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1.
Journal of Southern Medical University ; (12): 903-907, 2011.
Article in Chinese | WPRIM | ID: wpr-332520

ABSTRACT

<p><b>OBJECTIVE</b>To study the inhibitory effect of human umbilical cord mesenchymal stem cells (UC-MSCs) infected by a adenoviral vector containing interleukin 12 (IL-12) gene on the proliferation of ovarian carcinoma SKOV3 in vitro and the growth of tumor explants in nude mice.</p><p><b>METHODS</b>Cultured human UC-MSCs were infected with the recombinant adenovirus vector harboring IL-12 gene to establish the IL-12-expressing cell line AdIL-12-MSCs. Western blotting and RT-PCR were used to detect IL-12 expressions in AdIL-12-MSCs at the protein and mRNA levels, respectively. ELISA were used to detect IL-12 content in the supernatant of AdIL-12-MSCs, whose effect on the proliferation and apoptosis of ovarian carcinoma SKOV3 cells was evaluated with MTT assay and flow cytometry, respectively. In a nude mouse model bearing subcutaneous SKOV3 tumor explants, AdIL-12-MSCs were infused via the tail vein and the inhibitory effect on the tumor growth was observed.</p><p><b>RESULTS</b>The exogenous IL-12 gene was successfully transduced into UC-MSCs by the recombinant adenovirus vector, resulting in efficient IL-12 expression in the cell at both the protein and mRNA levels. The supernatant of AdIL-12-MSCs significantly inhibited the proliferation of SKOV3 cells and induced cellular apoptosis in vitro as compared with UC-MSC supernatant. In the tumor-bearing nude mouse model, the transplantation of AdIL-12-MSCs significantly inhibited the growth of SKOV3 tumor explants (P<0.05).</p><p><b>CONCLUSION</b>Human UC-MSCs with IL-12 gene transduction, which express IL-12 at protein and mRNA levels, can inhibit the proliferation and induce apoptosis of ovarian carcinoma SKOV3 cells in vitro, and suppress the growth of ovarian cancer explants in nude mice.</p>


Subject(s)
Animals , Female , Humans , Mice , Apoptosis , Cell Line, Tumor , Cell Proliferation , Genetic Therapy , Genetic Vectors , Interleukin-12 , Genetics , Mesenchymal Stem Cells , Cell Biology , Mice, Inbred BALB C , Mice, Nude , Neoplasm Transplantation , Ovarian Neoplasms , Genetics , Pathology , Therapeutics , Transfection , Umbilical Cord , Cell Biology
2.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 208-211, 2008.
Article in Chinese | WPRIM | ID: wpr-304034

ABSTRACT

<p><b>OBJECTIVE</b>To observe the effects of prenatal exposure to low level lead on the protein and mRNA expression of growth-associated protein (GAP-43) in hippocampus of rat's offspring, and to explore the molecular mechanisms of lead on learning and memory.</p><p><b>METHODS</b>The pregnant rats were randomizedly divided into 4 groups and provided with doubly evaporated water in control group and 125, 250, 500 mg/L lead acetate solution via drinking water in treatment groups respectively during pregnancy. When the rat's offspring was 1, 21, 60 days old, the lead content in hippocampus was measured by hydride generation atomic absorption spectrometry, and the GFAP protein and mRNA expression at hippocampal CA1 region were observed by immunohistochemistry and in situ hybridization.</p><p><b>RESULTS</b>The content of lead in the hippocampus was (1.64 +/- 0.32), (2.33 +/- 0.42) and (3.28 +/- 0.58) microg/L, and (0.94 +/- 0.18), (1.27 +/- 0.26) and (1.79 +/- 0.42) microg/L respectively in the low, middle and high lead dosage group when the rat's offspring was one day and 21 day old. When the rat's offspring was 1, 21 days old, the content of lead in hippocampus in treatment groups was significant higher than that of control (P < 0.05), the integral optical density of GAP-43 protein and mRNA expression (except low dosage treatment at 21 d) were significantly decreased compared with the control (P < 0.01, P < 0.05), but there was no significant difference at 60-day old offsprings for the parameters above.</p><p><b>CONCLUSION</b>Exposure to low level lead during pregnancy could inhibit the GAP-43 protein and mRNA expression in hippocampus of rat's offspring, which may be one of the molecular mechanisms of lead on learning and memory.</p>


Subject(s)
Animals , Female , Pregnancy , Rats , Environmental Exposure , GAP-43 Protein , Genetics , Metabolism , Hippocampus , Metabolism , Lead , Toxicity , Prenatal Exposure Delayed Effects , Metabolism , RNA, Messenger , Genetics , Rats, Wistar
3.
Chinese Journal of Oncology ; (12): 905-909, 2008.
Article in Chinese | WPRIM | ID: wpr-255588

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the variation in expression of ARHI, STAT3 and E2F1 and the correlation among them during carcinogenesis of ovarian serous carcinoma.</p><p><b>METHODS</b>Immunohistochemical staining was used to detect the expression of ARHI, STAT3 and E2F1 in samples of 25 normal ovaries, 35 ovarian serous cystadenomas, 18 borderline serous cystadenomas and 56 ovarian serous carcinomas. The variation in expression of the three genes and relationship among them were analyzed.</p><p><b>RESULTS</b>ARHI expression was detected in 22 of 25 (88.0%) normal ovaries and 30 of 35 (85.7%) cystadenomas, but only in 10 of 18 (55.6%) borderline serous cystadenomas and 22 of 56 (39.3%) ovarian serous carcinomas, significantly lower than that in the normal ovaries and ovarian serous cystadenomas (P < 0.05). STAT3 expression was found in 14 of 18 (77.8%) borderline serous cystadenomas and 49 of 56 (87.5%) ovarian serous carcinomas, significantly higher than that in the normal ovaries and ovarian serous cystadenomas (P < 0.05). To compare with E2F1 expression in the normal ovaries, serous cystadenomas and borderline serous cystadenomas, E2F1 expression in 46 of 56 (82.1%) ovarian serous carcinomas was significantly higher (P < 0.05). It was found that the expression of ARHI was inversely correlated with that of STAT3 and E2F1.</p><p><b>CONCLUSION</b>Our findings indicate that ARHI expression is down-regulated, but STAT3 and E2F1 expressions are up-regulated, with an inverse correlation between ARHI and STAT3 in the carcinogenesis of ovarian serous carcinoma.</p>


Subject(s)
Adult , Aged , Female , Humans , Middle Aged , Cystadenocarcinoma, Serous , Metabolism , Pathology , Cystadenoma, Serous , Metabolism , Pathology , E2F1 Transcription Factor , Metabolism , Gene Expression Regulation, Neoplastic , Immunohistochemistry , Ovarian Neoplasms , Metabolism , Pathology , Ovary , Metabolism , Pathology , STAT3 Transcription Factor , Metabolism , rho GTP-Binding Proteins , Metabolism
4.
Chinese Journal of Industrial Hygiene and Occupational Diseases ; (12): 206-209, 2005.
Article in Chinese | WPRIM | ID: wpr-346530

ABSTRACT

<p><b>OBJECTIVE</b>To analyze the treatment of 42 patients with acute methanol poisoning because of drinking alcohol containing methanol.</p><p><b>METHODS</b>Clinical data of 42 cases of methanol poisoning were collected and analyzed. Methanol concentration in drinking alcohol and blood was determined by gas chromatography (GC). National standard for occupational medicine (GBZ53-2002) was used to diagnose the cases.</p><p><b>RESULTS</b>The methanol concentration in the alcohol was 16% approximately 46%. 42 Patients (40 males, 2 females), at age of 46.1 (22 approximately 80), took 588.1 ml (50 approximately 2,000 ml) of the alcohol. The average methanol concentration in blood was 1.61 mmol/L (0.03 approximately 23.60 mmol/L). According to clinical diagnosis, there were 17 observed cases, 9 mild acute toxication, and 16 severe acute toxication. Among them, 35 (83.3%) patients were recovered, 2 (4.8%) blind, 4 (9.5%) with neuropsychic sequela and 1 (2.4%) dead after adopting 8 cure measures.</p><p><b>CONCLUSION</b>To start using emergency plan for public health events suddenly happened, designate a special treatment hospital, clear blood methanol as soon as possible, correct acidosis, adequately administer folacin and hormone, protect optic nerve and retina, and take comprehensive symptomatic treatment as well as strict monitoring are the keys of clinical cure.</p>


Subject(s)
Adult , Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Acute Disease , Methanol , Poisoning , Poisoning , Therapeutics , Public Health Practice
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