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Objective To investigate the effects of ovarian induction with raloxifene(RAL)versus clomi-phene citrate(CC)on the endometrial receptivity in mouse endometrium during perimplantation period. Methods 48 female Kun-ming mouse were randomly divided into four groups in equal number:RAL 240 mg group,RAL 180 mg group,CC group,natural conception group(NC),all treated with ovulation induction after drug administration.Successfully mated female mouse were killed,and uterus samples were collected for HE stain-ing and immunohistochemistry. Results HE staining showed that the endometrial morphology in the RAL 180 mg group and RAL 240 mg group and NC group were better than that of CC group.The expressions of COX-2 and LP-AR3 in the RAL 180 mg group and RAL 240 mg group were similar to NC group,without significant difference among the three groups(P > 0.05). But in the CC group,it was statistically significantly lower than other three groups(P<0.05),indicating ovarian induction with RAL did not decrease the expressions of COX-2 and LPAR3 in endometrium. Conclusion The mechanism of ovulation induction with RAL is similar to CC,but RAL has fewer adverse effects on the endometrial receptivity compared with CC.
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Objective The mechanism of celecoxib in influencing the migration of vascular endothelial cells is still not clear.The aim of this study was to investigate the effect of celecoxib against migration of vascular endothelial cells and its mechanism.Methods Human umbilical vein endothelial cells (HUVECs) were obtained from the cell bank of Central Laboratory of Nanjing General Hospital of Nanjing Military Command.Transwell was used to measure the migration rate of HUVECs after the administration of 0μmol/L, 10μmol/L and 20μmol/L celecoxib.Immunofluorescence, western blot, and qRT-PCR were used to detect protein and mRNA expression of COX-2 and PTPRJ in HUVECs.Results The expression of COX-2, PTPRJ in HUVECs were detected by immunofluorescence.After the administration of 20μmol/L, 10μmol/L and 0μmol/L celecoxib, HUVEC migration rate was (12.35±3.61), (32.80±5.92) and (63.15±5.83) respectively, representing significant difference (P<0.01).COX-2 protein expression in 20μmol/L group (0.16±0.03) and 10μmol/L group (0.36±0.05) decreased significantly compared with that of 0μmol/L group (0.77±0.07) (P<0.01).Moreover, COX-2 protein expression in 20μmol/L group significantly decreased compared with that of 10μmol/L group(P<0.05).PTPRJ protein expression in 20μmol/L group (0.82±0.05) and 10μmol/L group (0.51±0.02) was respectively higher than that of 0μmol/L group (0.27±0.04) (P<0.01).Moreover, PTPRJ protein expression in 20μmol/L group significantly increased compared with that of 10μmol/L group (P<0.05).COX-2 mRNA expression in 20μmol/L group (0.06±0.02) and 10μmol/L group (0.22±0.05) decreased significantly compared with that of 0μmol/L group (1.05±0.13) (P<0.01).PTPRJ mRNA expression in 20μmol/L group (60.27±11.31) and 10μmol/L group (16.50±3.18) increased significantly compared with that of 0μmol/L group (0.99±0.25) (P<0.01).Conclusion Celecoxib inhibits the migration of vascular endothelial cells, which may be related to the inhibition of COX-2 expression and the up-regulation of PTPRJ expression in vascular endothelial cells.
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Aim To investigated the possible effect of COX-2 on the BMP9-induced activation of PI3K/Akt signal in progenitor cells.Methods The activity of alkaline phosphatase(ALP) was measured using histochemical staining or chemiluminescence.The mRNA level of ALP was determined using real-time PCR assay.The protein levels of osteopontin(OPN), osteocalcin(OCN), COX-2, Akt1/2 and phosphorylated Akt1/2 were detected by Western blot.The mRNA level of COX-2 was assayed with RT-PCR, and the mineralization was measured with Alizarin Red staining.Results The ALP activity was apparently increased by BMP9 in C2C12 cells, as well as the protein level of OPN and OCN.The mineralization was also markedly induced by BMP9 in C2C12 cells.BMP9 increased the level of phosphorylated Akt1/2 greatly, although no substantial effect was observed on total protein level of Akt1/2.The BMP9-induced ALP activity was dramatically decreased by the inhibitor of PI3K.The mRNA and protein level of COX-2 were both increased by BMP9 in C2C12cells, and the BMP9-induced ALP activity and mineralization were greatly attenuated by the inhibitor of COX-2.The BMP9-induced phosphorylation level of Akt1/2 was increased by the exogenous expression of COX-2, but decreased by the inhibitor of COX-2.Conclusion Activation of PI3K/Akt signaling may be a critical event in BMP9-induced osteogenic differentiation, and this process may be mediated by the BMP9-upregulated COX-2 in stem cells at least.
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Objective To investigate the expression and significance of aromatase P450,COX-2,ER and PR in the patients with adenomysis.Methods The immunohistochemistry staining was used to detect the expression of aromatase P450,COX-2,ER and PR in ectopic endometrium and eutopic endometrium of 30 patients with adenomyosis and 30 cases in control group.Results The expression of aromatase P450,COX-2 in ectopic endometrium were significantly higher than those in eutopic endometrium (all P ＜ 0.05) ; The expression of ER,PR in ectopic endometrium were significantly lower than those in eutopic endometrium (all P ＜ 0.05),excepted the expression of PR in eutopic endometrium,the expressions of both ER and PR lose their periodical cycle.There was positive correlation between the expression of aromatase P450 and COX-2 in adenomysis group(P ＜ 0.05).In adenomyosis,the expression of aromatase P450,COX-2,ER and PR in dysmenorrhea subgroup were significantly higher than those in non-dys menorrhea subgroup(all P ＜ 0.05).Conclusion Aromatase P450,COX-2 and ER play important roles in the genesis and development of adenomyosis and dysmenorrheal,PR is not the main pathogenic factors of adenomyosis.The expressions of aromatase P450,COX-2 and ER in adenomyosis have nothing to do with endometrial cyclical change and are not subject to the regulation of ovarian hormones.
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Objective To investigate the expressions of cycloxygenase-2 (COX-2 ),vascular endothelial growth factor (VEGF),matrix metalloproteinase (MMP2 )and micro-vessel density (MVD)in papillary thyroid carcinoma (PTC)and the relationship between their expressions and clinicopathological features,so as to evaluate the malignancy and prognosis of PTC.Methods The expressions of COX-2,MMP2 and VEGF and MVD count in 32 cases of PTC and 18 cases of normal thyroid tissues were detected by immunohistochemical staining.Their relationship with clinicopathological characteristics was analyzed.Results ① The expression of COX-2,MMP2, VEGF and MVD in PTC was as follows:M(Q 3 -Q 1 )=5(1),M(Q 3 -Q 1 )=5.5(2),M(Q 3 -Q 1 )=5.5(1)and M (Q 3 -Q 1 )= 28 (5.75 ),respectively.It differed significantly from that in control group (P 0.5).Conclusion The high expressions of COX-2, VEGF and MMP2 in thyroid tissues may result in the occurrence of PTC and lymph node metastasis,which is related to the regulation of tumor new vessels.Detecting these expressions are of value in evaluating the malignancy and prognosis of PTC.
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Objective To study the effect of selective COX-2 inhibitor NS-398 on IL-1α and TNF a expression in HaCaT cells induced by UVA/UVB,and further to explore the mechanism on anti human skin photo damage. Methods The subcuhured HaCaT cells were divided into three groups:simple illuminated group was exposed to UVA/UVB directly,NS-398 interfered group was exposed to UVA/UVB after being treated with NS-398 in different concentrations,and the control group was cultured in normal without any treatment.The expression of IL -1α and TNF-α in supernarant was detected by ELISA kit.Results The level of IL-1α and TNF-α expression in supernatant from simple illuminated group was remarkably higher than that in the control group,NS-398 interfered group showed much lower level than the simple illuminated one,and the expression of IL-1α and TNF-α was dependent on the concentration of NS-398.Conclusions NS-398 can reduce IL-1α and TNF-α expression in HaCaT cells induced by ultraviolet rays,suggesting the possibility of anti human skin photo- damage effect.
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Objective To explore the role of COX-2 and VEGF in oncongensis and development of gestation-al trophoblastic disease,and evaluate prognosis of gestational trophoblastic tumor. Methods The expression of COX-2 and VEGF in normal chorion of early gestation and in gestational trophoblastic disease were detected by immunohis-tochemistry. Results In gestational trophoblastic tumor group,the positive rate of COX-2 and VEGF were significantly highter than that of normal chorion of early gestation group and the hydatidiform mole group respectively ( P < 0.01). There were positive correlation between COX-2 and VEGF in gestational trophoblastic tumor ( r = 0.795, P < 0.01). Conclusion The collaborative and over expression of COX-2 and VEGF were probably associated with the malignant change of trophoblastic cell,which suggest the worse prognosis of the gestational trophoblastic disease.
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Objective:The study was to investigate the effects of epidermal growth factor receptor (EGFR) antibody (cetuximab,C225) combined with cyclooxygenase 2(COX-2)inhibitor (nimesulide) on the proliferation and apoptosis of colon cancer HT-29 cells, and explore the potential molecular mechanism. Methods:C225 and nimesulide alone or in combination were incubated with HT-29 cells. MTT assay was used to measure the cell proliferation. AO/EB staining and flow cytometry were used to measure the cell apoptosis. RT-PCR was used to detect the COX-2 and non steroidal anti-inflammatory drug-activated gene (NAG-1) mRNA expression levels. The expression of Akt and phosphor-Akt protein was examined by Western blotting. Results:The inhibitory effect of nimesulide combined with C225 was significantly stronger than that of nimesulide alone [(72.8±2.3)% vs (51.8±1.8)% , P<0.05]at 48 h. Typical changes of apoptosis in HT-29 cells were observed in nimesulide combined with C225 treatment group. The apoptosis rate of combined group was significantly higher than that of single nimesulide group [(57.67±0.86)% vs(33.27±1.47)%]and single C225 group [(6.27±0.55)%,P<0.05]. C225 down-regulated the expression of COX-2 mRNA. The expression of NAG-1 mRNA was up-regulated in all treatment groups and the expression of phosphor-Akt was significantly down-regulated in combined treatment group than single nimesulide or C225 group. Conclusion:Nimesulide combined with C225 has obvious synergistic effects in inducing apoptosis. The potential mechanisms may be that EGFR signaling pathway is involved in the regulation of cycloxygenase-2 expression in HT-29 cells and finally influence the proliferation and apoptosis of HT-29 cells through the up-regulation of NAG-1 and down-regulation of phosphor-Akt expression.
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AIM: To investigate the association between cycloxygenase-2 (COX-2) expression and VEGF intervention as well as the inhibitory effect of Meloxicam on the cultured human pterygium fibroblasts (HPF).METHODS: Expression of COX-2 was measured by immunohistochemistry in the cultured HPF from twenty excised pterygium cases. Expression of COX-2 in HPF was measured by Western blot following the treatment of vascular endothelial growth factor (VEGF) at the different concentrations. In addition, the effect of Meloxicam on proliferation of HPF was studied by adding the different concentrations into the cultured HPF plates by Mono-nuclear cell direct cytotoxicity (MTT) reduction assay.RESULTS: COX-2 expression was present in the cultured HPF. The level of the expression increased following VEGF treatment. The proliferation of the cultured HPF decreased following addition of the different concentrations of Meloxicam (from 75μ mol/L to 300μ mol/L) and the magnitude of the inhibition was dose-time dependent.CONCLUSION: COX-2 levels in the cultured HPF werepositively associated with VEGF stimulation and Meloxicam was inhibitory to HPF proliferation.
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Objective:To explore the effects of Shenqi Compound Recipe on the expression of Cycloxygenase-2 (COX-2)mRNA in aorta in GK rats.There were five groups:GK group,model group,atorvastatin group,Shenqi Compound Recipe group and normal control group.During the experiment periods,each group was administrated correspondent substance respectively for 35 days.Serum concentrations of C reactive protein(CRP)were determined by ELISA.The mRNA expressions of COX-2 in aorta were detemined by reverse transcriptase PCR(RT-PCR).Results:Compared with model group,concentrations of CRP in serum and the mRNA expression of COX-2 all decreased in atorvastatin group and Shenqi Compound Recipe group(P
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AIM: To examine COX-2 expression in esophageal carcinoma,and to study relationships between COX-2 expression and clinicopathological features and prognosis of esophageal carcinoma patients.METHODS: 89 paraffin-embedded tissue samples from patients with esophageal carcinoma were collected,its clinicopathological features such as tumour differentiation,depth of invasion,length and site of the tumor,regional lymph node metastases,distant metastasis were recorded.Survival time of 81 cases were also recorded.By SP immunohistochemistry method,the expression of COX-2 in tumor samples was examined.RESULTS: COX-2 expression in esophageal carcinoma was markedly higher than that in nomal esophagus,the expression was higher in less differentiated and deeper invaded cases(P0.05).Cases of esophageal carcinoma with lower COX-2 expression had longer survival time than those with higher COX-2 expression(P