vitro.</p><p><b>METHODS</b>Effects of 24, 48, 72, 96 h incubation with different concentrations (0.25-1.5 g/L) of matrine injection on proliferation of SGC-7901 cells were evaluated using 3-4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide (MTT) assay. The cellular morphology of SGC-7901 cells was observed by transmission electron microscope (EM). Flow cytometry was used to analyze the apoptosis of SGC-7901 cells by staining with annexin V-FITC/PI. The expression of Fas/FasL was examined by flow cytometry using specific antibody. The activity of caspase-3 was measured by spectrofluorometry.</p><p><b>RESULTS</b>Matrine injection could inhibit the proliferation of SGC-7901 cells in a dose- and time-dependent manner. The typical morphological changes of apoptosis were observed after incubation with 1.0 g/L matrine injections for 48 h. The apoptosis rates of 0.5 g/L, 1.0 g/L and 1.5 g/L groups were 39.80%, 58.11% and 79.00% respectively. The apoptotic cells in matrine injection group were mainly early apoptotic cells, and those in 5-FU group were mainly late apoptotic cells and necrotic cells. Spectrofluorometry revealed FI levels of Fas and FasL were equal, which were both correlated with apoptosis rate. The activity of caspase-3 increased with the elevation of matrine concentration, and was correlated with the apoptosis rate.</p><p><b>CONCLUSION</b>Matrine injection can induce apoptosis of SGC-7901 cells through the up-regulation of Fas/FasL expression and activation of caspase-3.</p>

Therapeutic effects of a recombinant adeno-associated virus expressing fusion peptide NT4p53(C22)Ant on ICR mice bearing transplanted liver cancer / 南方医科大学学报

<p><b>OBJECTIVE</b>To study the therapeutic effects of recombinant adeno-associated virus (rAAV) expressing fusion peptide NT4p53(C22)Ant against transplanted liver cancer in ICR mice.</p><p><b>METHODS</b>NT4p53(C22)Ant was constructed, subcloned into recombinant AAV vector, and amplified in 293 packaging cells. The efficacy of rAAV-NT4p53(C22)Ant on tumors derived from H22 cells inoculated subcutaneously in IRC mice was evaluated according to the tumor weight, inhibition rate, survival time of the mice and the histological findings.</p><p><b>RESULTS</b>A single dose of rAAV-NT4p53(C22)Ant of 100 microl (2 x 10(11) pfu/ml) injected into the transplanted H22 tumors in the ICR mice resulted in tumor disappearance in 7 (totally 12) mice, and death occurred in only 1 mouse. The injection also resulted in decreased tumor weight and prolonged survival of the mice (for over 70 days). All the 7 mice with only rAAV injection or no treatment all died, with a mean survival of about 30 days. The tumor inhibition rate exceeded 90% in mice with rAAV-NT4p53(C22)Ant injection, significantly higher than that of mice without the injection. The histological examination revealed significantly decreased tumor cells in mice with rAAV-NT4p53(C22)Ant injection as compared with those without such treatment.</p><p><b>CONCLUSION</b>rAAV-NT4p53(C22)Ant can induce apoptosis of the H22 tumor cells transplanted in IRC mice to inhibit the tumor growth and prolong the survival of the mice.</p>

Effects of Ras antisense oligoribonucleotide on multidrug resistance of pancreatic carcinoma Pc-2 cells / 中国医学科学院学报

<p><b>OBJECTIVE</b>To investigate the role of Ras antisense oligoribonucleotide (ASODN) in multidrug resistance (MDR) of pancreatic carcinoma Pc-2 cells.</p><p><b>METHODS</b>Ras and P-gp expression was suppressed by Ras ASODN. Sensitivity of Pc-2 cells to chemotherapy was determined by the MTT assay. MDR-1 mRNA level was detected by fluorogenic probe quantitative reverse transcription polymerase chain (RT-PCR) method. Flow cytometry (FCM) was used to detect the accumulative concentration of adriamycin (ADR) in the cells.</p><p><b>RESULTS</b>Ras ASODN significantly inhibited the Ras and P-gp expression (P < 0.05), increased the sensitivity of Pc-2 cells to chemotherapeutic agents (P < 0.05), decreased MDR-1 gene level in Pc-2 cells (P < 0.05), and increased the intracellular intake of ADR in Pc-2 cells (P < 0.05).</p><p><b>CONCLUSION</b>Ras ASODN may enhance the sensitivity of multidrug-resistant pancreatic cancer Pc-2 cells to chemotherapeutic agents by regulating MDR-1 gene level.</p>

The study of the effect of antisense oligonucleotide specific to K-ras point mutation on human pancreatic carcinoma cell PC-2 / 中华外科杂志

<p><b>OBJECTIVE</b>To investigate the effects of antisense oligonucleotide specific to K-ras point mutation on human pancreatic carcinoma cell PC-2 in vitro.</p><p><b>METHODS</b>Human pancreatic carcinoma cell PC-2 was transducted with antisense oligonucleotide specific to K-ras point mutation by liposome; the expression of target gene was studied with immunohistochemistry and in situ hybridization. The effect on cell proliferation was studied by artificial count, MTT and mass test.</p><p><b>RESULTS</b>The expression degree of ras protein and K-ras mRNA transducted with antisense oligonucleotide decreased apparently compared with control group and sense oligonucleotide group 48 h after tansduction. The inhibitory effect on cell proliferation was confirmed by artificial count, MTT and mass test.</p><p><b>CONCLUSIONS</b>Antisense oligonucleotide specific to K-ras point mutation has an apparent inhibitory effect on target gene expression and cell proliferation of human pancreatic carcinoma cell in vitro.</p>