白癜风患者血清和皮肤提取液中氧化与抗氧化能力的比较研究

目的比较白癜风患者与正常对照组人群、进展期与稳定期白癜风患者皮肤和血清中氧化与抗氧化能力关键指标,探讨氧化应激在白癜风患者中的作用与其机制。方法经被检测人员同意,随机选取50例白癜风患者(标记为观察组其中进展期患者30例,稳定期患者20例)和50名健康志愿者(标记为对照组)。试剂盒检测皮肤和血清中T-AOC、SOD,CAT,GSH-Px的活性及MDA含量。结果观察组患者皮肤提取液和血清中MDA含量明显高于对照组(P0.05),而T-AOC与GSH-Px低于对照组(P0.05),SOD在血清中二组没有差异性,在皮肤提取液中低于对照组(P0.05);进展期患者皮肤提取液和血清中MDA的含量高于稳定期患者(P0.05),而T-AOC、SOD与GSH-Px活性低于稳定期白癜风患者(P0.05);观察组与对照组、进展期和稳定期白癜风患者皮肤提取液和血清CAT水平均无统计学意义(P0.05)。结论进展期患者的白癜风病情活动与皮肤和血清中氧化与抗氧化能力密切相关。     

白癜风患者血清及皮损中某些酶及微量元素改变研究

本研究检测白癜风患者血清中超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、黄嘌呤氧化酶(XOD)活性,丙二醛(MDA)水平及血清、皮肤中锌(Zn)、铜(Cu)、硒(Se)、铁(Fe)含量。结果表明:患者血清中GSH-Px、SOD活性及Cu含量低于对照组(P<0.01),MDA、Fe含量高于对照组(P<0.01).皮损处Zn、Cu、Se或Fe含量分别低于或高于周围外观正常皮肤,治疗后血清SOD、GSH-Px活性增高、Cu、Fe含量显著降低(P<0.01)。提示:白癜风患者自由基防御系统中部分酶活性降低,Zn、Cu、Se缺乏。     

白芍总苷对轻、中度寻常性银屑病氧化应激状态的影响

目的评估轻度和中度寻常性银屑病患者氧化还原状态及白芍总苷对其的作用。方法应用分光光度法测定30例轻度和中度寻常性银屑病患者及15例健康志愿者的血清总抗氧化能力(T-AOC)水平及抗氧化酶[包括超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)]的活性。分别采用ELISA法、免疫组化SP法检测患者及志愿者血清、皮肤中8-异前列腺素F2α的表达水平。患者口服白芍总苷及外用松馏油治疗6周后,再次测定上述指标并比较治疗前后的变化。结果银屑病患者血清T-AOC水平及SOD,GSH-Px活性较健康对照组显著下降(P均<0.01),CAT活性显著高于对照组(P<0.05);患者的血清及皮损中8-异前列腺素F2α水平较健康对照组明显升高(P均<0.01);白芍总苷治疗后,T-AOC水平、SOD及GSH-Px活性显著升高,CAT活性、血清及皮损中8-异前列腺素F2α水平降低,差异均有统计学意义(P均<0.01)。结论轻度和中度银屑病患者存在氧化应激,白芍总苷具有抗氧化作用,其治疗轻、中度银屑病有效可能与调节机体氧化还原状态并使之趋于正常有关。     

Nrf2-Keap1系统及相关因子在小鼠黄褐斑组织中的表达

目的:探讨核因子E2相关因子2(Nrf2)-Kelch样环氧氯丙烷相关蛋白1(Keap1)系统及相关因子在小鼠黄褐斑模型皮肤中的变化。方法:将24只Balb/c雌性小鼠随机分成2组,每组12只。模型组采用中波紫外线照射联合黄体酮注射方法造模,对照组肌肉注射同剂量的灭菌注射用水,采用q PCR相对定量检测小鼠皮肤的Nrf2和Keap1基因表达水平,化学比色法检测小鼠皮肤中丙二醛(MDA)含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性。结果:与对照组相比,模型组小鼠皮肤组织的Keap1 mRNA表达量明显增强(P<0.01),Nrf2 mRNA表达量无明显改变(P>0.05),模型组SOD和GSH-Px活性明显下降(P<0.01),MDA含量明显上升(P<0.01)。结论:氧化应激在黄褐斑发病中起着非常重要的作用,抗氧化损伤Nrf2-Keap1系统与黄褐斑的发病关系密切,可为黄褐斑的治疗提供新的靶点。     

生殖器疱疹患者的氧化应激状态研究

目的:检测生殖器疱疹患者的氧化应激状态,以探讨其与生殖器疱疹的关系。方法:本研究通过67例生殖器疱疹患者血清中超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)和一氧化氮(NO)的水平来评估生殖器疱疹患者的氧化应激状态。结果:生殖器疱疹患者SOD及GSH-Px活力低于正常人,MDA及NO浓度高于正常人(P<0.05),且NO浓度与SOD活力呈负相关,与MDA浓度呈正相关(P<0.05)。结论:生殖器疱疹患者氧化应激失衡,表现为氧化水平升高,抗氧化能力下降。     

天疱疮和大疱性类天疱疮患者体内氧化应激指标的检测

目的 :通过检测天疱疮及大疱性类天疱疮患者血清抗氧化防御水平及皮损中8-异前列腺素F2α(8-iso-PGF2α)的表达,来推测这两种疾病患者体内是否存在氧化应激状态,探讨氧化应激在其发病机制中的作用。方法:用分光光度法测定15例天疱疮患者、15例大疱性类天疱疮患者和15例健康对照者血清总抗氧化能力(T-AOC)水平及抗氧化酶包括超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)的活性;采用免疫组化(SP法)检测15例天疱疮患者、15例大疱性类天疱疮患者皮损及10例健康对照者皮肤组织中8-iso-PGF2α的表达水平。结果:1天疱疮组及大疱性类天疱疮组血清SOD活性分别为(35.408±5.322)k U/L及(33.076±2.962)k U/L,CAT活性分别为(4.475±1.999)k U/L及(4.318±1.487)k U/L,TAOC水平分别为(12.565±1.987)k U/L及(11.006±2.298)k U/L;均高于正常对照组[SOD(30.767±2.898)k U/L,CAT(3.187±0.818)k U/L,T-AOC(8.836±2.011)k U/L](P均0.05);而天疱疮组及大疱性类天疱疮组血清GSH-Px活性分别为(271.252±96.927)k U/L和(266.109±49.721)k U/L,均低于正常对照组[GSH-Px(479.383±40.451)k U/L](P均0.05)。2天疱疮组及大疱性类天疱疮组皮损中8-iso-PGF2α水平分别为(51.029±26.960)×10-3和(14.189±10.478)×10-3,均明显高于正常对照组(4.220±2.690)×10-3(P均0.05),差异有统计学意义。3天疱疮组和大疱性类天疱疮组皮损8-iso-PGF2α水平与血清GSH-Px、SOD、CAT活性和T-AOC水平无相关性。结论 :天疱疮及大疱性类天疱疮患者体内存在氧化产物增高、抗氧化能力发生改变等氧化应激状态。氧化应激可能在其发病过程中起一定作用。     

银屑病患者抗氧化能力及8-异前列腺素F2α的检测及意义

目的 探讨银屑病患者血清及皮损中8-异前列腺素F2α的水平和血清抗氧化防御水平及其与疾病严重程度的关系.方法 分光光度法测定50例寻常性银屑病患者及15例健康对照血清总抗氧化能力(T-AOC)水平及抗氧化酶包括超氧化物岐化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化酶(GSH-Px)的活性.分别采用酶联免疫吸附试验和免疫组化SP法检测患者及健康对照血清、皮损中8-异前列腺素F2α的表达水平.结果 银屑病患者血清T-AOC水平为(12.78±7.75) U/ml,SOD活性为(28.91±9.35) U/ml,GSH-Px活性为(180.64±47.70)U,较健康对照组[T-AOC (23.17±8.81) U/ml,SOD(51.36±7.92) U/ml,GSH-Px(244.20±66.68) U]显著下降(P值均＜0.01),且重度患者组T-AOC水平[(9.06±5.30) U/ml]、SOD活性[(21.63±5.28)U/ml]较轻中度患者组[T-AOC(15.27±8.18)U/ml,SOD (33.76±8.28) U/ml]下降更为明显(P值均＜ 0.01),轻中度患者CAT活性[(36.92±11.31) U/ml]显著高于对照组[(28.55±8.57)U/ml,P＜ 0.05]及重度患者[(24.15±9.36) U/ml,P＜ 0.01],患者血清及皮损中8-异前列腺素F2α水平[(88.77±25.27) ng/L,0.0186±0.0082]较健康对照组[(38.34±8.94) ng/L,0.0027±0.0014]升高(P值均＜0.01),且重度患者组[(114.24±13.93) ng/L,0.0279±0.0027]较轻中度患者组[(71.78±14.35) ng/L,0.0125±0.0030]升高更为明显(P值均＜0.01).患者T-AOC水平以及SOD、CAT活性与银屑病面积和皮损严重程度指数(PASI)评分均呈负相关,r值分别为-0.384、-0.573、-0.444,P值均＜0.01.血清及皮损中8-异前列腺素F2α水平均与PASI评分呈正相关,r值分别为0.710、0.783,P值均＜0.01.结论 银屑病患者血清及皮损处8-异前列腺素F2α水平较以往的氧化应激指标或许更能反映机体氧化应激状态.     

黄褐斑患者血中超氧化物歧化酶活性、丙二醛和维生素C、E含量的测定

通过测定 34例黄褐斑患者血中超氧化物歧化酶 (SOD)活性、丙二醛 (MDA)和维生素 C、 E(VitC|VitE)含量，并与 30例健康对照组比较。结果发现患者的 SOD和 VitE均明显低于对照组 (P< 0.05)。而 MDA则明显高于对照组 (P< 0.01)。且对氧自由基引发本病的机制作了进一步探讨。     

白癜风患者血清过氧化氢、过氧化氢酶和谷胱甘肽过氧化物酶的检测

目的探讨体内氧化物和抗氧化物与白癜风发病的关系。方法分别检测40例白癜风患者和10例健康对照者的血清过氧化氢(H2O2)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-PX)。结果白癜风患者CAT浓度(9.31±6.52)U/mL明显低于对照组(33.05±9.47)U/mL,其进展期CAT浓度(7.3±6.01)U/mL明显低于稳定期(13.05±6.11)U/mL,差异均有统计学意义(P均<0.01);而白癜风患者H2O2和GSH-PX水平与对照组比较,差异无统计学意义(P>0.05)。结论白癜风的发生可能与血清氧化物—抗氧化物水平的变化有一定的相关性。     

低强度脉冲式超声波对糖尿病勃起功能障碍的影响及其与血清同型半胱氨酸、一氧化氮、内皮素-1及氧化应激因子的关系

目的探讨低强度脉冲式超声波(Li-PUST)对糖尿病勃起功能障碍(DMED)的影响,并分析其与血清同型半胱氨酸(Hcy)、一氧化氮(NO)、内皮素-1(ET-1)及氧化应激因子的关系。方法选取2017年10月至2019年10月安康市中心医院收治的106例DMED患者作为研究对象。随机分为观察组(n=53)和对照组(n=53)。对照组给予常规治疗,观察组在对照组基础上给予Li-PUST。收集两组治疗前后国际勃起功能指数问卷表-5(IIEF-5)评分、性生活质量满意度和血清Hcy、NO、ET-1及丙二醛(MDA)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)水平。结果治疗后,与对照组比较,观察组总有效率和性生活满意度明显提高,观察组血清Hcy、ET-1和MDA水平明显降低,血清NO、SOD和GSH-Px水平明显升高,差异具有统计学意义(P0.05)。经Spearman相关分析得知,血清NO、SOD和GSH-Px与临床疗效呈明显正相关(P0.05);血清Hcy、ET-1和MDA与临床疗效呈明显负相关(P0.05)。经单因素和Logistic回归分析模型分析得知,治疗前IIEF-5评分和治疗方案是影响DMED临床疗效的重要因素(P0.05)。结论与常规治疗比较,联合Li-PUST可明显提高DMED临床疗效,与血清Hcy、NO、ET-1及MDA、SOD、GSH-Px均相关。     

The role of oxidants and antioxidants in generalized vitiligo

Oxidative stress may be induced by increasing the generation of reactive oxygen species (ROS) and other free radicals. The generation of ROS is known to be associated with a decrease in antioxidant levels. In the present study, the role of oxidative stress was assessed in the pathogenesis of generalized vitiligo. Superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH) levels in erythrocytes and serum malondialdehyde (MDA) and nitric oxide (NO) levels were investigated in 24 patients with generalized vitiligo and 20 healthy controls. Our results indicated that significantly increased levels of erythrocyte SOD, serum MDA, and NO were associated with a marked reduction of erythrocyte GSH-Px and GSH activities in patients with generalized vitiligo (p<0.05). Our observations suggest that the presence of an imbalance in the oxidant-antioxidant system might play a role in the pathogenesis of vitiligo. Our results further support the concept that free radical-mediated damage may be the initial pathogenic event in melanocyte degeneration in generalized vitiligo.     

OXIDATIVE STRESS IN EXPERIMENTAL VITILIGO C57BL/6 MICE

Aim:

To evaluate whether oxidative stress is implicated in melanocyte damage in vitiligo.

Background:

Vitiligo is a complex disorder characterized by gradually enlarging areas of depigmentation. A new unifying hypothesis for the etiology of this pigment disorder is proposed, in which we postulate that the final destruction of melanocytes in vitiligo results from a cascade of reactions initiated by a disregulation of melanogenesis, as the result of a breakdown in free radical defense.

Methods:

We evaluated 18 vitiligo mice and 12 controls that were age matched. Parameters of oxidative stress such as catalase (CAT), superoxide dismutase (SOD), and plasma malondialdehyde (MDA) were measured by spectrophotometry.

Results:

MDA levels in vitiligo mice were significantly higher than in controls (P < 0.001). CAT, SOD, and glutathione peroxidase (GPx) activities in mice were significantly lower than controls (P < 0.05 and P < 0.001, respectively).

Conclusion:

Our results confirmed that oxidative stress plays an important role in the pathogenesis of vitiligo. Melanocyte damage in vitiligo might be linked to generalized oxidative stress. This study is the first report on antioxidant parameters in experimental vitiligo mice.     

Oxidant-antioxidant enzymes and lipid peroxidation in generalized vitiligo

Vitiligo is a common pigmentary disorder of the skin with selective destruction of melanocytes. The pathogenetic mechanisms in vitiligo have not been completely clarified. The aim of our investigation was to evaluate the oxidative stress in the pathogenesis of generalized vitiligo. Twenty-seven patients with generalized vitiligo and 24 phototype-, age-, and sex-matched healthy controls were included in this study. We analysed serum levels of malondialdehyde (MDA), nitric oxide (NO), and serum activities of superoxide dismutase (SOD) and xanthine oxidase (XO) in the patients with vitiligo and in the controls. We found significantly higher levels of MDA and XO activity (P < 0.001 and P < 0.05, respectively), and a significantly lower level of serum SOD activity (P < 0.05) in patients with vitiligo compared with the controls. However, the increase in the level of serum NO was insignificant (P > 0.05). These results suggest that lipid peroxidation of cellular membrane of melanocytes by free radicals may have a significant role in the pathogenesis of generalized vitiligo.     

Sister chromatid exchange and micronucleus studies in patients with Behçet's disease

Background:  Genetic factors that predispose individuals to Behçet's disease (BD) are considered to play important roles in the development of the disease. The aim of this study was to determine, by counting sister chromatid exchange (SCE) and micronucleus (MN) frequencies, whether DNA damage have an effect on the pathogenesis of BD. Furthermore, our aim was to show if there is an association between oxidative stress and chromosome instability in BD.
Methods:  We analyzed lymphocytes from patients with BD (16 in active and 14 in inactive periods) and 20 healthy controls for SCE and MN frequencies. In addition, malondialdehyde (MDA) level, superoxide dismutase (SOD) level, glutathione peroxidase (GSH-Px) activity, erythrocyte sedimentation rate (ESR) and polymorphonuclear leukocyte (PMNL) count were determined in the all subjects.
Results:  The SCE and MN frequencies were significantly higher in both the active and inactive period patients than in the controls (p < 0.00001, p < 0.0001, p < 0.01 and p < 0.05, respectively), and the MDA level was significantly higher in both the active and inactive period patients than in the controls (p < 0.01 and p < 0.05, respectively). In contrast, the SOD and GSH-Px levels were significantly lower in both the active and inactive period patients than in the controls (p < 0.01, p < 0.05, p < 0.01 and p < 0.05, respectively).
Conclusions:  Our results suggest that increased plasma MDA level and decreased plasma GSH-Px and SOD levels reflect the increased levels of oxidative stress in BD patients, and this situation may impair genetic stability in BD patients.     

Protective effects of β-glucan against oxidative injury induced by 2.45-GHz electromagnetic radiation in the skin tissue of rats

In recent times, there is widespread use of 2.45-GHz irradiation-emitting devices in industrial, medical, military and domestic application. The aim of the present study was to investigate the effect of 2.45-GHz electromagnetic radiation (EMR) on the oxidant and antioxidant status of skin and to examine the possible protective effects of β-glucans against the oxidative injury. Thirty-two male Wistar albino rats were randomly divided into four equal groups: control; sham exposed; EMR; and EMR + β-glucan. A 2.45-GHz EMR emitted device from the experimental exposure was applied to the EMR group and EMR + β-glucan group for 60 min daily, respectively, for 4 weeks. β-glucan was administered via gavage at a dose of 50 mg/kg/day before each exposure to radiation in the treatment group. The activities of antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), as well as the concentration of malondialdehyde (MDA) were measured in tissue homogenates of the skin. Exposure to 2.45-GHz EMR caused a significant increase in MDA levels and CAT activity, while the activities of SOD and GSH-Px decreased in skin tissues. Systemic β-glucan significantly reversed the elevation of MDA levels and the reduction of SOD activities. β-glucan treatment also slightly enhanced the activity of CAT and prevented the depletion of GSH-Px activity caused by EMR, but not statistically significantly. The present study demonstrated the role of oxidative mechanisms in EMR-induced skin tissue damages and that β-glucan could ameliorate oxidative skin injury via its antioxidant properties.     

Serum antioxidant activities, malondialdehyde and nitric oxide levels in human cutaneous leishmaniasis

Leishmania sp. are obligate intracellular protozoa that infect and replicate within mammalian macrophages. Macrophages, neutrophils and other phagocytic cells are key components of the antimicrobial and tumoricidal immune responses. These cells are capable of generating large amounts of reactive oxygen species (ROS) and reactive nitrogen species (RNS). To examine antioxidant status and lipid peroxidation in cutaneous leishmaniasis (CL) patients, activities of two ROS scavenging enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and the levels of malondialdehyde (MDA) and nitric oxide (NO(.)) have been studied in serum. Blood samples were taken from CL patients before treatment (n = 27) and after the treatment (n = 18). NO(.) and MDA levels, SOD and GSH-Px activities were compared between untreated and treated CL patients and control subjects (n = 23). There was a significant decrease in SOD and GSH-Px activities in the CL patients (P < 0.0001). Significantly higher levels of serum MDA and NO(.) levels were found in CL patients, compared to controls and treated patients. It may be suggested that the overproduction of ROS and RNS results in oxidative stress and the acceleration of lipid peroxidation in CL patients, resulting from altered enzymatic antioxidant activities.     

Role of cellular oxidative stress and cytochrome c in the pathogenesis of psoriasis

Oxidative-free radicals and apoptosis have linked to chronic skin diseases. Higher levels of oxidative radicals and the release of mitochondrial cytochrome c may have a role in the pathogenesis of psoriasis. We investigated the possible role of cellular oxidative stress and release of cytochrome c of mitochondria in the pathogenesis of psoriasis. Disease severity was assessed by psoriasis area severity index score (PASI) of 55 psoriasis patients, they grouped as mild (11), moderate (20) and severe (24), also 20 healthy individuals used as controls. All groups were subjected for serum malondialdehyde (MDA), nitric oxide (NO·), superoxide dismutase (SOD), catalase (CAT), total antioxidant status (TAS) and serum cytochrome c concentrations. We found that, (1) Severity wise increase in MDA and NO·, and decrease in SOD, CAT and TAS levels in all patients with different degrees of psoriasis; (2) PASI showed positive correlation with the increase in MDA and NO·, and negatively with decreased SOD, CAT and TAS levels; (3) significant increase in cytochrome c level was observed among psoriasis patients which showed negative correlation to MDA and NO· levels in mild and positively with moderate and severe groups. The release of mitochondrial cytochrome c indicates the induction of apoptosis mediated via oxidative stress which ultimately plays role in the pathogenesis of psoriasis.     

绞股蓝皂甙对光损伤小鼠表皮中抗氧化应激酶的影响

目的观察不同浓度绞股蓝皂甙(GP)霜对小鼠皮肤光损伤模型中氧化应激相关酶活性的影响。方法采用多次UVB辐射Balb/C小鼠建立6组皮肤光损伤的动物模型,用可见光分光光度法和紫外线分光光度法测各组皮肤组织中超氧化物岐化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)、谷胱甘肽还原酶(GR)的含量。结果 1.5%绞股蓝皂甙霜组Balb/C小鼠表皮中SOD、CAT、GSH-Px、GR活力高于UVB组(P0.05),与维生素E霜组比较无明显差别。结论 1).1.5%绞股蓝皂甙霜可使UVB照射后光损伤Balb/C小鼠表皮中SOD,CAT,GSH-Px,GR活性得到恢复,其抗氧化作用与维生素E霜相似。2).1.5%绞股蓝皂甙霜有抗氧化损伤的作用,其保护的机制可能与清除氧自由基,提高部分抗氧化酶活性有关。