1.Effectiveness of intravenous low-dose erythromycin for feeding intolerance in preterm infants:a meta-analysis
Jun WEN ; Yufei SU ; Wenyi CHANG ; Lie WANG ; Shaoning LI ; Hua LI ; Jian XU
Chinese Pediatric Emergency Medicine 2013;20(5):479-483
Objective To evaluate the effectiveness of low-dose erythromycin for the treatment of feeding intolerance in preterm infants in China.Methods In this study,random clinical trials on the treatment of feeding intolerance in preterm infants with intravenous low-dose erythromycin published were searched at Chinese Journal Full-text Database,Chongqing Weipu Database and Wanfang database by using the methods of Cochrane systematic review.At the same time the information from related journals,professional data and network were hand-searched.The publishing deadline for the literatures reviewed in this study was August 2012.Statistical analysis of clinical data was performed by using RevMan 4.2 software provided by the Cochrane Collaboration.Results A total of 9 studies were included.The results showed that compared with the group of comprehensive therapy,the group of low-dose erythromycin was superior in the following aspects with significant differences(P < 0.05):the average length of hospital stay,time of parenteral nutrition,time to full feeding,the incidence rate of feeding intolerance (Z =3.44,P =0.000 6 ; Z =6.78,P <0.000 01 ; Z =3.96,P < 0.000 1 ; Z =2.51,P =0.01).Conclusion Low-dose erythromycin therapy for feeding intolerance in preterm infants is superior to the comprehensive therapy.It provides a prospective therapeutic method for feeding intolerance in preterm infants.However,large scale,multicenter and well-designed clinical trials should be adopted to confirm the conclusions.
2.Surgical treatment of familial adenomatous polyposis:a report of 45 cases
Yin WEN ; Jingbo LU ; Ming ZHU ; Chengtang WU ; Lie LI ; Wei ZHU
Chinese Journal of General Surgery 2001;0(09):-
Objective To summarize the clinical data of 45 cases of familial adenomatous polyposis(FAP) and the experiences of treatment and diagnosis of FAP. Methods Retrospectively analyzed of the clinical data was made on 45 FAP patients.The choice of operative procedure included total colectomy+ileostomy in 25 cases,subtotal colectomy+rectal polyposis electrocautery in 15,and total colectomy with ileo-anal anastomosis in 5. Results Average age of patients at first diagnosis was 33.5 years. A family history was found in 35 patients. Bleeding, diarrhea, pain are common clinical presentations, and the numbers of polyposis were all more than 100. All patients without malignant change survived for 3-21years;and metastasis of liver was the main cause of death in patients with malignant change. There were age differences between malignant and non malignant group. Conclusions FAP lacks typical clinical presentation, and misdiagnosis is not uncommon. Surgical therapy should be done on an individual basis and according to the actual condition of patients.
3.Activation of PACAP receptor could protect cultured hippocampal neurons against beta amyloid peptide induced neurotoxicity.
Lan-Run GUI ; Wen-Bin LI ; Bing-Lie ZHANG
Chinese Journal of Applied Physiology 2002;18(2):145-148
AIMTo observe the protective role of pituitary adenylate cyclase activating polypeptide (PACAP) on hippocampal neuronal apoptosis induced by beta amyloid peptide in the culture.
METHODSHippocampal neurons were isolated from 1d old SD rat and neuronal survival and apoptosis were measured by MTT assay and DNA ladder.
RESULTS25 micromol/L Abeta could induce neuron apoptosis while co-treatment with PACAP could increase the survival of hippocampal neurons. The antagonist of PACAP receptor, P6-27, could reverse the effect of PACAP.
CONCLUSIONPACAP could protects cultured neurons from the neurotoxicity of Abeta through the activation of PACAP receptor and may have a bright use in treatment of neurodegenerative disease.
Amyloid beta-Peptides ; toxicity ; Animals ; Apoptosis ; drug effects ; Cells, Cultured ; Hippocampus ; cytology ; Neurons ; drug effects ; metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide ; metabolism
4. Exploration of potential molecular mechanism of Chuanxiong in treatment of tension-type headache based on network pharmacology and molecular docking
Chun-Long HAN ; Xin-Jie ZHAO ; Chen BAI ; Meng-Jun LI ; Wen-Hui LI ; Xiang-Zhe LIU
Chinese Pharmacological Bulletin 2022;38(1):140-147
Aim To analyze the active ingredients of Chuanxiong, predict its target and signaling pathways in the treatment of tension-type headache, and clarify its therapeutic mechanism based on the principle of network pharmacology.Methods The effective active ingredients in Chuanxiong were retrieved from the Chinese herbal system pharmacology platform(TCMSP), and were performed by the ADME screen to collect the potential targets; the existing tension-type headache-related disease targets were collected through the GeneCards database.The targets corresponding to the active ingredients were intersected to obtain the common target as the key target.Cytoscape was used to construct and analyze the visual "drug-active ingredient-target-disease" network, and the String database was used to construct the PPI protein interaction network; through R language the GO function and KEGG pathway enrichment of common targets in the form of bubble graphs were analyzed.Lastly, molecular docking was used for preliminary verification.Results Finally 7 active ingredients, 105 compound targets and 2 139 tension-type headache-related target genes were obtained.There were 54 nodes in the protein interaction network.GO functional enrichment analysis yielded 215 entries, and KEGG pathway enrichment analysis yielded 68 signaling pathways.Molecular docking showed that FA, Chuanxiong quinone, sitosterol, ligustalin had strong affinity with CASP3, MAPK1, MAPK14.Conclusions It is suggested that Chuanxiong may treat tension-type headaches through anti-inflammatory, antioxidant and cytoprotective effects.
5.Recombinant human interleukin-10 inhibits proliferation of vascular smooth muscle cells stimulated by advanced glycation end products and neointima hyperplasia after carotid injury in the rat.
Ping OUYANG ; Li-Sheng PENG ; Hong YANG ; Wen-Lie PENG ; Wen-Yan WU ; An-Long XU
Acta Physiologica Sinica 2003;55(2):128-134
The purposes of this study was to determine the effects of recombinant human interleukin-10 (rhIL-10) on proliferation of vascular smooth muscle cells (VSMCs) stimulated by advanced glycation end products (AGE) and neointima hyperplasia after rat carotid arterial injury. Rat aortic VSMCs were cultured and treated with rhIL-10 or AGE respectively, and then co-treated with rhIL-10 and AGE. Proliferation of VSMCs was quantified by colormetric assay. Cell cycle analysis was performed by flow cytomertry. Sprague-Dawley rats were treated with recombinant human IL-10 (rhIL-10) for 3 d after carotid arteries injury. The ratio of neointima to media area at the site of arterial injury was measured 28 d after balloon injury. The p44/42 MAPK activity was evaluated by the immunoblotting technique using anti-p44/42 phospho-MAPK antibody. Compared to control, AGE stimulated VSMCs proliferation. rhIL-10 alone had no effect on VSMCs growth. With AGE stimulation, rhIL-10, at dose as low as 10 ng/ml, inhibited VSMCs growth (P<0.05). The cell number in G(0)/G(1) phase of AGE and rhIL-10 co-treatment group was higher than that of AGE treatment alone (P<0.01) by flow cytometry analysis. Compared with the control group of neointima hyperplasia in rats, the ratio of neointima to media area of recombinant human IL-10 group was reduced by 45% (P<0.01). The p44/42 MAPK activity was significantly enhanced by AGE. The AGE effects were opposed by rhIL-10. The anti-inflammatory cytokine rhIL-10 inhibits AGE-induced VSMCs proliferation. Recombinant human IL-10 also inhibited neointima hyperplasia after carotid artery injury in rats. The results suggest the possibility that recombinant human IL-10, as a potential therapeutic approach, prevents neointimal hyperplasia.
Animals
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Aorta, Thoracic
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cytology
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Atherosclerosis
;
physiopathology
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Carotid Artery Injuries
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pathology
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physiopathology
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Carotid Intima-Media Thickness
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Cell Proliferation
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drug effects
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Cells, Cultured
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Glycation End Products, Advanced
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antagonists & inhibitors
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pharmacology
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Hyperplasia
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prevention & control
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Interleukin-10
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pharmacology
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Male
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Muscle, Smooth, Vascular
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cytology
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Myocytes, Smooth Muscle
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drug effects
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Neointima
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drug therapy
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prevention & control
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Rats
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Rats, Sprague-Dawley
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Recombinant Proteins
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pharmacology
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Tunica Intima
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pathology
6.In vitro study on Hep G2 cell infected by hepatitis C virus.
Rui-lie CHEN ; Yong-wen HE ; Yong GAO ; Shu-li LI ; Xiao-ming YANG ; Duan-de LUO
Chinese Journal of Experimental and Clinical Virology 2005;19(2):156-158
OBJECTIVETo establish hepatitis C virus (HCV) infected cell model which is similar to the infection in vivo and can support HCV to replicate for a long time.
METHODSAfter infected with HCV-positive serum, Hep G2 cells were cultured for 60 days. Nested RT-PCR was used to detect plus and minus HCV RNA in cultured cells and supernatants.
RESULTSPlus HCV RNA was detected intermittently in Hep G2 cells during 2-30 days, minus HCV RNA was detected during 3-30 days after infection, the detection rate was similar to plus HCV RNA. Plus and minus HCV RNA can be still intermittently detected during 31-60 days after infection. However, the detection rate gradually declined. Plus HCV RNA was also found intermittently positive in the supernatant, and the detection rate was consistent to that in cells. Minus HCV RNA was not detected in the supernatant.
CONCLUSIONHep G2 cells were susceptible to HCV, and could support HCV to replicate for a relatively long time. Hep G2 is an ideal HCV infection cell model.
Cell Line, Tumor ; Hepacivirus ; genetics ; growth & development ; Humans ; RNA, Viral ; genetics ; isolation & purification ; Reverse Transcriptase Polymerase Chain Reaction ; Virus Replication
7.Relationship between amyloid beta-protein and oxidative stress and the protective role of pituitary adenylate cyclase activating polypeptide against oxidative stress induced damage on neuro-2a cells.
Lan-Run GUI ; Bing-Lie ZHANG ; Zheng-Yu FANG ; Wen-Bin LI
Chinese Journal of Applied Physiology 2003;19(2):171-174
AIMTo observe the relationship between amyloid beta-protein (Abeta) and oxidative stress and the protective role of pituitary adenylate cyclase activating polypeptide (PACAP, PACAP-27) against damage induced by oxidative stress (H2O2) in neurem-2a cells.
METHODSWith cultured neuro-2a cells the cell survival and apoptosis were measured by MTT assay, Hoechest33258 staining, DNA ladder and the percentage of small DNA fragment.
RESULTSConcentration-dependent toxicity was induced with H2O2 treatment for 24 h. The neurotoxicity of H2O2 was increased by about 10 times with cotreatment neurons with amyloid beta-protein fragment 25-35 (Abeta(25-35)). While decrease the percentage of small DNA fragmentation the cell survival was increased with co-treatment with PACAP-27(which were added to the culture everyday). The effect of PACAP was not reversed with antagonist of PACAP receptor, PACAP(6-27).
CONCLUSIONAbeta and H2O2 can promote each other's neurotoxicity. Cultured neurons were protected by PACAP27 from the neurotoxicity of H2O2 but not through the activation of PACAP-27 receptor.
Amyloid beta-Peptides ; toxicity ; Apoptosis ; Cell Survival ; Cells, Cultured ; Humans ; Hydrogen Peroxide ; pharmacology ; Neurons ; cytology ; drug effects ; Oxidative Stress ; Pituitary Adenylate Cyclase-Activating Polypeptide ; pharmacology
8.Plasma levels of adiponectin and tumor necrosis factor-alpha in children with obesity.
Wei-Jian YAN ; Jing WU ; Juan MO ; Chao-Wen HUANG ; Lie-Wu PENG ; Li XU
Chinese Journal of Contemporary Pediatrics 2009;11(1):47-50
OBJECTIVETo examine plasma adiponectin (ADPN) and tumor necrosis factor-alpha (TNF-alpha) levels and their correlation in children with obesity in order to investigate the roles of both in the development of childhood obesity.
METHODSOne hundred and forty-seven children with obesity and 118 normal children who were randomly sampled from five primary schools from the Kaifu District in Changsha were enrolled. Physical shape indexes, including height, weight, waist circumference, hip circumference, and waist to hip ratio (WHR) were measured. Body mass index (BMI) was calculated. Blood pressure was measured. Percentage of body fat (%BF) was measured with dual energy X-ray absorptiometry. Plasmal levels of ADPN and TNF-alpha were detected using ABC-ELISA. Blood concentrations of triglycerides (TG), total cholesterol (TC), high density lipoprotein-cholesterol (HDL-C) and low density lipoprotein-cholesterol (LDL-C) were measured by automatic biochemistry analyzer. Fasting blood glucose level was measured by glucose oxidase method. Fasting blood insulin level was assayed by radioimmunity. Homeostasis model assessment for insulin resistance (HOMA-IR) was performed.
RESULTSPlasma ADPN levels in obese children significantly decreased compared with those in normal children (8.12+/-2.54 mg/L vs 12.22+/-4.68 mg/L; p<0.05), and had a negative correlation with plasma TNF-alpha levels, BMI, WHR and HOMA-IR (p<0.01), and with %BF, fasting insulin, systolic blood pressure and TG (p<0.05). Plasma TNF-alpha levels in obese children significantly increased compared to normal children (171.38+/-34.33 ng/L vs 91.07+/-21.60 ng/L; p<0.01) and positively correlated with BMI, WHR, %BF, fasting insulin, HOMA-IR, TG and systolic blood pressure (p<0.01), and negatively with HDL (p<0.05). Multiple stepwise regression analysis showed that ADPN, BMI and TNF-alpha were main influential factors for %BF (R2=0.926, p<0.01). There was a significant interaction between ADPN and TNF-alpha (p<0.05).
CONCLUSIONSPlasma ADPN levels decreased and plasma TNF-alpha levels increased in children with obesity and both were main influential factors for %BF in children. There was an interaction between ADPN and TNF-alpha, suggesting that they both participate in the development of childhood obesity.
Adiponectin ; blood ; Adolescent ; Blood Pressure ; Body Mass Index ; Child ; Cholesterol, HDL ; blood ; Female ; Humans ; Insulin Resistance ; Male ; Obesity ; blood ; etiology ; Regression Analysis ; Tumor Necrosis Factor-alpha ; blood
9.Pituitary adenylate cyclase activating polypeptide protects neuro-2a cells from beta amyloid protein cytotoxicity by modulating intracellular calcium.
Lan-Run GUI ; Yan ZHOU ; Bing-Lie ZHANG ; Wen-Bin LI
Acta Physiologica Sinica 2003;55(1):42-46
MTT analysis and intracellular calcium measurement by using confocal laser scanning microscopy were used to study the possible mechanism of protective effect of pituitary adenylate cyclase activating polypeptide 27 (PACAP27) from beta amyloid protein (Abeta)-induced neurotoxicity. The results showed that treatment with PACAP (less than 0.1 micromol/L) increased the survival and reproductive ability of neuro-2a cells and protected the neuro-2a cells from being injured by Abeta. The protective effect of PACAP27 was reversed by the competitive PACAP receptor antagonist PACAP6-27. An increase in intracellular calcium was observed when the cells were challenged with Abeta and PACAP. But the calcium increase induced by Abeta kept stable for a long time while PACAP caused a transient rise in intracellular calcium. The intracellular calcium increase induced by Abeta was blocked by pretreatment with PACAP for 10 min. It is suggested that the neuroprotective effect of PACAP against neuronal damage induced by Abeta may result from its role in inhibiting the sustained rise in intracellular calcium.
Amyloid beta-Peptides
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antagonists & inhibitors
;
toxicity
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Calcium
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metabolism
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Calcium Channels
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metabolism
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Cell Line, Tumor
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Humans
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Neuroblastoma
;
pathology
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Neuroprotective Agents
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pharmacology
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Pituitary Adenylate Cyclase-Activating Polypeptide
;
pharmacology
10.Stirred Bioreactor Cultivation Enhances the Efficiency of Embryoid Bodies Formation and Differentiation into Cardiomyocytes
Wen-Jun HE ; Ling-Ling YE ; Shi-Chong LI ; Hong LIU ; Qi-Wei WANG ; Hai-Tao WANG ; Jing XIE ; Zhao-Lie CHEN ;
China Biotechnology 2006;0(11):-
Objective:To determine the optimal condition for mouse embryonic stem cells (mESC) culture with stirred bioreactor,and to develop a method for mass production of embryoid bodies (EB). Methods:The different initial cell concentrations of mESC and the initial stirring speed of bioreactor were investigated to determine the optimal condition for EB formation. Induced by ascorbic acid,the differentiation of EBs formed in stirred bioreactor into cardiomyocytes was compared with EBs formed in Petri dish. Immunofluorescence staining and RT-PCR were used to identify the cardiomyocytes derived from mESC. Results:The formation of a large number of uniform relatively EBs was achieved in stirred bioreactor when mESC were seeded initially with 1?105~3?105 cells/ml and stirring speed was set to 15~30r/min. Most of cells in the EBs formed in bioreactor were viable. EBs produced in bioreactor differentiated into cardiomyocytes more efficiently compared with EBs from Petri dish. The cardiac specific genes were expressed in ESC-derived cardiomyocytes. Conclusions:Stirred bioreactor culture could enhance the efficiency of EB formation and differentiation into cardiomyocytes,which may be a more ideal culture system for EB formation.