1.Inhibition effect of PPARγ agonist on proliferation of human pterygium fibroblasts
Chinese Journal of Experimental Ophthalmology 2011;29(4):341-345
Background Recurrence of pterygium is a common complication after the surgical excision of pterygium,and this procedure is related to cell proliferation,inflammation and neovascularization.Researches determined that rosiglitazone can suppress inflammation and neovaseularization and inhibit proliferation,hut few studies concerning the effect of rosiglitazone on pterygium were performed. Objective The aim of this study was to investigate the effect of peroxisome proliferator-activated receptor γ agonist on the proliferation and apoptosis of human pterygium fibroblasts(HPFs)in culture and search for a new drug to prevent and cure the recurrence after pterygium surgery. Methods Human pterygium samples were obtained during surgery and HPFs were cultured and purified using an explant method and 0.25%trypsin digestion,respectively.The identity of cultured HPFs was confirmed by immunohistochemistry using anti-vimentin and keratin antibodies.Rosiglitazone with the concentrations of 0(control),5,10,25,50,75,100,150,200,400μmol/L was then added in the culture medium for 12,24 or 72 hours.1%DMSO was used as blank control.The MTT method was used to assay the biologic effects of rosiglitazone on HPFs.Cell cycle distribution and apoptosis of HPFs after rosiglitazone treatment were studied by flow cytometic analysis.The expression of proliferating cell nuclear antigen(PCNA)mRNA in HPFs was detected by real-time PCR. Result Cultured HPFs radially migrated outward from the pterygium block,and then grew in long fusiform shape,showing positive response for vimentin and negative for keratin.The HPFs became round and thin with loose distribution after the addition of rosiglitazone.Following 25-125 μmol/L rosiglitazone administration for 12,48 or 72 hours,the A490 value of HPFs significantly declined with the increase of dosage(F=158.312,P=0.006)and lapse of time(F=1.924,P=0.135).Following the treatment of 25,75 or 125 μmol/L rosiglitazone for 24 hours,the number of HPFs in G0/G1 phase was markedly elevated;while the cell numbers in S phase decreased significantly in comparison with the control group(P<0.05).The apoptotic rate of HPFs in the 25,75 and 125 μmol/L rosiglitazone groups significantly increased with the increase of rosiglitazone concentration(P<0.05).Real-time PCR revealed that after 24 hours of rosiglitazone treatment,the expression of PCNA mRNA in HPFs was suppressed in a dose-dependent manner(F=3244.329,P<0.05). Conclusion Rosiglitazone inhibits HPFs proliferation,arrests their cell cycle progression in G0/G1 phase,induces apoptosis of HPFs and depresses the synthesis of PCNA in a dose-and time-dependent manner.
2.COX-2 and its inhibitor Celecoxib in corneal neovascularization
Yuan, DONG ; Ming-Chang, ZHANG
International Eye Science 2006;6(3):523-526
AIM: To observe the expression of COX-2 in rat corneal neovascularization (CNV) and its relationship to CNV, and to explore the inhibition of Celecoxib, a COX-2 inhibitor, to CNV.METHODS: The distribution and quantification of COX-2and VEGF was detected by immunohistochemistry. Expression of COX-2 and VEGF mRNA was quantified by RT-PCR.The difference in protein and mRNA expressions of COX-2and VEGF was analyzed to find the correlation between them.RESULTS: Expression of activated COX-2 and VEGF protein and mRNA in CNV had a dynamic change. VEGF and COX-2co-localized. Compared with the control group, expression of both protein, mRNA of COX-2 and VEGF in experimental group Ⅱ and Ⅲ had significant difference (P<0.05), indicating the correlation between COX-2 and VEGF, while that in experimental group I had no statistical difference (P>0.05).CONCLUSION: COX-2 expression was up-regulated in inflammatory CNV. COX-2 modulates the expression of VEGF,playing a very important role in CNV. Celecoxib inhibit COX-2expression so as to hold back the CNV.
3.Effect of dihydromyricetin on proliferation and apoptosis of breast cancer MCF-7 cells
Ming LI ; Weixing ZHANG ; Lu YUAN
International Journal of Laboratory Medicine 2017;38(13):1762-1764
Objective To investigate the effect of dihydromyricetin on proliferation and apoptosis of breast cancer MCF-7 cells.Methods From March 2014 to February 2015,breast cancer MCF-7 cells were treated with 99% pure DMY as an inhibitor.MTT assay,flow cytometry and immunocytochemistry were used to analyze the proliferation,apoptosis and protein expression of breast cancer cell MCF-7.Results When the DMY concentration was higher than 20 μg/mL,the inhibitory effect appeared,but not good.When 40 and 80 μg/mL DMY were used,the proliferation of MCF-6 cells were significantly inhibited,and have different degrees of sensitivity to it.When DMY was 80 μg/mL,the IC50 was 226.9 μg/mL.The inhibition rate and IC50 were compared with 0 μg/mL DMY,there was significant difference(P<0.05).Indicating that the relatively high concentration of DMY could significantly improve the patient′s condition of breast cancer;MCF-6 cells treated with 40 and 80 μg/mL DMY could induce G2/M phase arrest in DMY with concentration greater than 20 μg/mL(P<0.01),and showed significant cell apoptosis death phenomenon.At the same time,G0/G1 phase was also blocked and S phase cells decreased significantly,the difference was significant(P<0.05).The positive rate of PCNA in breast cancer MCF-6 cells significantly decreased(P<0.01) when the DMY concentration was higher than 50 μg/mL,the positive rate was> 50%,especially in DMY with 80 μg/mL,the positive rate was 10.00%.Compared with 0 μg/mL DMY,the difference was significant(P<0.05).Conclusion The use of dihydromyricetin in breast cancer patients can effectively inhibit the rapid increase of cancer cells,accelerate apoptosis,slow down the patient′s condition,the effect is outstanding.
4.Achillis Tendon-Sliding Procedure and Subtalar Joint Capsula Release by the Same Cut and Individualization in Treatment of Congenital Clubfoot
jing-dong, ZHANG ; yuan-ming, OU-YANG
Journal of Applied Clinical Pediatrics 1986;0(01):-
Objective To explore achillis tendon-sliding procedure and subtalar joint capsula release by the same cut and individualization treatment used in the correction of congenital clubfoot.Methods Forty eight cases (76 feet) of congenital clubfoot who were first visit were treated by achillis tendon-sliding procedure and subtalar joint capsula release by the same cut,meantime,footplate fascia release and transfer of the anterior tibial tenden were made by individualization.Results All cases were followed-up,the average time follow-up was 1 year and 6 months,excellent were 71% and good were 15.7%.Five cases were recurrence and its rate was 6.94%.Conclusions Achillis tendon-sliding procedure and subtalar joint capsula release by the same cut can solve rotation of displacement between calcaneus and talus and individualization treatment can also solve high arch deformity and adduction of foot.This technique is a simple,safe and effective treatment for congenital clubfoot.
5.Effect of radiotherapy combined with elemene injection on lung cancer treatment
Ming ZHANG ; Fuwei YANG ; Changji YUAN
Chinese Journal of Biochemical Pharmaceutics 2014;(1):132-134
Objective To study the clinical effects on patients with brain metastases from lung cancer combined with Elemene Injection and radiotherapy. Method 86 patients with brain metastases from lung cancer were randomly divided into control group and treatment group, 43 cases in each group. Control group was given conventional radiotherapy treatment, while treatment group combined Elemene Injection with radiotherapy. Results Compared with control group, treatment group’s disease control effect was obviously better. Survival rates after treatment for six months, one year, three years were higher than control group, and the number of adverse reactions were lower. Serum MMP-2 and MMP-9 levels were significantly greater. Radiotherapy plan time and total time in hospital for treatment were significantly shorter. Conclusion The combination of Elemene Injection with radiotherapy treatment for patients with brain metastases from lung cancer is very obvious.
6.The Inhibitory effect of pigment epithelium-derived factor on invasion of gliomas
Tao ZHANG ; Ming GUAN ; Yuan LV
Chinese Journal of Laboratory Medicine 2003;0(12):-
Objective To assess the impact of recombinant pigment epithelium-derived factor (rPEDF) on the growth and invasion of the glioma cells.Methods The level of vascular enthothelial growth factor (VEGF) and thrombospondin-1 (TSP-1) were evaluated by enzyme-linked immunoadsorbent assay (ELISA); cell proliferation assays were performed by MTT assay; the cell migratory assay was used for evaluating its inhibitory migration rate.Results The VEGF expression (0.29?0.03) of A172_ PEDF (added the PEDF to the A_ 172 cells) decreased 4.4 times compared with the A172_ con (not added the PEDF to the A_ 172 cells, 1.31?0.02, P
7.Relationship between matrix metalloproteinase-9 expression and MRI characteristics of glioma
Lihua LIU ; Ming ZHANG ; Yuan WANG
Chinese Journal of Medical Imaging Technology 2009;25(12):2197-2200
Objective To investigate the levels of matrix metalloproteinase-9 (MMP-9) expression in different grades of glioma and the relationship with MRI characteristics. Methods Thirty-one patients of glioma confirmed pathologically were divided into two groups: low grade group (grade Ⅰ and Ⅱ, n=20) and high grade group (grade Ⅲ and Ⅳ, n=11). MMP-9 expression levels were evaluated with immunohistochemical staining. Plain and enhanced MR scan were performed in all patients before operation. Peritumoral edema index (EI), enhance percentage (EP) and the tumor's maximum diameter were recorded as characteristics of MRI. Results The expression levels of MMP-9, EI, EP and the tumor's maximum diameter were significantly higher in the high grade group than those in the low grade group (t=6.312, 4.405, 6.286 and 5.026, respectively, all P<0.05). The expression of MMP-9 were found significantly correlated to EI, EP and the maximum diameter of tumor (r=0.516, 0.554 and 0.676, respectively, all P<0.05). The expression levels of MMP-9 were significantly different between tumors with heterogeneity and even signal (t=2.637, P<0.05), but not between tumors with unclear border and clear border definition (t=0.906, P>0.05). Conclusion MMP-9 expression have close relationship with invasion of glioma. EI, EP, the maximum diameter and signal of tumor can reflect the level of MMP-9 expression, and may be used to estimate tumor's malignant behavior, being able to provide the evidence for future clinical operation.
8.The effect of pigment epithelium-derived factor on apoptosis of glioma cells
Tao ZHANG ; Ming GUAN ; Yuan Lü
Chinese Journal of Laboratory Medicine 2008;31(4):421-424
Objective To assess the impact of pigment epithelium-derived factor(PEDF)on the proliferation and apoptosis of the glioma cells by detecting expression of apoptosis related proteins.Methods U87 cells were treated with PEDF(1000μg/ml,U87PEDF),or without PEDF(U87com0),cell proliferation assays were performed by MTT assay to test the effect of PEDF on proliferation of glioma cells;Apoptosis assays were performed by flow-cytometric analysis;Western-blot Was used for evaluating the expression of p16 protein.Results The induced inhibitony rates of glioma cells by PEDF were(54.29±0.62)% Compaxed with the control(t=2.63,P<0.05).The apoptosis assay showed that(21.84±0.36)% of PI- negative/annexin V-positive Was present in the U87 PEDF cells.The appoptosis was associated with the incteases of p16 protein(0.82±0.09)compared with tlle control(0.43±0.03,P<0.05).Conciusion PEDF may play a significant role in apoptosis regulation and proliferation of glioma cell accompanied with the increase of the p16 protein.
9.The inhibitory effect of pigment epithelium-derived factor on migration of gliomas
Tao ZHANG ; Ming GUAN ; Yuan Lü
Chinese Journal of Laboratory Medicine 2008;31(2):200-203
Objective To assess the impact of pigment epithelium-derived factor(PEDF) on the migration of the glioma cells.Methods PEDF(100 ng/ml)was added to U87 cells(U87PFDF),and VEGF of 0.25μg/ml was added to U87PEDF+VEGF while U87 cells as control(U87con).The cell migratory assav was used tbr evaluating its inhibitory migration rate of PEDF.Real time RT-PCR was used for evaluating the expression of Laminin-8 gene.Results The number of migratory cells was higher than those with added PEDF,and the inhibitory rate of migratory was 38% even in the presence of VEGF.Real time RT-PCR revealed that the mRNA expression levels of α4,β1,γl were(1.043±0.090),(0.823±0.012).(0.762±0.05) copy/μl,which were higher than those treated by PEDF(0.633±0.004),(0.442±0.005).(0.424±0.002)copy/μl,respectively (P<0.05).Conclusion PEDF could decrease the migmtory capacity of the glioma cells even in the presence of VEGF because of the regulation of Laminin-8 in part.
10.Combination treatment in acute myocardial infarction-thrombolysis and immediate early PTCA in acute myocardial infarction
Ming ZHANG ; Zhangquan LI ; Long YUAN
Journal of Interventional Radiology 2004;0(S2):-
Objective The study evaluated the efficiency and safety of a short-acting full-dose fibfinolytic regimen to promote early infarct-related artery (IRA) patency during the inherent delay experienced by infarction patients referred for angioplasty as the principal recanalization modality. Method Accepted aspirin and heparin, 75 patients were treated by an intravenous bolus of 20 mg recombined tissue-type plasminogen activator (rt-PA), then followed by 80 mg over 30 minutes. Patients were to undergo angiography as soon as possible following study drug. If the IRA was occlude (TIMI flow grade 0 or 1),or was open but with ≥50% stenosis, immediate early PTCA at the same time. The end point included patency rates on catheterzation laboratory (cath Lab) arrival, technical results when PTCA was performed, complication rates, clinical adverse events rates and left ventricular (LV) function by treatment assignment in two weeks. Results Patency on Cath lab arrival was 88% with combination treatment group (26% Thrombolysis in myocardia infarction trial TIMI-2, 66%TIMI-3), and 36%with primary PTCA group (20%TIMI-2, 16%TIMI-3), (P