Intragingival injection of Porphyromonas gingivalis-derived lipopolysaccharide induces a transient increase in gingival tumour necrosis factor-a, but not interleukin-6,in anaesthetised rats

This study used in vivo microdialysis to examine the effects of intragingival application of lipopolysaccharide（LPS） derived from Porphyromonas gingivalis（Pg-LPS） on gingival tumour necrosis factor（TNF）-a and interleukin（IL）-6 levels in rats. A microdialysis probe with an injection needle attached to the surface of the dialysis membrane was implanted into the gingiva of the upper incisor. For comparison, the effects of LPS derived from Escherichia coli（Ec-LPS） on IL-6 and TNF-a levels were also analysed. Pg-LPS（1 mg/1 m L） or Ec-LPS（1 or 6 mg/1 m L） was applied by microsyringe, with gingival dialysates collected every hour. Enzyme-linked immunosorbent assay（ELISA） revealed that gingival dialysates contained approximately 389 pg？m L21 of IL-6 basally; basal TNF-a levels were lower than the detection limit of the ELISA. Pg-LPS failed to alter IL-6 levels but markedly increased TNF-a levels, which remained elevated for 2 h after treatment. Neither IL-6 nor TNF-a were affected by Ec-LPS. Reverse transcriptase-polymerase chain reaction（RT-PCR） analysis revealed that the gingiva expresses Toll-like receptor（TLR） 2 and TLR4 m RNA. Immunohistochemical examination showed that TLR2 and TLR4 are expressed by gingival epithelial cells. The present study provides in vivo evidence that locally applied Pg-LPS, but not Ec-LPS, into the gingiva transiently increases gingival TNF-a without affecting IL-6. The present results suggest that TLR2 but not TLR4 expressed on gingival epithelial cells may mediate the Pg-LPS-induced increase in gingival TNF-a in rats.

Anti-tumour necrosis factor agent and liver injury:literature review,recommendations for management

Abnormalities in liver function tests,including transient and self-limiting hypertransaminasemia,cholestatic disease and hepatitis,can develop during treatment with anti-tumour-necrosis-factor(TNF)therapy.The optimal management of liver injury related to antiTNF therapy is still a matter of debate.Although some authors recommend discontinuing treatment in case of both a rise of alanine aminotransferase more than5 times the upper limit of normal,or the occurrence of jaundice,there are no standard guidelines for the management of anti-TNF-related liver injury.Bibliographical searches were performed in Pub Med,using the following key words:inflammatory bowel disease(IBD);TNF inhibitors;hypertransaminasemia;drugrelated liver injury;infliximab.According to published data,elevation of transaminases in patients with IBD treated with anti-TNF is a common finding,but resolution appears to be the usual outcome.Anti-TNF agents seem to be safe with a low risk of causing severe drugrelated liver injury.According to our centre experience,we found that hypertransaminasemia was a common,mainly self-limiting finding in our IBD cohort and was not correlated to infliximab treatment on both univariate and multivariate analyses.An algorithm for the management of liver impairment occurring during antiTNF treatment is also proposed and this highlights the need of a multidisciplinary approach and suggests liver biopsy as a key-point in the management decision in case of severe rise of transaminases.However,hepatic injury is generally self-limiting and drug withdrawal seems to be an exception.

Increased expression of tumor necrosis factor-a is associated with advanced colorectal cancer stages

AIM:To detect the expression of tumor necrosis factor-a(TNF-a)in colorectal cancer(CRC)cells among Saudi patients,and correlate its expression with clinical stages of cancer.METHODS:Archival tissue specimens were collected from 30 patients with CRC who had undergone surgical intervention at King Khalid University Hospital.Patient demographic information,including age and gender,tumor sites,and histological type of CRC,was recorded.To measure TNF-a m RNA expression in CRC,total RNA was extracted from tumor formalin-fixed,paraffinembedded,and adjacent normal tissues.Reverse transcription and reverse transcription polymerase chain reaction were performed.Colorectal tissue microarrays were constructed to investigate the protein expression of TNF-a by immunohistochemistry.RESULTS:The relative expression of TNF-a m RNA in colorectal cancer was significantly higher than that seen in adjacent normal colorectal tissue.High TNF-a gene expression was associated with StageⅢandⅣneoplasms when compared with earlier tumor stages(P=0.004).Eighty-three percent of patients(25/30)showed strong TNF-a positive staining,while only 10%(n=3/30)of patients showed weak staining,and 7%(n=2/30)were negative.We showed the presence of elevated TNF-a gene expression in cancer cells,which strongly correlated with advanced stages of tumor.CONCLUSION:High levels of TNF-a expression could be an independent diagnostic indicator of colorectal cancer,and targeting TNF-a might be a promising prognostic tool by assessment of the clinical stages of CRC.

Zinc-α2-glycoprotein 1 attenuates non-alcoholic fatty liver disease by negatively regulating tumour necrosis factor-α

BACKGROUND Zinc-α2-glycoprotein 1 (AZGP1) plays important roles in metabolism-related diseases. The underlying molecular mechanisms and therapeutic effects of AZGP1 remain unknown in non-alcoholic fatty liver disease (NAFLD). AIM To explore the effects and potential mechanism of AZGP1 on NAFLD in vivo and in vitro. METHODS The expression of AZGP1 and its effects on hepatocytes were examined in NAFLD patients, CCl4-treated mice fed a high fat diet (HFD), and human LO2 cells. RESULTS AZGP1 levels were significantly decreased in liver tissues of NAFLD patients and mice. AZGP1 knockdown was found to activate inflammation;enhance steatogenesis, including promoting lipogenesis [sterol regulatory elementbinding protein (SREBP)-1c, liver X receptor (LXR), fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and stearoyl CoA desaturase 1 (SCD)-1], increasing lipid transport and accumulation [fatty acid transport protein (FATP), carnitine palmitoyl transferase (CPT)-1A, and adiponectin], and reducing fatty acid β-oxidation [farnesoid X receptor (FXR) and peroxisome proliferator-activated receptor (PPAR)-α];accelerate proliferation;and reverse apoptosis in LO2 cells. AZGP1 overexpression (OV-AZGP1) had the opposite effects. Furthermore, AZGP1 alleviated NAFLD by blocking TNF-α-mediated inflammation and intracellular lipid deposition, promoting proliferation, and inhibiting apoptosis in LO2 cells. Finally, treatment with OV-AZGP1 plasmid dramatically improved liver injury and eliminated liver fat in NAFLD mice. CONCLUSION AZGP1 attenuates NAFLD with regard to ameliorating inflammation, accelerating lipolysis, promoting proliferation, and reducing apoptosis by negatively regulating TNF-α. AZGP1 is suggested to be a novel promising therapeutic target for NAFLD.

Effects of erythropoietin on the expression of tumor necrosis factor-alpha and Bax after facial nerve axotomy in rats

This study sought to evaluate the effect of high-dose erythropoietin （EPO; 5 000 IU/kg） on the expression of tumor necrosis factor-alpha （TNF-α） and Bax in the facial nucleus after facial nerve transection in rats. A total of 42 Wistar rats of both genders were used in this study, and 40 rats were randomly divided into 2 groups： EPO group and model group. The EPO group was treated with EPO once a day for 5 days at a dose of 5 000 IU/kg body weight. The model group was treated with saline of the same amount. At day 3 after EPO （or saline） treatment, the right facial nerves of the 40 rats were transected at the level of the stylomastoid foramen, with the left sides untreated. The remaining 2 rats that did not undergo axotomy served as the control group. The surviving motor neurons in operated rats were counted in coronal paraffin sections of the facial nucleus. The expression of TNF-a and Bax in the facial nucleus was detected by immunohistochemical staining at days 3, 7, 14, 21, and 28 after axotomy. At days 14, 21, and 28 after facial nerve axotomy, a significantly greater proportion of facial motor neurons survived in the EPO group than in the model group. After axotomy, the expression of TNF-a and Bax increased in motor neurons in both the EPO and the model groups. TNF-o expression reached its peak level at day 14 after axotomy, while Bax expression reached its peak level at day 21. TNF-α expression was much lower in the EPO group than in the model group at all time points. No significant difference in Bax expression was found between the EPO and the model groups. These results indicate that high-dose EPO treatment attenuates the increase in TNF-α expression in the facial nucleus and reduces the loss of motor neurons after facial nerve transection in rats. However, high-dose EPO treatment has little effect on Bax expression.

Nitric oxide and tumour necrosis factor alpha in the process of pseudoexfoliation glaucoma

AIMTo establish the role of nitric oxide (NO), ascorbic acid and tumour necrosis factor-α (TNF-α) in the pathogenesis of pseudoexfoliation glaucoma (XFG).METHODSOur study included 120 patients who were referred for cataract surgery. All patients were divided into four groups according to clinical findings: XFG, early and late pseudoexfoliation syndrome (XFS), and cataract (without pseudoexfoliation). Serum and aqueous humour levels of the ascorbic acid, NO and TNF-α were measured. The concentrations of the ascorbic acid and NO were measured by an appropriate spectrophotometric method. Enzyme-linked immunosorbent assay (ELISA) was used to determine TNF-α level.RESULTSAqueous humour concentration of ascorbic acid was significantly lower in patients with late XFS (0.61±0.11 mmol/L) and XFG (0.48±0.15 mmol/L) compared to patients with early XFS (0.9±0.15 mmol/L) and cataract (1.16±0.22 mmol/L), while there was no difference in serum concentration in all examined groups. Aqueous humour concentration of NO was significantly higher in patients with XFG (77.7±11.4 µmol/L) compared to patients with early XFS (50.27±9.34 µmol/L) and cataract (49.77±7.1 µmol/L), while serum concentration was increased in the early stage of XFS (73.26±8.29 µmol/L). Aqueous humour level of proinflammatory cytokine TNF-α was increased in patients with XFS (early 460.04±18.32 pg/mL; late 502.42±53.23 pg/mL) and XFG (510.34±43.07 pg/mL), while there was no difference in serum level in all examined groups of patients.CONCLUSIONReduced ascorbic acid and elevated NO and inflammation related cytokine TNF-α level in aqueous humour of the patients with developed XFG suggest that oxidative stress induces local inflammation.

Up-regulation of tumor necrosis factor-a pathway survival genes and of the receptor TNFR2 in gastric cancer

BACKGROUND Gastric carcinogenesis can be induced by chronic inflammation triggered by Helicobacter pylori(H. pylori) infection. Tumor necrosis factor(TNF)-α and its receptors(TNFR1 and TNFR2) regulate important cellular processes, such as apoptosis and cell survival, and the disruption of which can lead to cancer. This signaling pathway is also modulated by microRNAs(miRNAs), altering gene expression.AIM To evaluate the mRNA and miRNAs expression involved in the TNF-α signaling pathway in gastric cancer(GC) tissues and its relationship.METHODS Quantitative polymerase chain reaction(qPCR) by TaqMan? assay was used to quantify the RNA transcript levels of TNF-α signaling pathway(TNF, TNFR1,TNFR2, TRADD, TRAF2, CFLIP, NFKB1, NFKB2, CASP8, CASP3) and miRNAs that targets genes from this pathway(miR-19 a, miR-34 a, miR-103 a, miR-130 a,miR-181 c) in 30 GC fresh tissue samples. Molecular diagnosis of H. pylori was performed by nested PCR for gene HSP60. A miRNA:mRNA interaction network was construct using Cytoscape v3.1.1 from the in silico analysis performed using public databases.RESULTS Up-regulation of cellular survival genes as TNF, TNFR2, TRADD, TRAF2, CFLIP,and NFKB2, besides CASP8 and miR-34 a was observed in GC tissues, whereas mediators of apoptosis such as TNFR1 and CASP3 were down-regulated. When the samples were stratified by histological type, the expression of miR-103 a and miR-130 a was significantly increased in the diffuse-type of GC compared to the intestinal-type. However, no influence of H. pylori infection was observed on the expression levels of mRNA and miRNAs analyzed. Moreover, the miRNA:mRNA interaction network showed several interrelations between the miRNAs and their target genes, highlighting miR-19 a and miR-103 a, which has as predicted or validated target a large number of genes in the TNF-α pathway,including TNF, TNFR1, TNFR2, CFLIP, TRADD, CASP3 and CASP8.CONCLUSION Our findings show that cell survival genes mediated by TNF/TNFR2 binding is up-regulated in GC favoring its pro-tumoral effect, while pro-apoptotic genes as CASP3 and TNFR1 are down-regulated, indicating disbalance between apoptosis and cell proliferation processes in this neoplasm. This process can also be influenced by an intricate regulatory network of miRNA:mRNA.

Single nucleotide polymorphism in the tumor necrosis factor-alpha gene affects inflammatory bowel diseases risk

AIM: To investigate the role that single nucleotide polymorphisms (SNPs) in the promoter of the tumour necrosis factor-alpha (TNF-α) gene play in the risk of inflammatory bowel diseases (IBDs) in a New Zealand population, in the context of international studies. METHODS: DNA samples from 388 patients with Crohn's disease (CD), 405 ulcerative colitis (UC), 27 indeterminate colitis (IC) and 201 randomly selected controls, from Canterbury, New Zealand were screened for 3 common polymorphisms in the TNF-α receptor: -238 G→A, -308 G→A and -857C→T, using a TaqmanR assay. A meta-analysis was performed on the data obtained on these polymorphisms combined with that from other published studies. RESULTS: Individuals carrying the -308 G/A allele had a significantly (OR = 1.91, χ2 = 17.36, P < 0.0001) increased risk of pancolitis, and a 1.57-fold increased risk (OR = 1.57, χ2 = 4.34, P = 0.037) of requiring a bowel resection in UC. Carrying the -857 C/T variant decreased the risk of ileocolonic CD (OR = 0.56, χ2 =4.32, P = 0.037), and the need for a bowel resection (OR = 0.59, χ2 = 4.85, P = 0.028). The risk of UC was reduced in individuals who were smokers at diagnosis, (OR = 0.48, χ2 = 4.86, P = 0.028). CONCLUSION: TNF-α is a key cytokine known to play a role in inflammatory response, and the locus for the gene is found in the IBD3 region on chromosome 6p21, known to be associated with an increased risk for IBD. The -308 G/A SNP in the TNF-α promoter is functional, and may account in part for the increased UC risk associated with the IBD3 genomic region. The -857 C/T SNP may decrease IBD risk in certain groups. Pharmaco- or nutrigenomic approaches may be desir- able for individuals with such affected genotypes.

AN EXPERIMENTAL STUDY OF THE TUMOUR NECROSIS FACTOR LEVELSIN AQUEOUS HUMOR AFTER TRAUMATIC CATARACT AND INTRAOCULAR LENS IMPLANTATION

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Withdrawal of anti-tumour necrosis factor α therapy in inflammatory bowel disease

Anti-tumour necrosis factor α(anti-TNFα) therapy is an established treatment in inflammatory bowel disease.However, this treatment is associated with high costs and the possibility of severe adverse events representing a true challenge for patients, clinicians and health care systems.Consequently, a crucial question is raised namely if therapy can be stopped once remission is achieved and if so, how and in whom.Additionally, in a real-life clinical setting, discontinuation may also be considered for other reasons such as the patient's preference, pregnancy, social reasons as moving to countries or continents with less access, or different local policy or reimbursement.In contrast to initiation of anti-TNFα therapy guidelines regarding stopping of this treatment are missing.As a result, the decision of discontinuation is still a challenging aspect in the use of anti-TNFα therapy.Currently this is typically based on an estimated, case-by-case, benefit-risk ratio.This editorial is intended to provide an overview of recent data on this topic and shed light on the proposed drug withdrawal strategies.

An Experimental Study of the Tumour Necrosis Factor Level in Aqueous Humor after Transscleral Fixation of Intraocular Lens

Purpose: The tumour necrosis factor (TNF) level in aqueous humor after transscleral fixation of intraocular lens (IOL) implantation in rabbits and discuss the effect of TNF on postoperative anterior ocular inflammation.Methods: Twenty - seven pigmented rabbits were divided into three groups. Group 1: transscleral fixation of posterior chamber (PC) IOL implantation;Group 2; Lens of rabbits was removed without IOL implantation; Group 3; the comtrol group, without surgical intervention. On the 1st, 3rd, 7th and 14th postoperative days,aqueous humor samples were obtained. An modified double antibodies indirect sandwich ELISA was used to detected for the presence of TNF. The data were analyzed by using analysis of variance of SAS software. Results: It was found that TNF level in aqueous humor was increased after transscleral fixation of IOL implantation. TNF level reached its maximum on the 14th postoperative day in the IOL implanted group. TNF level on 1st, 3rd, 7th and 14th days postoperatively was

Tumour Necrosis Factor Alpha and Oxidative Stress in the Breath Condensate of Those with Non-Small Cell Lung Cancer

Background and Aims: Lung cancer is a leading cause of cancer mortality worldwide and is associated with the release of tumour necrosis factor-α (TNF-α), subsequent cellular apoptosis and the generation of oxidative stress. Exhaled breath condensate (EBC) analysis is a non-invasive method for sampling biofluids from the lower respiratory tract. This study aimed to evaluate possible biomarkers of lung cancer by measuring the levels of TNF-α and the oxidation of ascorbic acid in EBC. Patients with lung cancer were enrolled into the study prior to treatment, during treatment and post-treatment, and results compared with an age-matched control population. Material and Methods: Patients with Stage II-IV non small cell lung cancer (NSCLC) were recruited prior to and at stages of their treatment. EBC levels of TNF-α, and rate of ascorbic acid oxidation were measured. Results: A total of 19 patients with NSCLC (mean age 71.37 ± 7.77 yrs) and 25 age-matched control subjects were enrolled. Levels of EBC TNF-α were elevated in the EBC of patients with lung cancer compared with control subjects (1.02 ± 0.07 pg/ml vs. 0.51 ± 0.06 pg/ml, p < 0.0001). Moreover, the rate of ascorbic acid oxidation was significantly greater in the EBC of patients with lung cancer compared with control subjects (2.20% [0.4 – 11.0] vs. 1.00% [0.1 – 8.5], p = 0.0244). Conclusion: TNF-α and the rate of ascorbic acid oxidation was elevated in the EBC of patients with lung cancer regardless of treatment. Longitudinal studies in a larger population are required to evaluate these markers for the effect of treatment and prognosis.

Effects of propofol on Bax and Bcl-2 expression induced by tumour necrosis factor-α in mouse spinal cord neurons in vitro

Objective:To study the effects of propofol on Bax and Bcl-2 expression induced by tumour necrosis factor-α(TNF-α) in mouse spinal cord neurons in vitro. Methods:Spinal cord neurons were isolated from fetal mice and cultured in Neurobasal medium with B27 supplement. On the 7^th day, cultured neurons were randomly divided into 6 groups: control group, propofol (50 umol/L)group, TNF-α group, propofol (25 umol/L) with TNF-α group, propofol (50 umol/ L) with TNF-α group, and propofol ( 100 umol/L)with TNF-α group. Propofol was added to the cultured cells respectively and the cells were incubated for 30 min. Then TNF-α was added to the cultured cells(the final concentration of TNF-α was 2 000 U/ml) and incubated for 24 h. The Bax and Bcl-2 expression were measured by immunocytochemical technique. Results:In TNF-α group, the expression of Eax increased and the expression of Bcl-2 decreased (P<0.01, vs control). However, treatment with various concentrations of propofol (25, 50, 100 umol/L) decreased the expression of Bax and increased the expression of Bcl-2 (P<0.05, P<0.05, P<0.05, vs TNF-α). Conclusion: Propofol can inhibit the apoptosis induced by TNF-α by modulating the expression of Bax and Bcl-2.

What is left when anti-tumour necrosis factor therapy in inflammatory bowel diseases fails?

The inflammatory bowel diseases(IBDs) are chronic incurable conditions that primarily present in young patients. Being incurable, the IBDs may be part of the patient's life for many years and these conditions require therapies that will be effective over the long-term. Surgery in Crohn's disease does not cure the disease with endoscopic recurrent in up to 70% of patients 1 year post resection. This means that, the patient will require many years of medications and the goal of the treating physician is to induce and maintain long-term remission without side effects. The development of the antitumour necrosis factor alpha(TNFα) agents has been a magnificent clinical advance in IBD, but they are not always effective, with loss of response overtime and, at times, discontinuation is required secondary to side effects. So what options are available if of the anti-TNFα agents can no longer be used? This review aims to provide other options for the physician, to remind them of the older established medications like azathioprine/6-mercaptopurine and methotrexate, the less established medications like mycophenolate mofetil and tacrolimus as well as newer therapeutic options like the anti-inte-gins, which block the trafficking of leukocytes into the intestinal mucosa. The location of the intestinal inflammation must also be considered, as topical therapeutic agents may also be worthwhile to consider in the longterm management of the more challenging IBD patient. The more options that are available the more likely the patient will be able to have tailored therapy to treat their disease and a better long-term outcome.

Effects of Tryptergium Wilfordii Polyglyco-sidium on the Tumour Necrosis Factor Levels in Aqueous Humor after Intraocular Lens Implantation

Purpose : Effects of Tryptergium Wilfordii Polyglycosidium (TWP) on the Tumour Necrosis Factor (TNF) levels in aqueous humor after intraocular lens (IOL) implantation were studied in rabbits.Methods: Twenty-seven pigmented rabbits were divided into three groups. In the first group, the IOL were placed in the capsular bag after lens extraction. In the second group, rabbits received TWP therapy after IOL implantation. And in the third group, rabbit received prednisone therapy after IOL implantation. Aqueous humor samples were aspirated on the 1st, 3rd, 7th, and 14th postoperative day. A modified double antibodies indirect sandwich EL ISA was used to detect for the presence of TNF. The data were closely studied by means of analysis of variance with SAS software.Results; It was found that TNF level in aqueous humor reached its maximum on the 7th postoperative day in the group with IOL implantation. It was also found that the TNF levels in aqueous humor on the 7th and 14th postoperative day were

Relationship of Tumor Necrosis Factor-α and Nitrogen Oxide with Treatment of Frequent Relapse Nephrotic Syndrome by Shenkangling(肾康灵)Granule in Children

Objective: To observe the relationship of tumor necrosis factor-o (TNF-a) and nitrogen oxide (NO) with the treatment of frequent relapse nephrotic syndrome (FRNS) and to explore the patho-genesis of FRNS and the therapeutic mechanism of Shenkangling (肾康灵,SKL) Granule in children. Methods: Sixty children suffering from FRNS were randomly divided into the treated group and control group, 30 in each, and the other 30 healthy children were taken as healthy group. The patients were treated with prednisone for a long-term course, and those with no effect or partial effect shown were treated with additional Tripterygium or Cytoxan in the control group, while in the treated group patients were treated with prednisone and additional SKL. The two groups were compared as to their changes of TNF-a, NO before and after treatment, and the relapses after treatment. Results: The levels of TNF-a and NO in the sick children before treatment were markedly higher than those after treatment and normal group (P< 0. 01). The positive correlation between TNF-o of FRNS cases and relapse risk displayed more significance than that between the relapse of FRNS and NO. The difference between treated group and control group was significant (P<0. 01). Conclusion: TNF-a can be regarded as the monitoring parameter of the active phase in FRNS, and the higher the level, the more possible the relapse would occur. SKL could markedly reduce the relapse rate of FRNS in children.

强直性脊柱炎合并急性早幼粒细胞白血病及弥散性血管内凝血1例并文献复习

目的探讨强直性脊柱炎(ankylosing spondylitis,AS)合并急性早幼粒细胞白血病(acute promyelocytic leukemia,APL)及弥散性血管内凝血(disseminated intravascular coagulation,DIC)的临床特点、诊断和治疗,深入了解三者之间的潜在关系和机制。方法报告1例AS合并APL及DIC的临床特点及治疗,结合文献进行归纳总结。结果患者APL达到完全缓解期,继续巩固治疗。AS、APL和DIC之间的关系涉及到人白细胞抗原-B27、肿瘤坏死因子-α和白介素-23/17轴和其他免疫功能。结论AS与APL、DIC之间的关系千丝万缕,从基因到免疫功能都存在着潜在的发病机制,其中的奥妙仍需探索。

土藤草颗粒对微晶型尿酸钠致家兔急性痛风性关节炎的药效学研究

目的观察土藤草颗粒对微晶型尿酸钠(monosodium urate,MSU)致家兔急性痛风性关节炎模型的药效学作用。方法选用取雄性日本大耳白兔,随机分为正常对照组,模型对照组,阳性药秋水仙碱组(0.18 mg·kg^(-1)),土藤草颗粒高、中、低剂量组分别为600、300、150 mg·kg^(-1)。通过家兔左后肢膝关节腔内注入MSU的方式建立急性痛风性关节炎模型,给药5天后收集关节液,检测关节腔积液中的白细胞数,测定关节液中炎症细胞因子白介素-6(interleukin-6,IL-6)、白介素-8(interleukin-8,IL-8)、肿瘤坏死因子-α(tumour necrosis factor-α,TNF-α)、白介素-1β(interleukin-1β,IL-1β)、前列腺素E2(prostaglandin E2,PGE2)含量;采血检测血尿酸值,给药前后血清中尿素(urea,UREA)、胆固醇(cholesterol,CHO)、血肌酐(serum creatinine,Cre)、血糖(glucose,GLU)及甘油三酯(triglyceride,TG)含量。结果土藤草颗粒高、中、低剂量组给药5 d后关节腔内白细胞数均有所下降,中剂量组与模型对照组比较有显著性差异(P<0.01);高、中剂量组有降低血尿酸的趋势;土藤草颗粒对家兔血清中UREA、CHO、Cre、GLU及TG含量均无影响;与模型对照组比较,土藤草颗粒高、中、低剂量组IL-6、IL-8、TNF-α及PGE2含量均明显降低,其中高、中、低剂量组的IL-6、TNF-α含量,高、中剂量组IL-8含量及中剂量组PGE2含量与之比较有显著性差异(P<0.01);土藤草颗粒高、中、低剂量组可以一定程度上降低关节液中IL-1β含量。结论土藤草颗粒对MSU致急性关节炎家兔模型有明显的治疗作用,可以减少动物关节腔内白细胞数量、抑制炎症细胞因子的表达,降低血清中尿酸含量。

血清IL-10/TNF-α比值对卵巢子宫内膜异位症患者腹腔镜术后疾病复发的预测价值

目的分析血清白介素-10(IL-10)/肿瘤坏死因子-α(TNF-α)比值对卵巢子宫内膜异位症(OEMs)患者腹腔镜术后疾病复发的预测价值。方法选取2019年1月至2021年12月唐山市妇幼保健院收治的223例OEMs患者作为研究对象,均接受腹腔镜保守性手术治疗。根据术后随访1年疾病复发情况分为复发组(n=27)与未复发组(n=196),比较两组基线资料及出院前末次检查时实验室指标,分析出院前血清IL-10/TNF-α比值对OEMs患者腹腔镜术后疾病复发的预测价值。结果223例患者术后随访1年期间疾病复发27例,复发率为12.11%。与未复发组相比,复发组术前病灶最大直径更大,美国生育医学会修订(r-ASRM)分期更高,出院前血清IL-10及TNF-α水平、IL-10/TNF-α比值更高(P<0.05)。受试者工作特征(ROC)曲线结果显示,出院前血清TNF-α水平预测OEMs患者腹腔镜术后疾病复发的曲线下面积(AUC)为0.640,预测价值较低;出院前血清IL-10水平及IL-10/TNF-α比值预测OEMs患者腹腔镜术后疾病复发的AUC分别为0.847、0.860,具有一定预测价值,且IL-10/TNF-α比值预测价值更高。结论出院前血清IL-10/TNF-α比值与OEMs患者腹腔镜术后疾病复发有关,可用于患者术后疾病复发的早期预测中。

血清CTRP9、AMH对多囊卵巢综合征患者IVF-ET助孕结局的预测价值

目的探讨行体外受精-胚胎移植(in vitro fertilization and embryo transfer,IVF-ET)助孕的多囊卵巢综合征(polycystic ovary syndrome,PCOS)患者血清中补体C1q/肿瘤坏死因子相关蛋白9(complement C1q/tumour necrosis factor-related protein 9,CTRP9)、抗苗勒管激素(anti-mullerian hormone,AMH)对治疗结果的预测价值。方法选取2022年3月—2023年7月于重庆医科大学附属第一医院生殖中心行IVF-ET的85例PCOS患者。根据妊娠结局分为临床妊娠组43例与临床未妊娠组42例。记录2组患者的一般资料,测定血清CTRP9和AMH水平,分析其与妊娠结局的关系。结果临床未妊娠组血清CTRP9为(290.19±58.97)ng/mL,AMH为3.39(2.09,5.42)ng/mL,均低于临床妊娠组的(413.63±89.56)ng/mL、7.42(5.45,9.90)ng/mL(P<0.05)。血清CTRP9、AMH水平、优胚数是PCOS患者IVF-ET妊娠成功的保护因素(P<0.05)。血清CTRP9预测行IVF-ET的PCOS患者妊娠成功的敏感度与特异度为74.40%和90.50%,曲线下面积(area under the curve,AUC)值为0.836;血清AMH预测敏感度与特异度为83.70%和73.80%,AUC值为0.859;血清CTRP9和AMH联合预测的敏感度和特异度分别为88.40%和92.90%,AUC值为0.924,高于单独使用CTRP9或AMH预测的价值。结论血清CTRP9、AMH与PCOS患者IVF-ET治疗结局密切相关,且与单一指标检测比较,两者联合检测可提高预测价值。