AIM： Prostaglandin G/H synthase 2 （PTGS2 or COX2） is one of the key factors in the cellular response to inflammation. PTGS2 is expressed in the affected intestinal segments of patients with inflammatory bowel disea...AIM： Prostaglandin G/H synthase 2 （PTGS2 or COX2） is one of the key factors in the cellular response to inflammation. PTGS2 is expressed in the affected intestinal segments of patients with inflammatory bowel diseases （IBD）. In IBD patients, non-steroidal anti-inflammatory drugs, which have been shown to reduce both the production and activity of PTGS2, may activate IBD and aggravate the symptoms. We aimed at examining genetic variants of PTGS2 that may be risk factors for IBD. METHODS： We genotyped 291 individuals diagnosed with IBD and 367 controls from the Dutch population for the five most frequent polymorphisms of the PTG52 gene. Clinical data were collected on all patients. DNA was extracted via normal laboratory methods. Genotyping was carried out using multiplex PCR followed by the Invader Assay and the 5＇ exonuclease assay （TaqMan）. New polymorphism screening was performed by pre-screening with denaturing high-performance liquid chromatography, followed by fluorescent sequencing. RESULTS： Allele 5209G was weakly associated with Crohn＇s disease （odds ratio [OR] 1.63, 95% confidence interval [CI] 1.03-2.57）, and allele 8473T with ulcerativecolitis （OR 1.50, 95%CI 1.00-2.27）. The haplotype including both alleles showed a strong association with IBD （OR 13.15, 95%CI 3.17-116.15）. This haplotype, while rare （-0.3%） in the general population, is found more frequently in patients （3.5%）. CONCLUSION： Our data suggest that this haplotype of PTGS2 contributes to the susceptibility of IBD.展开更多
Objective:To observe the effects of electroacupuncture(EA)on uterine prostaglandin F2α(PGF2α),cyclooxygenase 2(COX-2)and nuclear factorκB(NF-κB)in rats with primary dysmenorrhea(PD)and to discuss the possible mech...Objective:To observe the effects of electroacupuncture(EA)on uterine prostaglandin F2α(PGF2α),cyclooxygenase 2(COX-2)and nuclear factorκB(NF-κB)in rats with primary dysmenorrhea(PD)and to discuss the possible mechanism in EA intervening PD.Methods:Forty Sprague-Dawley female rats were randomly divided into a blank group,a model group,an EA group and an ibuprofen group,with 10 rats in each group.The PD model was established using estradiol benzoate combined with oxytocin in the model group,EA group and ibuprofen group.At the same time of modeling,rats in the EA group were given EA at Guanyuan(CV 4)and Sanyinjiao(SP 6)once a day for 20 min each time for 10 consecutive days.Ibuprofen was intragastrically administered once a day for 10 consecutive days in the ibuprofen group.The same amount of normal saline was intragastrically administered once a day for 10 consecutive days in the blank group and model group.The number of writhing of rats in each group within 30 min was compared on the 11th day just after the interventions.The uterine homogenate supernatant was separated and the PGF2αlevel was detected by enzyme-linked immunosorbent assay.Western blot was applied for the detection of the expression levels of COX-2,phospho-NF-κB p65 and NF-κB p65 proteins in uterine tissues.Results:Compared with the blank group,the number of writhing in the model group increased significantly(P<0.01),and the expression levels of PGF2α,COX-2,phospho-NF-κB p65 and NF-κB p65 proteins in uterine tissues were significantly increased(all P<0.01).Compared with the model group,the number of writhing in the EA group and ibuprofen group were significantly reduced(both P<0.01),and the expression levels of PGF2αand COX-2 protein in uterine tissues were significantly reduced(both P<0.01).Compared with the model group,the phospho-NF-κB p65 level in uterine tissues in the EA group was significantly reduced(P<0.01).Compared with the ibuprofen group,the phospho-NF-κB p65 level in the EA group was significantly reduced(P<0.01).Conclusion:The mechanism of EA for PD rats may be related to inhibiting the phosphorylation of NF-κB and reducing the levels of COX-2 and PGF2αin uterine tissues.展开更多
基金Supported by The Grants from the International Agency for Research on Cancer (Special Training Award to DGC)the French Association for Research on Cancer (grant #7478)the Crohn's and Colitis Foundation of America (to ASP)
文摘AIM： Prostaglandin G/H synthase 2 （PTGS2 or COX2） is one of the key factors in the cellular response to inflammation. PTGS2 is expressed in the affected intestinal segments of patients with inflammatory bowel diseases （IBD）. In IBD patients, non-steroidal anti-inflammatory drugs, which have been shown to reduce both the production and activity of PTGS2, may activate IBD and aggravate the symptoms. We aimed at examining genetic variants of PTGS2 that may be risk factors for IBD. METHODS： We genotyped 291 individuals diagnosed with IBD and 367 controls from the Dutch population for the five most frequent polymorphisms of the PTG52 gene. Clinical data were collected on all patients. DNA was extracted via normal laboratory methods. Genotyping was carried out using multiplex PCR followed by the Invader Assay and the 5＇ exonuclease assay （TaqMan）. New polymorphism screening was performed by pre-screening with denaturing high-performance liquid chromatography, followed by fluorescent sequencing. RESULTS： Allele 5209G was weakly associated with Crohn＇s disease （odds ratio [OR] 1.63, 95% confidence interval [CI] 1.03-2.57）, and allele 8473T with ulcerativecolitis （OR 1.50, 95%CI 1.00-2.27）. The haplotype including both alleles showed a strong association with IBD （OR 13.15, 95%CI 3.17-116.15）. This haplotype, while rare （-0.3%） in the general population, is found more frequently in patients （3.5%）. CONCLUSION： Our data suggest that this haplotype of PTGS2 contributes to the susceptibility of IBD.
文摘Objective:To observe the effects of electroacupuncture(EA)on uterine prostaglandin F2α(PGF2α),cyclooxygenase 2(COX-2)and nuclear factorκB(NF-κB)in rats with primary dysmenorrhea(PD)and to discuss the possible mechanism in EA intervening PD.Methods:Forty Sprague-Dawley female rats were randomly divided into a blank group,a model group,an EA group and an ibuprofen group,with 10 rats in each group.The PD model was established using estradiol benzoate combined with oxytocin in the model group,EA group and ibuprofen group.At the same time of modeling,rats in the EA group were given EA at Guanyuan(CV 4)and Sanyinjiao(SP 6)once a day for 20 min each time for 10 consecutive days.Ibuprofen was intragastrically administered once a day for 10 consecutive days in the ibuprofen group.The same amount of normal saline was intragastrically administered once a day for 10 consecutive days in the blank group and model group.The number of writhing of rats in each group within 30 min was compared on the 11th day just after the interventions.The uterine homogenate supernatant was separated and the PGF2αlevel was detected by enzyme-linked immunosorbent assay.Western blot was applied for the detection of the expression levels of COX-2,phospho-NF-κB p65 and NF-κB p65 proteins in uterine tissues.Results:Compared with the blank group,the number of writhing in the model group increased significantly(P<0.01),and the expression levels of PGF2α,COX-2,phospho-NF-κB p65 and NF-κB p65 proteins in uterine tissues were significantly increased(all P<0.01).Compared with the model group,the number of writhing in the EA group and ibuprofen group were significantly reduced(both P<0.01),and the expression levels of PGF2αand COX-2 protein in uterine tissues were significantly reduced(both P<0.01).Compared with the model group,the phospho-NF-κB p65 level in uterine tissues in the EA group was significantly reduced(P<0.01).Compared with the ibuprofen group,the phospho-NF-κB p65 level in the EA group was significantly reduced(P<0.01).Conclusion:The mechanism of EA for PD rats may be related to inhibiting the phosphorylation of NF-κB and reducing the levels of COX-2 and PGF2αin uterine tissues.
