萆薢总皂苷对大鼠慢性高尿酸血症和肾小管尿酸转运体1表达的影响

目的: 研究萆薢总皂苷对大鼠慢性高尿酸血症的防治作用及对肾脏尿酸转运体1(urate transporter 1,URAT1)表达的影响。 方法: 90只雄性SD大鼠随机分为正常组、模型组、萆薢总皂苷(total saponin of Dioscorea,TSD)高、中、低剂量组(300,100,30 mg·kg^-1)、苯溴马隆(10 mg·kg^-1)组。以氧嗪酸钾联合乙胺丁醇复制大鼠慢性高尿酸血症模型,第3周开始灌胃给药,每天1次,连续4周,测定血尿酸、尿尿酸、尿酸排泄量、黄嘌呤氧化酶(XOD)活性;RT-PCR法、免疫组化法分别测定大鼠肾小管细胞URAT1 mRNA和URAT1蛋白的表达。 结果: 模型组大鼠血尿酸水平显著升高,尿尿酸排泄减少,肾脏URAT1 mRNA和URAT1蛋白高表达。TSD能剂量依赖性地降低高尿酸血症大鼠的血清尿酸水平,增加尿尿酸浓度和尿酸排泄量,降低肾脏URAT1 mRNA和URAT1蛋白的高表达,其作用与苯溴马隆相近;对高尿酸血症大鼠XOD、尿量无明显影响。 结论: TSD有明显的抗高尿酸血症作用,可能是通过抑制大鼠肾脏URAT1的高表达而减少尿酸的重吸收。     

CA—50和二胺氧化酶联合检测对恶性胸水的诊断价值

本研究测定了４５例良恶性胸水患者胸水，血清ＣＡ—５０和二胺氧化酶水平。结果表明，癌性胸水和血清ＣＡ—５０、二胺氧化酶均明显高于良性胸水。如胸水和血清ＣＡ—５０以２０ｕ／ｍｌ作为界值，其敏感性为７７．８％和５９．２％，特异性９４．４％。若胸水二胺氧化酶以２５０ｕ／ｍｌ作为界值，其敏感性为７０．４％，特异性８８．９％。综合测定胸水ＣＡ一５０，二胺氧化酶，可提高癌性胸术诊断率。     

The protective effect of alpha-lipoic acid in experimental ovarian ischaemia-reperfusion injury

BACKGROUND: We investigated the effect of alpha-lipoic acid (LA) on reperfusion injury in a rat ovarian torsion-detorsion model. The changes in tissue and plasma levels of malondialdehyde (MDA), end-product of lipid peroxidation, superoxide dismutase (SOD), xanthine oxidase (XO) and nitric oxide (NO), were determined. Ovarian histopathological findings were scored and compared among groups. MATERIALS AND METHODS: Thirty-two female Sprague-Dawley rats were divided into four groups. Sham operation was performed in group I; in group II only ovarian torsion was performed. Group III received intraperitoneal injections of saline, and group IV received LA via intraperitoneal injections (LA group: aqueous solution at 36 mg/kg of body weight per day, saline group: equal volume of saline) 21, nine, and one hour before torsion of the ovary. Rats in the torsion group were killed after 360 degrees clockwise adnexial torsion for three hours, and ovaries were harvested. After three hours of adnexial detorsion, the rats in saline group and LA group were killed and adnexa were surgically removed. RESULTS: Ovarian tissue damage scores were significantly different among groups and were seen to correlate with tissue MDA levels. Ovarian tissue and serum MDA, NO and serum XO levels in the group III were significantly higher than those of the groups I and IV (P<0.05). The serum levels of SOD in the group III were significantly lower than those of the groups I and IV (P<0.05). CONCLUSION: These results suggest that LA pretreatment has beneficial effects in the prevention of ischaemia-reperfusion injury of the ovaries.     

自发性蛛网膜下腔出血患者血清及脑脊液中单胺类递质的变化

目的 探讨自发性蛛网膜下腔出血(SAH)患者血清和脑脊液中单胺类递质水平与SAH发病的关系.方法 30例自发蛛网膜下腔出血患者与30例健康对照组分别采集血清和脑脊液,运用反相高效液相色谱荧光法,检测去甲肾上腺素(NE)、多巴胺(DA)和5-羟色胺(5-HT)含量.结果 SAH患者血清中DA含量较对照组显著升高(P＜0.05),而NE和5-HT含量与对照组比较差异无统计学意义(P＞0.05).两组脑脊液中NE、DA比较差异无统计学意义(P＞0.05),SAH组5-HT含量低于对照组(P＜0.05).结论 血清DA升高和脑脊液中5-HT下降可能与SAH密切相关,其机制需进一步探讨.     

Nox2 underpins microvascular inflammation and vascular contributions to cognitive decline

Chronic microvascular inflammation and oxidative stress are inter-related mechanisms underpinning white matter disease and vascular cognitive impairment (VCI). A proposed mediator is nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (Nox2), a major source of reactive oxygen species (ROS) in the brain. To assess the role of Nox2 in VCI, we studied a tractable model with white matter pathology and cognitive impairment induced by bilateral carotid artery stenosis (BCAS). Mice with genetic deletion of Nox2 (Nox2 KO) were compared to wild-type (WT) following BCAS. Sustained BCAS over 12 weeks in WT mice induced Nox2 expression, indices of microvascular inflammation and oxidative damage, along with white matter pathology culminating in a marked cognitive impairment, which were all protected by Nox2 genetic deletion. Neurovascular coupling was impaired in WT mice post-BCAS and restored in Nox2 KO mice. Increased vascular expression of chemoattractant mediators, cell-adhesion molecules and endothelial activation factors in WT mice post-BCAS were ameliorated by Nox2 deficiency. The clinical relevance was confirmed by increased vascular Nox2 and indices of microvascular inflammation in human post-mortem subjects with cerebral vascular disease. Our results support Nox2 activity as a critical determinant of VCI, whose targeting may be of therapeutic benefit in cerebral vascular disease.     

福建口岸三蚊种COI基因序列分析

〔目的〕分析福建口岸白纹伊蚊、中华按蚊和骚扰阿蚊细胞色素C氧化酶亚基I(COI)基因序列,为建立蚊种分子鉴定方法奠定基础。〔方法〕扩增并测定在福建口岸采集的白纹伊蚊、中华按蚊和骚扰阿蚊COI基因序列,与GenBank中相应序列进行对比分析。〔结果〕三蚊种COI基因扩增片段长度约500bp,A+T含量为65.61%~68.73%。核苷酸同源性分析结果表明,同一蚊种COI基因同源性为98.1%~100%,三蚊种间基因同源性为84.4%~87.7%;COI部分基因系统进化关系显示,三蚊种COI分子鉴定与形态学鉴定结果一致,阿蚊属与伊蚊属聚类为库蚊亚科,按蚊亚科位于系统进化树另一分支。〔结论〕COI基因核苷酸序列分析可应用于福建国境口岸三蚊种的区分,弥补形态特征信息量不足等传统分类鉴定方法的缺点,为建立外来或新发现蚊种分子鉴定方法奠定基础。     

LOX与VEGF蛋白在人喉鳞癌中的表达及其相关性研究

目的检测赖氨酰氧化酶（LOX）、血管内皮生长因子（VEGF）蛋白在人喉鳞癌中的表达,探讨其对喉鳞癌转移及预后的影响及意义。方法采用免疫组织化学方法检测14例有淋巴结转移的喉鳞癌及24例未见淋巴结转移的原位癌组织中LOX及VEGF的表达情况,并分析其表达的相关性。结果①LOX、VEGF在喉鳞癌组织中表达显著高于癌旁正常组织（P均〈0．05）。②VEGF在淋巴结转移组与无转移组表达阳性率分别为100％和71％,具有显著性差异（P〈0．05）;LOX在淋巴结转移组与无转移组表达无显著性差异（P〉0．05）。③LOX、VEGF的表达与患者的年龄、性别、临床分型及临床分期等临床病理因素无关。④LOX与VEGF在人喉鳞癌组织中表达呈正相关。结论LOX与VEGF存在正相关性,可作为喉癌治疗的一个新靶点。VEGF的高表达可能是造成LOX表达变化的重要影响因素之一。     

Histone deacetylase inhibitors inhibit cervical cancer growth through Parkin acetylation-mediated mitophagy

Parkin, an E3 ubiquitin ligase, plays a role in maintaining mitochondrial homeostasis through targeting damaged mitochondria for mitophagy. Accumulating evidence suggests that the acetylation modification of the key mitophagy machinery influences mitophagy level, but the underlying mechanism is poorly understood. Here, our study demonstrated that inhibition of histone deacetylase (HDAC) by treatment of HDACis activates mitophagy through mediating Parkin acetylation, leading to inhibition of cervical cancer cell proliferation. Bioinformatics analysis shows that Parkin expression is inversely correlated with HDAC2 expression in human cervical cancer, indicating the low acetylation level of Parkin. Using mass spectrometry, Parkin is identified to interact with two upstream molecules, acetylase acetyl-CoA acetyltransferase 1 (ACAT1) and deacetylase HDAC2. Under treatment of suberoylanilide hydroxamic acid (SAHA), Parkin is acetylated at lysine residues 129, 220 and 349, located in different domains of Parkin protein. In in vitro experiments, combined mutation of Parkin largely attenuate the interaction of Parkin with PTEN induced putative kinase 1 (PINK1) and the function of Parkin in mitophagy induction and tumor suppression. In tumor xenografts, the expression of mutant Parkin impairs the tumor suppressive effect of Parkin and decreases the anticancer activity of SAHA. Our results reveal an acetylation-dependent regulatory mechanism governing Parkin in mitophagy and cervical carcinogenesis, which offers a new mitophagy modulation strategy for cancer therapy.     

中国上海汉族人群NAD(P)H氧化酶p22phox亚基C242T基因多态性与脑卒中相关性

目的:研究NAD(P)H氧化酶p22phox亚基C242T基因多态性与脑卒中的相关性?方法:收集118例脑出血患者?125例脑梗死患者和147例正常对照组,研究对象均来自上海地区汉族人群,3组在年龄?性别构成比?体质指数(BMI)等基线指标均没有明显差异,分别进行血糖?血脂等各项指标的测定,用聚合酶链反应?限制性片段长度多态性分析(PCR－RFLP)和基因测序方法比较其在不同人群中的基因突变频率?结果:脑出血组?脑梗死组CT + TT基因型(9.3%?9.6%)和T等位基因(4.7%?5.2%),均明显高于对照组(2.0%和1.0%,P < 0.05),脑梗死组中发现1例TT基因型,出血组与正常对照组均未发现TT基因型,与基因测序结果一致?采用二分类Logistic回归分析p22phox亚基C242T基因多态性与脑出血的相关性(β = 1.712,OR = 5.537,95%CI:1.120~27.381,P = 0.036),与脑梗死的相关性(β = 1.432,OR = 4.187,95%CI:0.934~18.774,P = 0.061),表明C242T基因多态性可能是脑出血?脑梗死的危险因素?结论:NAD(P)H氧化酶p22phox亚基C242T多态性与脑出血?脑梗死均有一定的相关性,可能是脑卒中的一个危险因素?但与高血压和饮酒等传统危险因素相比,C242T多态性对脑梗死的影响并不显著?     

鬼箭羽三种提取物对氧自由基作用的影响

目的观察鬼箭羽(Euonymus Alatus,EA)主要提取物对氧自由基的影响.方法从鬼箭羽中分离出总黄酮(Total Flavonolds of Euonymus Alatus,TFEA)、总甾体(Total Steroids of Euonymus Alatus,TSEA)和总多糖(Total Polysaccharide of Euonymus Alatus,TPEA),利用黄嘌呤/黄嘌呤氧化酶(Xanthine/Xanthine oxidase,Xan/XO)和多形核白细胞(Polymorphonuclear leaukocytes.PMN)呼吸爆发介导鲁米诺化学发光(Chemluminesence,CL)体系H2O2诱导大鼠肝匀浆脂质过氧化体系进行实验,观察3种成分对氧自由基作用的影响.结果 TFEA和TSEA有良好的清除氧自由基作用,其中TFEA效果最好,TSEA次之.结论鬼箭羽提取物具有抗氧化作用,其主要成分是TFEA、TSEA和TPEA.