二甲亚砜和戊二醛治疗根尖周炎临床报告

目的观察二甲亚砜和戊二醛治疗根尖周炎的疗效。方法选择急慢性根尖周炎172例,采用二甲亚砜和戊二醛作根管消毒剂。结果二甲亚砜和戊二醛治疗根尖周炎总有效率为93.03%。结论用二甲亚砜和戊二醛治疗根尖周炎临床疗效显著。     

二甲亚砜治疗深龋及早期牙髓炎的近期疗效观察

龋病和牙髓病的治疗是临床工作重要组成部分,占有大量比例,传统治疗是以干髓、塑化等疗法保存牙齿,操作复杂,复诊多次,远期疗效差,为此我们选用20％二甲亚砜与氢氧化钙联合盖髓,以提高炎症性牙髓炎治疗效果,经临床应用观察,抗炎作用明显加强,获得了较好疗效,现概述如下。     

二甲亚砜凝胶治疗运动损伤

目的：探索二甲亚砜凝胶对运动所致软组织损伤的疗效。方法：将１６０例闭合性软组织损伤病人，按就诊的先后次序分为２组。治疗组８０例，其中男性４８例，女性３２例，年龄２０．０±ｓ１．０ａ，用二甲亚砜凝胶药膏每天局部贴敷，更换药膏２次。对照组８０例，男性４４例，女性３６例，年龄２０±３ａ，用伤湿止痛膏，每天更换药膏２次。２组全疗程均为７ｄ。结果：治疗组总有效率为９５％，对照组总有效率为７５％（Ｐ＜０．０１）。２组用药过程未见明显副作用。结论：二甲亚砜凝胶是治疗软组织损伤疗效较好的外用药，其疗效优于伤湿止痛膏。     

二甲亚砜,人参总皂甙对大鼠呼吸窘迫综合征的防治作用及机理探讨

观察二甲亚砜（DMSO）和人参总皂甙（GS）对大鼠油酸型呼吸窘迫综合征（RDS）的防治作用。发现DMSO及GS不能明显减轻肺水肿，但DMSO和GS均可保护过氧化物歧化酶（SOD）活性、减少血浆丙二醛（MDA）生成及减少动脉血氧分压（PaO2）下降。DMSO还能减少肺蛋白渗出及红细胞外漏，电镜显示DMSO能减轻呼吸膜损伤，GS可减少Ⅱ型肺泡上皮细胞内空泡变性极层体。提示DMSO、GS对油酸所致RDS具有一定防治作用。     

药用辅料二甲亚砜有关物质测定方法改进

摘 要 目的：参考各国药典对药用辅料二甲亚砜中有关物质的测定方法进行改进。 方法: 采用气相色谱法,以二苯甲烷为内标,Agilent DB wax毛细管柱（0.32 μm×30 m, 0.5 μm）,柱温:150℃,进样口温度:230℃,FID检测器温度:250℃,分流比：20∶1,进样量:2 μl。 结果: 在该色谱条件下,二甲亚砜中各杂质能完全分离;二甲基砜在6.58～526.50 μg·ml-1 的浓度范围线性关系良好（r=0.999 9）;平均回收率为101.27%（RSD=0.46%,n=6）。 结论: 本方法准确度高、重复性好,可用于二甲亚砜有关物质的测定。     

红强二甲亚砜搽剂治疗局限性神经性皮炎60例

目的 观察红强二甲亚砜搽剂治疗局限性神经性皮炎的临床疗效及安全性。方法 局限性神经性皮炎120例，随机分为治疗组和对照组各60例。治疗组外用红强二甲亚砜搽剂，对照组外用复方吲哚美辛酊，tid，每周复诊1次，共3周。结果 治疗组和对照组总有效率分别为93．3％，63．3％（P〈0．01）；复发率分别为18．3％，36．7％（P〈0．05）。两组不起反应发生率差异无显著性。结论 红强二甲亚砜搽剂治疗神经性皮炎是一种安全、有效、止痒迅速、价廉适用的外用药。     

高效液相色谱法测定倍他米松二甲亚砜溶液的含量

目的建立测定倍他米松二甲亚砜溶液中倍他米松含量的高效液相色谱法。方法固定相：Hyeril ODS2色谱柱(250 mm ×4.6 mm，5 μm);流动相：甲醇-纯化水(70∶30);检测波长：240 nm;流速：1.0 mL·min^-1;进样量：20 μL;柱温：35 ℃。结果线性关系良好，回收率为99.67%，RSD＝0.9%(n＝9)。结论该方法简便，结果准确，可作为倍他米松二甲亚砜溶液的质量控制方法。     

三聚甲醛伍用二甲亚砜作为牙髓失活剂的临床应用

在牙髓病治疗过程中,主要采用亚砷酸失活剂。因其对根尖周组织的损害和严格的复诊时间给医生和患者带来许多不便,而三聚甲醛失活剂作用缓慢,治疗牙髓病常需要1～3wk时间,也给医患带来一些麻烦。为此,我们将学者们提出的三聚甲醛和二甲亚砜作为牙髓失活剂用于临床。二甲亚砜不仅能加速甲醛分子进入牙髓过程,而且也使失活剂增强了镇痛、杀菌和抑菌作用。上述失活剂临床效果较好,而且无明显副作用。其中的二甲亚砜容易通过非损伤性生物膜进行渗透。     

Protection of rabbit kidney from ischemia/reperfusion injury by green tea polyphenol pretreatment

Reactive oxygen species (ROS) have been implicated in the pathogenesis of renal injury after ischemia/reperfusion (I/R). Recently, green tea polyphenols (GTP) have been found to protect the myocardium and liver against II/R injury. Less attention, however, has been paid to the protective effects of GTP with respect to the kidneys. This study was designed to determine whether GTP could protect renal cells from ischemic injury. The rabbits were divided into three groups of equal size: control (sham-operated), I/R + vehicle (normal saline) and I/R + GTP groups. Each group consisted of six rabbits. Animals underwent 30, 60, 90 and 120 min of ischemia, followed by 24 h of reperfusion, respectively. GTP (200 microg/kg) or the vehicle was administered 45 min prior to commencement of I/R. The results demonstrated that GTP administration resulted in a significant (P < 0.05) reduction of renal damage after 90 min of ischemia, as indicated by the decreased levels of creatinine and urea nitrogen in serum. These results were confirmed by histological examinations, which showed that GTP pretreatment inhibited necrosis and sloughing of the proximal tubules induced by I/R. Examinations also showed decreased necrotic areas in the medulla and decreased glomerular collapse in the I/R-injured rabbits. Moreover, the infiltration of CD8+ T cells was considerably decreased in GTP-treated kidneys. The results of this study suggest that GTP can reduce renal injury by preventing the oxidative stress dependent on I/R and may be used in renal transplantation as an antioxidant.     

酒石酸亚铁比色法测定黄鹂芽中茶多酚的含量

目的测定黄鹂芽茶中茶多酚的含量。方法采用国家标准酒石酸亚铁比色法,在535nm处测定吸光度,用对照品标准曲线法测定黄鹂芽茶中茶多酚的含量。结果茶多酚在10～100μg.L-1呈良好的线性关系;回归方程:Y=8.104 X-0.000 9,r=0.999 8,平均加样回收率为96.5%,RSD为2.1%(n=5)。结论酒石酸亚铁比色法测定茶多酚准确、可靠,可作为黄鹂芽中茶多酚的含量测定方法。     

复方茶多酚片预防性降脂减肥作用研究

目的研究复方茶多酚片对高血脂大鼠降脂及减肥作用。方法采用预防性脂代谢紊乱模型法,对复方茶多酚片进行降血脂和减肥试验。结果复方茶多酚片150和750 mg/kg剂量组具有显著降低高脂大鼠体重、内脏脂肪(P<0.05)和血清总胆固醇(P<0.01)的作用,750 mg/kg剂量组具有降低脂体比作用(P<0.05)。复方茶多酚片30,150和750 mg/kg剂量组均具有降低血清甘油三酯作用(P<0.01)和不同程度提高高密度脂蛋白与总胆固醇作用(P<0.05,P<0.01)。结论复方茶多酚片具有降脂减肥作用。     

Synergistic cytotoxicity and DNA strand breaks in cells and plasmid DNA exposed to uranyl acetate and ultraviolet radiation

Depleted uranium (DU) has a chemical toxicity that is independent of its radioactivity. The purpose of this study was to explore the photoactivation of uranyl ion by ultraviolet (UV) radiation as a chemical mechanism of uranium genotoxicity. The ability of UVB (302 nm) and UVA (368 nm) radiation to photoactivate uranyl ion to produce single strand breaks was measured in pBR322 plasmid DNA, and the presence of adducts and apurinic/apyrimidinic sites that could be converted to single strand breaks by heat and piperidine was analyzed. Results showed that DNA lesions in plasmid DNA exposed to UVB‐ or UVA‐activated DU were only slightly heat reactive, but were piperidine sensitive. The cytotoxicity of UVB‐activated uranyl ion was measured in repair‐proficient and repair‐deficient Chinese hamster ovary cells and human keratinocyte HaCaT cells. The cytotoxicity of co‐exposures of uranyl ion and UVB radiation was dependent on the order of exposure and was greater than co‐exposures of arsenite and UVB radiation. Uranyl ion and UVB radiation were synergistically cytotoxic in cells, and cells exposed to photoactivated DU required different DNA repair pathways than cells exposed to non‐photoactivated DU. This study contributes to our understanding of the DNA lesions formed by DU, as well as their repair. Results suggest that excitation of uranyl ion by UV radiation can provide a pathway for uranyl ion to be chemically genotoxic in populations with dermal exposures to uranium and UV radiation, which would make skin an overlooked target organ for uranium exposures. Copyright © 2014 John Wiley & Sons, Ltd.     

人支气管上皮细胞5-脂氧合酶介导4-氨基联苯的活化及DNA损伤

目的探讨人支气管上皮(HBE)细胞内5-脂氧合酶(5-LOX)对4-氨基联苯(4-ABP)的氧化活化及所致DNA损伤,为LOX作为前致癌物氧化活化的代谢途径提供依据。方法①体外酶系统实验:4-ABP在含有大豆脂氧合酶(SLO)的体外酶体系中反应,用分光光度法检测体系中反应产物生成。②细胞实验:4-ABP 100～800μmol.L-1染毒HBE细胞,MTT法检测HBE细胞存活率;Western印迹法检测5-LOX蛋白表达;单细胞凝胶电泳检测DNA损伤。同时,检测特异性5-LOX抑制剂AA861对5-LOX蛋白表达和多种酶抑制剂对细胞存活率和DNA损伤的影响。结果在过氧化氢参与下,SLO可以协同氧化4-ABP,LOX抑制剂去甲二氢愈创木酸可抑制该协同氧化作用。4-ABP可以使HBE细胞内5-LOX蛋白表达增加,AA861对5-LOX蛋白表达没有影响;4-ABP 400μmol.L-1可以使HBE细胞产生明显的DNA损伤,彗星细胞的阳性率达47.7%(P<0.01),AA861和萘普生可以抑制该浓度4-ABP所致的DNA损伤,最大保护率分别为58.1%和21.7%。结论 4-ABP上调HBE的5-LOX蛋白表达。5-LOX可能通过介导4-ABP协同氧化,导致DNA损伤,这可能是4-ABP致癌的机制之一。     

Genotoxicity of short single-wall and multi-wall carbon nanotubes in human bronchial epithelial and mesothelial cells in vitro

Although some types of carbon nanotubes (CNTs) have been described to induce mesothelioma in rodents and genotoxic effects in various cell systems, there are few previous studies on the genotoxicity of CNTs in mesothelial cells. Here, we examined in vitro DNA damage induction by short multi-wall CNTs (MWCNTs; 10–30 nm × 1–2 μm) and single-wall CNTs (SWCNTs; >50% SWCNTs, ∼40% other CNTs; <2 nm × 1–5 μm) in human mesothelial (MeT-5A) cells and bronchial epithelial (BEAS 2B) cells, using the single cell gel electrophoresis (comet) assay and the immunoslot blot assay for the detection of malondialdehyde (M₁dG) DNA adducts. In BEAS 2B cells, we also studied the induction of micronuclei (MN) by the CNTs using the cytokinesis-block method. The cells were exposed to the CNTs (5–200 μg/cm², corresponding to 19–760 μg/ml) for 24 and 48 h in the comet assay and for 48 and 72 h in the MN and M₁dG assays. Transmission electron microscopy (TEM) showed more MWCNT fibres and SWCNT clusters in BEAS 2B than MeT-5A cells, but no significant differences were seen in intracellular dose expressed as area of SWCNT clusters between TEM sections of the cell lines. In MeT-5A cells, both CNTs caused a dose-dependent induction of DNA damage (% DNA in comet tail) in the 48-h treatment and SWCNTs additionally in the 24-h treatment, with a statistically significant increase at 40 μg/cm² of SWCNTs and (after 48 h) 80 μg/cm² of both CNTs. SWCNTs also elevated the level of M₁dG DNA adducts at 1, 5, 10 and 40 μg/cm² after the 48-h treatment, but both CNTs decreased M₁dG adduct level at several doses after the 72-h treatment. In BEAS 2B cells, SWCNTs induced a statistically significant increase in DNA damage at 80 and 120 μg/cm² after the 24-h treatment and in M₁dG adduct level at 5 μg/cm² after 48 h and 10 and 40 μg/cm² after 72 h; MWCNTs did not affect the level of DNA damage but produced a decrease in M₁dG adducts in the 72-h treatment. The CNTs did not affect the level of MN. In conclusion, MWCNTs and SWCNTs induced DNA damage in MeT-5A cells but showed a lower (SWCNTs) or no (MWCNTs) effect in BEAS 2B cells, suggesting that MeT-5A cells were more sensitive to the DNA-damaging effect of CNTs than BEAS 2B cells, despite the fact that more CNT fibres or clusters were seen in BEAS 2B than MeT-5A cells. M1dG DNA adducts were induced by SWCNTs but decreased after a 3-day exposure to MWCNTs and (in MeT-5A cells) SWCNTs, indicating that CNTs may lead to alterations in oxidative effects within the cells. Neither of the CNTs was able to produce chromosomal damage (MN).     

Efficient protection of human bronchial epithelial cells against sulfur and nitrogen mustard cytotoxicity using drug combinations.

The aim of this study was to test the efficacy of several candidate molecules against sulfur mustard (SM) and nitrogen mustard (HN2) using a human bronchial-epithelial cell line (16HBE14o-). Candidate molecules were chosen on the basis of the known cytotoxicity mechanisms of mustards or their efficacy previously observed on other cellular models. It included the sulfhydryl-containing molecules N-acetyl-cysteine (NAC) and WR-1065, the nucleophile hexamethylenetetramine (HMT), the energy-level stabilizer niacinamide (NC), the antioxidant dimethylthiourea (DMTU), L-arginine analogues such as L-thiocitrulline (L-TC) and L-nitroarginine methyl ester (L-NAME), and the anti-gelatinase doxycycline (DOX). Their efficacy was determined using 2-(4-[3-iodophenyl)-3-(4-nitrophenyl)-5-(2, 4-disulfophenyl)-2Htetrazolium (WST-1) reduction by viable cells 24 h after initial exposure to 100 microM HN2 or SM. On individual immediate cotreatment, some molecules exhibited selective protection against only one mustard, such as DMTU and WR-1065 against HN2 and DOX against SM, whereas NAC and L-TC were effective against both SM and HN2 cytotoxicity. However, as the level of protection against SM was always weak compared to HN2, several combinations were investigated against SM to improve the protection. The effective combinations (L-TC + DOX, NAC + DOX, NAC + DMTU, NAC + HMT, NC + DOX) combined agents, reducing the bioavailability of the mustard with compounds possibly acting on the consequences of alkylation. One of these combinations, NAC + DOX, appeared to be the most interesting, as these agents are already used in human therapy. It exhibited good efficacy in delayed cotreatment (up to 90 min) against SM.     

红景天苷对力达霉素诱导人二倍体成纤维细胞衰老的干预作用

目的:研究红景天苷对力达霉素导致DNA损伤后所诱导的细胞衰老的调节作用。方法:采用MTT法测定药物对人胚肺二倍体成纤维细胞2BS活力的影响;衰老相关的β-半乳糖苷酶染色法观察细胞衰老形态变化;流式细胞术检测细胞周期分布以及γ-H2AX蛋白表达变化;蛋白免疫印迹技术观察p53和p21蛋白表达水平变化。结果:较低浓度(低于0.1 nmol.L-1)力达霉素能够抑制2BS细胞增殖,诱导β-半乳糖苷酶染色率显著升高和G2/M期阻滞,并使DNA损伤相关的γ-H2AX蛋白以及p53和p21蛋白表达升高。红景天苷能够显著干预力达霉素诱导的上述细胞衰老样表型及相关分子信号变化。结论:红景天苷能够抑制基因毒药物所致DNA损伤及其诱导的细胞衰老。     

茶多酚有效成分对淋巴细胞增殖的抑制和抗氧化作用

研究表明,茶多酚具有很强的消除有害自由基、抗衰老等多种药理作用[1],茶多酚临床治疗白癜风具有较明显的效果,但其各类组分在临床治疗白癜风所发挥的作用还未见报道。1材料与方法1.1动物C57BL/6(B6)小鼠,体质量(20±2)g,由浙江中医药大学实验动物中心提供。1.2主要药品与试剂H2O2、EGCG均购自美国Sigma公     

Cytogenetic analysis of micronuclei and cell death parameters in epithelial cells of pesticide exposed tea garden workers

Buccal micronucleus cytome assay was carried out in 47 exposed (sprayers and leaf harvesters), 47 non-exposed (controls) to determine the extent of damage working in the tea plantations of Terai region of West Bengal, India. As the pesticide exposed male workers were found to consume alcohol and smoked cigarettes/bidis, 35 smokers and 30 alcoholics were also included for comparison. Results showed a significant difference in micronuclei (9.91?±?2.74, p?≤?.001), nuclear bud (4.98?±?1.31, p?≤?.001), binucleate (6.26?±?2.84, p?≤?.001), karyorrhectic (8.36?±?2.28, p?≤?.001), pyknotic (5.62?±?1.78, p?≤?.05) as well as karyolytic (6.81?±?3.00, p?≤?.001) nuclei compared with control. Comparison also revealed a higher frequency of micronuclei (6.11?±?2.55, p?≤?.01), nuclear bud (4.06?±?1.97, p?≤?.05), binucleate (4.34?±?1.85, p?≤?.001), karyorrhectic (6.83?±?2.12, p?≤?.001), and karyolytic (6.20?±?2.54, p?≤?.001) nuclei except pyknotic cell in the smoker than control. Frequency of binucleate (3.80?±?1.73, p?≤?.05), karyorrhectic (5.57?±?2.34, p?≤?.05), pyknotic (5.50?±?1.36, p?≤?.05), and karyolytic (6.30?±?2.71, p?≤?.001) nuclei was higher in the alcoholics than control (non-alcoholics), whereas the micronuclei and nuclear bud were found to be non-significant compared with the control. Our analyses also revealed a higher proportion of the micronucleus and the cell death parameters in the pesticide exposed males than females, which indicated that pesticide, smoking, and alcohol may act synergistically to cause more damage to the buccal epithelial cells. However, age and the exposure duration have no influence on the micronucleus and other cell death parameters.