The dynamic changes of the serum levels of interleukin-1β, tumor necrosis factor-α, cyclooxygenase-2 in acute gouty arthritis patients / 中华风湿病学杂志

Objective To investigate the dynamic changes of serum interleukin (IL)-1β,tumor necrosis factor (TNF)-α,cyclooxygenase (COX)-2 levels in patients with acute gouty arthritis with various severityes and to provide evidence for the course of anti-inflammatory drug used in patients with acute gouty arthritis.Methods Ninety patients with gouty arthritis were randomly selected including sixty acute gouty arthritis patients and thirty gout patients in remission (observation group 3).Sixty acute gouty arthritis patients were divided into severe (observation group 1) and mild (observation group 2) subgroups according to the chief complaints and pain score points (VRS-4 method).All acute gouty arthritis patients were given the same dose and duration of etoricoxib and colchicine (14 days in all).Serum IL-1β,TNF-α,COX-2 levels were detected by enzyme-linked immunosorbent assay (ELISA) after the 1,3,7,10 and 14 days after onset.The 2-tailed independent samples t test was used for the analysis of measurement data.ANOVA were adapted for the comparison between groups.Results The serum levels of IL-1β,TNF-α in the observation group 1,2 were significantly higher than those in the control group in day 1 and 7 (P＜0.01),and almost completely returned to normal at day 10 to 14 day anti-inflammatory therapy.The serum COX-2 levels in observation group 1,2 were significantly higher than those in the control group (P＜0.01) in day 1 to 3,and returned to normal at day 7 to 10 after anti-inflammatory therapy.There were no significant differences between observation group3 and the control group (t=-0.880,-1.201,-0.548; P=0.383,0.235,0.586).② The serum levels of IL-1β,TNF-α were significantly higher in observation group 1 than those in observation group 2 [(24±5) pg/ml and(19±3) pg/ml,(323±84) ng/ml and (234±29) ng/ml; P=0.001,0.002],while there was no significant differences between observation group 2 and the control group (P=0.357).The serum COX-2 levels in observation group 1 were significantly higher than those in observation group 2 at day 7 [(12.9±2.0) pg/ml and (9.1±1.6) pg/ml],while there was no significant difference between observation group 2 and the control group (P=0.941).Conclusion Inflammatory factor can return to normal completely after anti-inflammatory therapy for acute gouty arthritis for 10 to 14 days.This study provides evidence for the course of anti-inflammatory drug used in patients with acute gouty arthritis.

Expression of NF-κB,COX-2 and the MMP-9 in hypopharyngeal carcinoma / 肿瘤研究与临床

Objective To study the quantitative expression and the correlation of the NF-κB p65,COX-2 and MMP-9 Drotein in the hypopharyngeal carcinoma tissue.Methods FCM method was performed to detect the quantitative expression of the NF-κB p65,COX-2 and MMP-9 protein in 48 cases of hypopharyngeal carcinoma fresh sample and 48 cases of para-carcinoma tissue.Fluorescence Index wasdeftned as the quantitative expression index of the three proteins.Results The quantitative expression of the NF-κB p65,COX-2 and MMP-9 in hypopharyngeal carcinoma tissues(1.16,1.32 and 1.26) was remarkably higher than in para-carcinoma(1.03,1.04 and 1.04).The quantitative expression of three proteins in metastasis group was obviously higher than in non-metastasis group.The expression of NF-κB p65 and COX-2 protein in hypopharvngeal carcinoma tissues was positively related (P＜0.05). Conclusion The high expression of NF-κB p65 and COX-2 is closely related in hypopharyngeal carcinoma tissues.NF-κB p65 might improve the expression of COX-2.

Expression of COX-2 and VEGF and their relation with cervical lymph metastases of papillary thyroid carcinoma / 中国耳鼻咽喉头颈外科

OBJECTIVE To investigate the relation of cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) expression with cervical lymph metastases in papillary thyroid carcinoma. METHODS The expression of COX-2 and VEGF in 79 specimens of papillary thyroid carcinoma were evaluated with SP immunohistochemical methods. In all the 79 cases, there were 46 cases with cervical lymph node metastases and 33 cases without cervical lymph node metastasis. RESULTS The positive expression rates of COX-2 and VEGF in the cases with cervical metastases were 81.6 % and 86.8 % respectively, and in the cases without cervical lymph metastases were 54.5 % and 66.7 % respectively. There was a significant difference in the positive expression rates of COX-2 and VEGF between two groups (P

Inflammatory reaction and expression of adhesion molecules and cyclooxygenase-2 after reperfusion in focal cerebral ischemia rats / 中华神经科杂志

Objective To clarify the possible role of cyclooxygenase-2(COX-2), intercellular adhesion molecule-1(ICAM-1) and E-selectin in the inflammatory injury induced by cerebral ischemia and reperfusion. Methods The focal cerebral ischemia and reperfusion model was induced by a suture occlusion of the right middle cerebral artery. The rats were randomly assigned to four groups: sham operated group; 4 h,22 h and 46 h reperfusion groups. The expression of ICAM-1, E-selectin and COX-2 were detected by immuno-Western blot and immunohistochemical method. Myeloperoxidase (MPO) activity was detected by a commercial MPO kit. Results In the right cortex and striatum of the sham operated group and the 4 h, 22 h and 46 h reperfusion groups, the relative values of COX-2 were 0.7642?0.0763, 1.5382?0.1047, 1.6491?0.3265, 1.8020?0.3719 and 0.7104?0.0891, 2.2061?0.2143, 1.7897?0.3537, 1.8018?0.5703 respectively; the relative values of ICAM-1 were 0.6845?0.0531, 0.9115?0.0422, 0.9426?0.0407, 1.0756?0.0467 and 0.6583?0.0361, 0.9439?0.0746, 0.9975?0.1532, 0.8808?0.0497 respectively. Significant increase of MPO activity and expression levels of COX-2, ICAM-1 and E-selectin were shown from 4 h to 46 h in the striatum and cortex of rats following reperfusion. Immunohistochemical staining showed that the number of ICAM-1 and E-selectin positive vessels was increased in the border of ischemia. The positive cells of COX-2 were almost neurons in the cortex, but in the striatum, the cells were neurons, glias and vessel endothelium. Positive correlation between COX-2 and ICAM-1 expression in the cortex(n=6,r=0.973,P

Expression of cyclooxygenase in rat spinal cord with acute contusion / 中华创伤骨科杂志

Objective To characterize the localization and expression of cyclooxygenase (COX) in thoracic spinal cord before and after acute contusion. Methods 48 Sprague Dawley rats, 250 to 300 g in weight, were used for the study. The injuries of spinal cord were induced at the T8,9 level by dropping a weight of 10.24 g form a height of 50 mm (Allen’ s model). All the animals with spinal cord injury were sacrificed at time points ranging from 2 to 48 hours (2, 4, 8, 16, 24, and 48 hours) after management. Expressions of COX- 1 and COX- 2 in the thoracic spinal cords, normal and injured, were studied with immunohistochemistry. Results COX- 1 immunoreactivity was found to constitutively express in cytoplasmof glial cells and neuropils in white matter. Tiny COX- 1 immunoreactivity was found in glial cells, neuropils and neurons in the gray substance. It was found that COX- 2 immuno- labeling expressed constitutively in cytoplasm and closely surrounding the nucleus of neurons in both ventral and dorsal horns. Contusion to the spinal cord did not result in changes of COX- 1 protein localization and expression according to evaluation of immunohistochemistry. COX- 2 immunoreactivity improved only in neurons 4 hours following contusion. The positive COX- 2 protein reactivity reached the peak 24 hours after contusion. Conclusions In contrast to their expression in the majority of peripheral tissues, both COX isoforms express constitutively in the normal rat thoracic spinal cord. The major isoform of COX involved in the secondary spinal cord injury is COX- 2 after the spinal cord is mechanically injured.

Regulation of Cytokine and Cyclooxygenase Expression in Palatine Tonsils from Recurrent Tonsillitis in Children / 대한이비인후과학회지

BACKGROUND AND OBJECTIVES: Prostanoids are converted from arachidonic acid via cyclooxygenase (COX), which has two isoforms, COX-1 and COX-2. It has recently been shown that prostanoids may have a novel role in mediating cytokine release in some cells. We investigated the baseline expression and regulation of interleukin (IL)-6, IL-8, COX-1 and COX-2 in palatine tonsils from pediatric recurrent tonsillitis. MATERIALS AND METHOD: Palatine tonsils were obtained from 12 children with recurrent tonsillitis during elective tonsillectomy and adenoidectomy. Tonsil cells were incubated with culture media only or with proinflammatory cytokines (IL-1beta and TNF-alpha) or inhibitors of transcription (actinomycin D) or translation (cycloheximide). In these groups, IL-6, IL-8, COX-1, COX-2 mRNAs and COX-1, COX-2 proteins were analyzed by reverse transcriptasepolymerase chain reaction and Western blot, respectively. RESULTS: The baseline expressions of IL-6, IL-8, COX-1 and COX-2 mRNAs were detected although tonsillectomy was done in the silent phase without acute infection. The culture of tonsil cells with pro-inflammatory cytokines increased the expression of IL-6, IL-8 and COX-2 mRNAs and COX-2 protein. The expressions of IL-6, IL-8 and COX-2 mRNAs and COX-2 protein induced by pro-inflammatory cytokines was significantly inhibited by actinomycin D, not by cycloheximide. CONCLUSION: Tonsil cells isolated from pediatric recurrent tonsillitis are in constantly inflamed state. The expression of COX-2 mRNA induced by pro-inflammatory cytokines is accompanied by the induction of IL- 6 and IL-8 mRNAs. The regulation of these effects occurs at the transcriptional level. Furthermore, the regulation of cytokines and COX-2 may provide an understanding of mechanism of prostanoids synthesis in chronic tonsillitis.

Interleukin-1beta stimulates matrix metalloproteinase-2 expression via a prostaglandin E2-dependent mechanism in human chondrocytes

IL-1beta is known promote cyclooxygenase-2 (COX- 2) and matrix metalloproteinase-2 (MMP-2) expression. This study focuses on the characterization of the signaling cascade associated with IL-1beta-induced matrix metalloproteinase-2 (MMP- 2) regulation in human chondrocytes. The decrease in collagen levels in the conditioned media was prevented by a broad spectrum MMP inhibitor, suggesting that IL-1beta promotes the proteolytic process leading to MMP-2 activation. IL-1beta-related MMP-2 expression was found to be dependent on prostaglandin E2 (PGE2) production. In addition, the induction of COX-2 and MMP-2 was inhibited by the pretreatment of chondrocytes with a SB203580 or Ro 31-8220, indicating the involvement of protein kinase C (PKC) or p38 mitogen-activated protein kinase (MAPK). However, there is no cross-talk between PKC and p38 MAPK in the IL-1beta-induced MMP-2 activation. Taken together, these results demonstrated that IL-1beta induces MMP-2 expression through the PGE2-dependent mechanism in human chondrocytes.

Peripheral Analgesic and Anti-inflammatory Effects of Diclofenac, SC-560 and NS-398 on Acute Arthritic Model in Rats / 대한마취과학회지

BACKGROUND: Non-steroidal anti-inflammatory drugs (NSAIDs) are generally attributed to suppression cyclooxygenase enzymes, leading to decreased products of the arachidonic acid cascade. Since the discovery of two isoenzymes of cyclooxygenase, inhibition of cyclooxygenase-2 has been suggested to be responsible for therapeutic effects of NSAIDs without side effects. In the present study, to investigate the extent to peripheral nociception and inflammation of cyclooxygenase-1 and cyclooxygenase-2, diclofenac (non-selective inhibitor), SC-560 (selective cyclooxygenase-1 inhibitor) and NS-398 (selective cyclooxygenase-2 inhibitor) are injected intra-articularly on acute arthritic model in rats. METHODS: Arthritis was induced with 2% lamda-carrageenan (suspended in 50microliter normal saline) into the right knee joint cavity under enflurane anesthesia (2-4%). Before and after the injection, rats were allowed to walk freely through a pathway constructed to record weight load by means of 8 weight sensors (strain gauge type) attached to 8 plates which function independently. The weight load, diameter of both knee joints and weight of rat were measured at each test. At 4 hours and 30 minutes, diclofenac, SC-560 and NS-398 dissolved in 10% dimethyl sulfoxide were injected intra-articularly (50microgram/50microliter). RESULTS: The weight loads increased in diclofenac group at 6 and 9 hours and in NS-398 group at 24 and 48 hours after induction of arthritis. The diameter ratio decreased in diclofenac group at 12 hours after induction of arthritis. CONCLUSIONS: These results suggest that peripheral nociception and inflammation in acute model of arthritis in rats are likely related with both cyclooxygenase-1 and cyclooxygenase-2 pathways.

Expression of Cyclooxygenase-2 and Its Correlation with Clinicopathologic Factors of Ampulla of Vater Cancer

There has been no report for the expression of cyclooxygenase-2 (COX-2) and its clinicopathologic and biologic significance in ampulla of Vater cancer. This study was aimed for the clarification of COX-2 expression and its biologic roles in ampulla of Vater cancer. Fourty-six patients with ampulla of Vater cancer were enrolled and their COX-2 expression and clinicopathologic features were analyzed. The median age of patients was 60 yr and the mean duration of follow-up was 35 months (range: 14-82 months). Immunohistochemical stainings for COX-2, Ki-67, CD34 and TUNEL staining were performed. The immunoreactive COX-2 expression was present in 24 (52.2%) patients of ampulla of Vater cancer and mainly localized in cytosolic and perinuclear region. There was no significant difference in the length of survival between COX-2 postive and negative group (p=0.9420 by Log Rank test). Also, there were no significant differences of proliferation index (p=0.326), apoptotic index (p=0.764) and microvessel density (p=0.135) between COX-2 positive and negative group. Initial pTNM stage (p=0.0028 by Log Rank test) and blood transfusion over 4 pints during operation (p=0.0254 by Log Rank test) were independent prognostic factor in patients with ampulla of Vater cancer. It is suggested that immunoreactivity of COX-2 is not correlated with clinicopathologic and biologic features of ampulla of Vater cancer.

Dexamethasone differentiates NG108-15 cells through cyclooxygenase1 induction

Cyclooxygenase (COX) is a key enzyme in the conversion of arachidonic acid into prostanoids which participate in various cellular functions including apoptosis, mitogenesis, inflammation, immune modulation and differentiation. Moreover, the synthetic glucocorticoid, dexamethasone has immune modulating and anti-inflammatory effects in vivo. Recently, dexamethasone was found to enhance retinoic acid-induced neuronal differentiation. In this study, we investigated the mechanisms of dexamethasone-mediated neuronal differentiation. Immunoblotting and morphological analysis demonstrated that dexamethasone induced neuronal differentiation through COX 1 induction. This phenomenon was inhibited by indomethacin, a COX inhibitor. In addition, the addition of exogenous prostaglandin E2 (PGE2), a substance produced by the COX-mediated pathway, triggered neurite outgrowth of cells treated with COX inhibitor. Taken together, COX 1 appears to play an important role in dexamethasone-mediated neuronal differentiation.

The Expression of Cyclooxygenase-2 in Several Epidermal Tumors / 中华皮肤科杂志

Objective To explore the expression of cyclooxygenase-2 (COX-2) in different epidermal tumors and its significance. Method The expression of COX-2 was detected by immunohistochemical staining of skin specimens from 10 cases of basal cell carcinoma (BCC), 8 squamous cell carcinoma (SCC), 8 Bowen′s disease (BD), 12 seborrheic keratosis (SK) and 10 normal volunteers. Results Compared with normal epidermal cells, COX-2 expression was significantly increased in BCC, SCC and BD cells. Especially, COX-2 expression in SCC was the most intensive. COX-2 expression in SK cells was similar to that of normal epidermal cells. Conclusion The up-regulation of COX-2 expression may play a potential role in the pathogenesis of epidermal tumors.

Effects of Sex Hormones on Nociception and the Analgesic Action of NSAIDs / 대한마취과학회지

BACKGROUND: The effects of sex hormones on nociception and the analgesic actions of non-steroidal anti-inflammatory drugs (NSAIDs) in an acute arthritic pain model were investigated. METHODS: Rats were ovariectomized and randomly assigned to three experimental groups. The estrogen group (n = 45) received a 0.25 mg pellet of 17beta-estradiol, the placebo group (n = 45) received a 0.25 mg pellet of a placebo and the progesterone group (n = 45) received a 25 mg pellet of progesterone. Arthritis was induced by injecting 2% carrageenan into the knee joint cavity of the right hind leg. Before and after the injection, rats were allowed to walk freely through a weight load apparatus. The weight load and the weight of the rat were measured for each test. One hour after injection, ibuprofen or NS-398, dissolved in dimethyl sulfoxide, was injected intraperitoneally (1 mg/kg/ml). RESULTS: The carrageenan injection into the knee joint cavity of the right hind leg of the rat resulted in a significant decrease in the weight load on the injected leg. Estrogen-treated rats showed lower weight load reduction than the placebo and progesterone groups, NS-398 increased the weight load compared to rats not receiving NSAIDs. CONCLUSIONS: These results suggest that the nociceptive response after acute inflammation was reduced by estrogen, and that only NS-398 had a good analgesic effect in the placebo and progesterone groups. It is likely that the analgesic effect of NSAIDs on the estrogen group was unremarkable compared to those of the placebo and progesterone groups because of the antinociceptive action of estrogen.

NF-kappaB Binding Activity and Cyclooxygenase-2 Expression in Persistent betaCCI(4)-Treated Rat Liver Injury

The involvement of NF-kappaB binding activity is known to be important in the mechanism of acute liver injury and in the induction of cyclooxygenase (COX-2). This study was performed to evaluate NF-kappaB binding activity and the expression of COX-2 in chronic liver injury induced by carbon tetrachloride (betaCCI(4)). Liver tissues from Sprague - Dawley rats were collected at 1, 3, 5, and 7th week after intraperitoneal injection of 0.1 mL of betaCCI(4)/100 g body weight twice a week. Reactive oxy-gen species (ROS) were measured in the postmitochondrial fraction by dichlorofluorescein formation with a fluorescent probe. An electrophoretic mobility shift assay was performed for NF-kappaB binding activity. Western blot was performed to measure the level of COX-1, COX-2, p65, p50, and I B proteins. ROS and NF-kappaB activity increased during the CCl4-induced chronic liver injury. The expression of nuclear p65 protein and p50 protein increased compared with that of the control, while the cytoplasmic I B protein decreased as the inflammation persisted. The expression of COX-2 in betaCCI(4)-treated rat liver increased compared with that of the control. It could be suggested that ROS produced by betaCCI(4) treatment increased NF-kappaB binding activity and thereby COX-2 expression, and these might be implicated in the progress of chronic liver damage.

Cyclooxyenase-2 expression in endometrium carcinoma / 中华妇产科杂志

Objective To investigate the expression of cyclooxyenase 2 (COX 2)in carcinogensis and development of endometrium carcinoma Methods Immunostainings, westernblotting and quantitve reverse transcription polymerase chain reaction (RT PCR) assay were utilized to measure levels of protein and mRNA expression of COX 2 in following five study groups: 25 cases with proliferative phase, 25 cases with secretory phase,25 cases with endometritis, 23 cases with atypical proliferative phase and 34 cases with endometrium carcinoma Results COX 2 expression of both RNA and protein in patients with endometrial carcinoma was higher significantly than patients with proliferative phase, secretary phase,endometritis,atypical proliferate phase Immunostaining score was 5 46?0 12 vs 3 20?0 18,4 78?0 12,6 10?0 25,8 70?0 93, average absorbent value was 0 75?0 23 vs 0 41?0 45, 0 56?0 31, 1 10?0 56,1 46?0 41;concentration of mRNA [(93?8) vs (65?11),(79?6),(299?11),(493?30) fpg/?g respectively] Successively the expression of COX 2 in atypical proliferation group was higher than normal endometrial and endometritis group The expression in proliferative phase group was higher significantly than secretory phase group ( P

Expression of cyclooxygenase-2 and 15-prostaglandin dehydrogenase of placenta and fetal membranes in patients of preterm labor / 中华妇产科杂志

0.05). IH scores of 15-PGDH in chorion of placenta and fetal membranes in PL were 1.5?0.6,2.3?0.8, respectively, in TL were 2.6?0.8,3.0?0.7, respectively, and in control group were 4.4?1.1, 4.1?1.2,respectively. IH scores in PL and TL were obviously lower than those in control group(P

Expression of cyclooxygenase-1 and -2 in rheumatoid arthritis synovium

The aim of this study was to investigate the expression and localization of cyclooxygenase-1 and -2 (COX-1 and COX-2) in synovial tissues from patients with rheumatoid arthritis (RA). Synovial tissues from 9 patients with RA and 5 patients with osteoarthritis (OA) were examined for COX-1 and COX-2 expressions by immunohistochemical staining using 2 polydonal COX-1 and COX-2 antibodies. In RA synovia, synovial lining cells showed intense immunostaining for COX-1, whereas slight to moderate staining was observed in inflammatory cells, stromal fibroblast-like cells and vascular endothelial cells. There was no significant difference in COX-1 expression between RA and OA synovia. The localization of COX-2 expression dearly differed from that of COX-1 expression, being most intense in inflammatory cells. However, there was no difference in COX-1 and COX-2 expressions between RA and OA synovial tissues. Our observations support that inflammatory mechanisms modulated by COX-1 and COX-2 in chronic RA synovium might be similar to those in chronic OA synovium.

Effect of NS-398 on invasion of colon cancer HT-29 cells in vitro and its regulation by CD44v6 and nm23-H1 genes / 中国病理生理杂志

AIM: To study the anti-invasive effect of NS-398 on colon cancer cell line HT-29 in vitro an its regulation by CD44v6 and nm23-H1 genes. METHODS: Flow cytometry was used to detect the expression of COX-2 and CD44v6 in HT-29 cells. MTT was used for cell survival rate tests. The modified Boyden chamber model was used for quantitative invasion assay. RT-PCR was used to detect the expression of nm23-H1 mRNA. RESULTS: Flow cytometry analysis showed that COX-2 was positive in HT-29 cells. NS-398 had significant inhibitory effects on invasion of HT-29 cells, which had no relation with its cytotoxicity. NS-398 down-regulated the expression of CD44v6 and up-regulated the expression of nm23-H1 mRNA. CONCLUSION: NS-398 has an anti-invasive effect on HT-29 cells in vitro. Down-regulation of CD44v6 and up-regulation of nm23-H1 may be its underlying mechanisms.

Expression of cyclooxygenase-2 in IL-1?-stimulated mesangial cells is medicated by NF-?B/I?B signal pathway / 中国病理生理杂志

AIM: To investigate the role of NF-?B/I?B signal pathway in the regulation of (cyclooxygenase-2) (COX-2) expression in human mesangial cells (HMC). METHODS: The PGE_2 concentration in supernatants of HMC was measured by radioimmunoassay. COX-2 mRNA and protein expression were determined by RT-PCR and Western blot. Electrophoretic mobility shift assay (EMSA) and Western blot were used to detect the activity of NF-?B and degradation of I?B. RESULTS: IL-1? significantly upregulated COX-2 expression and PGE_2 production in HMC. Significant up-regulation of NF-?B activation, nuclear translocation of p65 subunit, and degradation of I?B ? and I?B ? were observed in IL-1?-induced HMC. CONCLUSION: Expression of COX-2 in IL-1?-induced HMC is mediated by NF-?B/I?B signal pathway. [

Effects of NS-398 on the proliferation and apoptosis of HepG2 cells / 中国病理生理杂志

AIM: To evaluate the effects of NS-398, a cyclooxygenase-2(COX-2) inhibitor, on the proliferation and apoptosis in HepG2 cells. METHODS: The effects of NS-398 on the proliferation of HepG2 cells was evaluated by MTT. DNA fragmentation gel analysis was used to analyze the apoptotic cells; DNA ploidy and apoptotic cell percentage were examined by flow cytometry. Furthermore, the expression of COX-2 and Bcl-2 mRNA was identified by competitive RT-PCR. RESULTS: NS-398 inhibited cell proliferation and induced apoptosis in HepG2 in a concentration-dependent manner. DNA ploidy analysis showed that S phase cells were significantly decreased with NS-398 concentration increasing. The quiescent G_0/G_1 phase was accumulated with decreasing of Bcl-2 mRNA. Whereas NS-398 had no effect on the expression of COX-2 mRNA, no correlations were found between COX-2 mRNA and the HepG2 cell proliferation and apoptosis induced by NS-398 (r=0.056 and r=0.119, respectively). CONCLUSION: NS-398 significantly inhibits the proliferation and induces apoptosis in HepG2. Mechanisms may be involved in accumulation of quiescent G_0/G_1 phase and decrease in Bcl-2 mRNA expression, but independent to COX-2 mRNA expression. [

Effects of cyclooxygenase-2 inhibitors on gastric epithelial cell proliferating and gastric healing following hydrochloric acid-induced injury in rats / 中国病理生理杂志

AIM: To clarify the effects of specific and non-specific cyclooxygenase-2 (COX-2) inhibitors on gastric epithelial cell proliferating and gastric healing following acid-induced damage. METHODS: Male Sprague-Dawley rats were given 1 mL of 0.6 mol/L hydrochloric acid (HCl) into the stomach. Ten minutes after the administration of the acid,the animals were given NS-398 (COX-2 inhibitor) or indomethacin. Levels of COX-1 and COX-2 in the gastric mucosa before and after HCl-administration were analyzed using western blotting and immunohistochemical staining. Proliferating cell nuclear antigen (PCNA) was detected using immunohistochemistry for epithelial cell proliferation. Gastric lesion index (LI) was assessed using planimetry. RESULTS: Expression of COX-2 was enhanced mainly in surface epithelial cells and neck cells following HCl-administration. At 24 h following acid administration,PCNA labeling index (PCNA-LI) was (22.72?4.33) % and (21.98?5.18) % in the groups treated with 40 mg/kg of NS-398 and indomethacin respectively,which was significantly lower than that in the control group [ (34.46?3.61) %,P