肾癌病理组织中核转录因子κB的表达及其意义

目的:探讨核转录因子κB(NF-κB)表达在肾癌发生、发展中的意义。方法:采用免疫组化方法检测66例肾癌病理标本(肾癌组)中NF-κB的表达情况,并与40例非癌肾组织病理标本(对照组)中NF-κB的表达情况比较。结果:肾癌组NF-κB阳性表达率为75.8%,对照组NF-κB阳性表达率为15.0%,肾癌组明显高于对照组(P<0.05)。NF-κB的表达与肾癌病理组织学分级之间无明显的相关性(P>0.05);NF-κB的表达与肾癌的TNM分期之间呈显著的正相关(P<0.05)。结论:肾癌病程中存在NF-κB的异常激活,NF-κB的表达与肾癌病理组织学分级之间无明显的相关性;NF-κB的表达与肾癌的TNM分期之间呈显著的正相关关系。

重组人脑利钠肽对慢性心力衰竭患者血浆sRAGE、NF-κB及心功能的影响

目的探讨重组人脑利钠肽(rhBNP)对慢性心力衰竭患者血浆可溶性晚期糖基化终末产物受体(sRAGE)、核转录因子-κB(NF-κB)及心功能的影响。方法选取2014年1月~2016年2月于解放军总医院第一附属医院住院治疗的86例慢性心力衰竭患者,按照随机数字表法分为对照组(n=43)和rhBNP组(n=43)。对照组给予硝酸甘油治疗,rhBNP组在对照组基础上加用rhBNP治疗。观察两组的临床疗效及不良反应,采用酶联免疫吸附法检测血浆sRAGE、NF-κB水平,分析两组患者治疗前后心功能及血浆sRAGE、NF-κB水平。结果 rhBNP组总有效率(83.7%)显著高于对照组(65.1%)(P<0.05)。两组治疗后左室收缩末期内径(LVESD)、左室舒张末期内径(LVEDD)、左室内径(LADD)明显低于治疗前(P<0.01),心指数(CI)、左室射血分数(LVEF)明显高于治疗前(P<0.05或P<0.01)。与对照组治疗后比较,rhBNP组各心功能指标改善更明显(P<0.05或P<0.01)。两组治疗后血浆sRAGE、NF-κB较治疗前降低(P<0.05或P<0.01);与对照组治疗后比较,rhBNP组血浆sRAGE、NF-κB水平改善更明显(P<0.05)。两组不良反应发生率比较,差异无统计学意义(P>0.05)。结论 rhBNP治疗可有效改善心功能,降低慢性心力衰竭患者血浆sRAGE、NF-κB水平。

白细胞介素32γ通过活化核转录因子κB通路诱导LX-2细胞表达基质金属蛋白酶9

目的：研究白细胞介素-32（Interleukin-32， IL-32）可否诱导肝星状细胞LX-2表达基质金属蛋白酶9（matrix metalloproteinase 9， MMP-9）。方法用不同浓度的IL-32γ与LX-2细胞共培养，收集细胞培养上清，用TRizol试剂提取细胞总RNA，用定量 PCR检测MMP-9 RNA表达水平， MMP-9蛋白质表达水平用酶联免疫吸附试验（ enzyme-linked immunosorbent assay， ELISA）试剂盒检测。接下来将Nuclear factor kappa B （ NF-κB）亚基p50、 p65真核表达载体pCMV-p50、 pCMV-p65单独或联合转染LX-2细胞，48 h后收集细胞培养上清，酶联免疫吸附测定（ enzyme linked immunosorbent assay， ELISA）检测MMP-9蛋白质表达水平。将不同浓度的NF-κB抑制剂SN50加入IL-32γ与LX-2细胞共培养的培养液中，48 h后收集细胞培养上清，用ELISA检测MMP-9蛋白质表达水平。结果 IL-32γ可以诱导人LX-2细胞表达MMP-9，且其表达水平随IL-32γ浓度增加而增强； NF-κB亚基p50、 p65可以诱导LX-2细胞MMP-9表达增高； NF-κB抑制剂SN50阻断NF-κB通路可降低IL-32γ诱导的MMP-9表达。结论 IL-32γ通过活化NF-κB通路诱导LX-2细胞表达MMP-9， IL-32可能通过诱导肝星状细胞表达MMP-9参与肝纤维化形成。

Effects of Bushen Huoxue Yin(补肾活血饮) on brain NF-κB and NO content in the parkinson's disease model mouse

OBJECTIVE:To observe the effects of Bushen Huoxue Yin(补肾活血饮,BSHXY) on nuclear transcription factor kappa B(NF-κB) and nitric oxide(NO) in the brain of the Parkinson's disease(PD) model mouse.METHODS:Forty-five C57BL/6 mice were randomly divided into three groups;normal,model and BSHXY treatment groups.Concentrations of NF-κB and NO in mouse brain tissue were determined by ELISA and spectrophotometry,respectively.RESULTS:NF-κB concentration in brain tissue in the model group was 14.04±4.38 μg· L-1,which was higher than that in normal(P<0.01) and BSHXY(P< 0.05) groups.NO content in brain tissue in the model group was 5.93±0.79 μmol · gprot-1,which was also higher than that in model(P<0.01) and BSHXY(P<0.01) groups.However,there were no significant differences in the content of NF-κB and NO between BSHXY and normal groups(P>0.05).CONCLUSION:The mechanism of BSHXY for treatment of PD is possibly related to inhibition ofNF-κB activation and decreased NO content in the brain.

Functional characterization of the promoter of carbonyl reductase 1 gene in porcine endometrial cells

Prostaglandins （PGs） play a critical role in porcine reproduction, of which prostaglandin E2 （PGE2） and prostaglandin F2a （PGF2a） exert antiluteolytic and luteolysis actions, respectively. As a rate-limiting enzyme, carbonyl reductase 1 （CBR1） catalyzes the conversion of PGE2 to PGF2a. A high ratio of PGE2：PGF2a is beneficial to the establishment and maintenance of porcine pregnancy. PG is essential for the establishment of pregnancy which resembles the proinflammatory response and nuclear factor KB （NF-KB） is involved in the process. Bioinformatic analysis has shown that NF-KB is a possible factor bound to two cis-regulatory elements in CBRI promoter. In this study, we cloned the 2997 bp （-2875/＋122） of the promoter, and constructed six 5＇-deleted dual-luciferase reporter recombinant vectors. In endometrial cells, the region of P2 （-16401＋7） exhibited the greatest transcriptional activity at driving luciferase expression, but not significantly different from that of P1 （-2089/＋7）. The activity of P1, P2, and P3 （-1019/＋7） was highly significantly higher than that of others （P〈0.01）, suggesting that two positive regulatory elements were likely present in the regions of -1640/-1019 and -1019/-647. The results also showed that the -1640/ -647 region was indispensable for the promoter. The results of chromatin immunoprecipitation （CHIP） demonstrated that the NF-KB subunit p65 binds to one site around -15451-1531. Using four reference genes, we found that the over-expression of p65 enhanced the expression of CBR1 （P〈0.05） in porcine endometrial epithelial cells, while knockdown of the p65 did not down-regulate the CBRI expression. These results indicated that NF-KB （p65） could bind to the special element of CBR1 gene promoter in porcine endometrial epithelial cells in vitro. The binding site of NF-KB was a positive regulator for the CBR1 gene promoter, but was not necessary for the basic expression.