褪黑素对糖尿病合并创伤应激大鼠细胞因子及氧化应激的影响

目的 :探讨褪黑素干预治疗对糖尿病合并严重创伤应激大鼠血清TNF α、IL 6及氧化应激指标的影响。方法 :对糖尿病大鼠行左下肢截肢术作为创伤应激 ,术后给予褪黑素 1mg/kg/赋型剂腹腔注射 ,观察术后 2h、6h、12h、2 4h、72h各组大鼠血清TNF α、IL 6、SOD、MDA及GSH水平的变化。结果 :对糖尿病大鼠行截肢术后 ,血清TNF α、IL 6水平升高 ,SOD、GSH水平均明显降低 ,MDA水平明显升高 (P <0 .0 1) ,褪黑素干预组血清TNF α、IL 6水平降低 ,SOD、GSH水平均明显升高 ,MDA水平下降 (P <0 .0 5 )。结论 :褪黑素干预治疗可使糖尿病合并严重创伤应激大鼠前炎症细胞因子下降 ,抗氧化应激能力提高     

2型糖尿病并发不同程度肾病患者血清APN和VEGF表达与氧化应激的相关性

目的探讨2型糖尿病(T2DM)并发不同程度肾病患者血清脂联素(APN)和血管内皮生长因子(VEGF)表达与氧化应激的相关性。方法选择T2DM并发不同程度肾病患者90例,按肾损害程度不同分为观察1组、观察2组、观察3组各30例,另选择同期健康体检者30例设为对照组。分别检测和比较4组血清APN、VEGF及氧化应激指标超氧化物歧化酶(SOD)、丙二醛(MDA)、谷胱甘肽过氧化物酶(GSH-Px)水平,并分析其指标相关性。结果 3个观察组患者空腹血糖(FPG)水平较对照组明显升高(P<0.05);4组患者腰臀比(WHR)及总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)、高密度脂蛋白(HDL-C)水平比较差异无统计学意义(P>0.05);观察2、观察3组患者24 h蛋白排泄量(UAER)水平较观察1组显著升高(P<0.05)。观察1、观察2、观察3组患者血清APN及SOD、GSH-Px较对照组明显下降,且观察3组下降程度明显高于观察1组和观察2组(P<0.05);血清VEGF和MDA较对照组明显上升,且观察3组上升程度明显高于观察1组和观察2组(P<0.05)。相关性回归分析显示,T2DM患者血清APN水平与SOD、GSH-Px呈明显正相关,与MDA呈明显负相关(P<0.05);VEGF水平与SOD、GSH-Px呈明显负相关,与MDA呈明显正相关(P<0.05)。观察1、观察2、观察3组患者血清APN与VEGF均表现为明显负相关(r=-0.72,P<0.05)。结论 T2DM并发不同程度肾病患者血清APN和VEGF表达与氧化应激反应具有显著相关性,可作为临床T2DM并发不同程度肾病患者诊断及治疗的重要指标。     

菊粉对代谢综合征患者炎症及氧化应激水平的影响

目的研究菊粉对代谢综合征(MS)患者炎症因子及氧化应激水平的影响。方法将204例未采用药物治疗的MS患者随机分为菊粉组和对照组,分别给予菊粉和安慰剂治疗,两组同时给予饮食及运动指导治疗。于治疗前及治疗8 w后检测丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、白细胞介素(IL)-6、超敏C反应蛋白(hs-CRP)、空腹血糖(FPG)、空腹胰岛素(FIns)水平,并计算胰岛素抵抗指数(HOMA-IR)。结果治疗后菊粉组MDA、IL-6、hs-CRP、FPG、FIns、HOMAIR显著下降,SOD、GSH-Px水平显著升高(P0.05);对照组FPG、HOMA-IR显著下降(P0.05);其余指标治疗前后比较差异无统计学意义(P0.05);治疗后菊粉组MDA、hs-CRP、IL-6、FPG、HOMA-IR明显低于对照组,SOD、GSH-Px水平明显高于对照组(P0.05);两组FIns差异无统计学意义(P0.05)。结论菊粉能降低MS患者hs-CRP、IL-6、MDA水平,提高抗氧化物SOD、GSH-Px水平并改善胰岛素抵抗(IR)。     

糖尿病脂质过氧化物及抗氧化酶活性与高脂血症的关系

本文通过对糖尿病患者血清内二醛(MDA),超氧化物歧化酶(SOD)及全血谷胱甘肽过氧化酶(GSH-Px)与高脂血症关系的研究.结果表明糖尿病患者MDA含量升高,SOD、GSH-Px活性下降,当合并高脂血症时,其升高与下降更明显,与糖尿病血脂正常组比较有显著性差异(P＜0.01).糖尿病高脂血症组血管病变发生率明显高于糖尿病血脂正常组(P＜0.01).提示在临床工作中控制血糖、纠正高脂血症及中止脂质过氧化损伤是防止血管病变的关键.     

褪黑素对糖尿病应激状态垂体—肾上腺轴功能的影响

目的 :探讨褪黑素对糖尿病应激状态垂体 肾上腺轴功能影响及改善糖代谢紊乱作用的神经内分泌机制。方法 :采用随机、单盲、安慰剂平行对照的方法 ,连续观察 3天外源性褪黑素及安慰剂对 37例糖尿病急性并发症患者垂体 肾上腺轴及糖尿病急性代谢紊乱相关指标的影响 ;并观察给药两周后患者糖代谢控制情况。结果 :①患者下丘脑 垂体 肾上腺 (HPA)轴处于激活状态 ,于药物干预前血浆ACTH和皮质醇水平均高于正常值 ,两组间血浆ACTH和皮质醇水平的差异无显著意义 (P >0 .0 5 ) ;②药物干预后第 1天两组间血浆ACTH和皮质醇水平均有所下降 ,但差异无显著意义 (P >0 .0 5 ) ;药物干预后第 2天和第 3天褪黑素组血浆ACTH和皮质醇下降程度均明显高于安慰剂组 ,两组间差异具显著意义 (P <0 .0 5 ) ;③药物预后 3d内褪黑素对血浆血糖、HCO3 -、阴离子间隙及血浆渗透压等糖尿病急性代谢紊乱相关指标无明显影响。给药两周后褪黑素组患者血浆空腹血糖、餐后血糖及果糖胺水平均较安慰剂组明显下降 ,两组间差异具显著意义 (P <0 .0 5 )。结论 :褪黑素对糖尿病应激状态垂体 肾上腺功能有一定抑制作用 ,适度的抑制糖尿病急性并发症患者HPA轴功能可能对糖代谢的控制及疾病预后转归有利。     

褪黑素对糖尿病大鼠急性创伤时糖、脂代谢的作用研究

目的:观察急性创伤应激状态下糖尿病大鼠糖、脂代谢水平的变化,并探讨褪黑素对其的影响。方法:设正常对照组、糖尿病对照组、糖尿病 溶媒组、糖尿病 褪黑素1组、糖尿病 褪黑素2组,观察糖尿病大鼠经17d褪黑素处理后在创伤应激时血糖、血清甘油三酯、胆固醇水平的变化。结果:创伤应激后糖尿病大鼠血糖明显升高,血清甘油三酯、胆固醇水平无明显改变。每日腹腔注射0.1mg/kg或0.2mg/kg的褪黑素对创伤应激前、后糖尿病大鼠血糖、血清甘油三酯、胆固醇水平无显著影响(P>0.05)。结论:急性创伤应激可使糖尿病大鼠血糖升高(P<0.05),而对血清甘油三酯、胆固醇水平无明显影响(P>0.05);褪黑素对糖尿病大鼠创伤应激前、后血糖、血清甘油三酯、胆固醇水平无显著影响(P>0.05)。     

解毒化瘀方对内毒素血症大鼠肝细胞线粒体氧化损伤的影响

目的:观察解毒化瘀方对内毒素血症( endotoxemia,ETM)大鼠肝细胞线粒体氧化损伤的影响.方法:将56只大鼠随机分为正常对照组及内毒素注射后6小时、12小时、24小时组和解毒化瘀方6小时、12小时、24小时组.眼眶取血,检测大鼠血清肿瘤坏死因子(TNF)-α水平,同时取肝组织分离线粒体,测定其丙二醛(MDA)的含量及超氧化物岐化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性.结果:在注射内毒素6小时后,大鼠血清TNF-α水平及线粒体MDA的含量升高,线粒体SOD、GSH-Px活性下降,随着时间的延长,TNF-α水平及MDA的含量进一步升高,SOD、GSH-Px活性明显下降.与对应的内毒素组比较,经解毒化瘀方处理后,TNF-α水平及MDA的含量均降低,SOD、GSH-Px活性均升高.结论:解毒化瘀方对内毒素刺激Kupffer细胞释放TNF-α有抑制作用,同时减少内源性自由基的生成,提高机体的抗氧化损伤能力,具有保护肝细胞的作用.     

下肢血管病变与体内自由基

目的 研究自由基产生和抗氧化能力改变在糖尿病及出现下肢血管病变患者中的变化情况,探讨体内自由基水平与下肢血管病变的联系.方法 根据踝臂指数和B型超声将100例糖尿病患者分为A、B两组.A组,糖尿病伴下肢血管病变组60例;B组,糖尿病不伴下肢血管病变组40例.根据空腹血糖将A组分为两组,A1组31例血糖在7.0～15.0 mmoL/L之间,A2组29例血糖≥15.0 mmol/L,无酮症酸中毒及糖尿病高渗性昏迷.各组患者肾功、肝功和心脏功能正常.25例健康成人做对照.分别检测各组患者血清活性氧(ROS)、丙二醛(MDA)及符胱甘肽过氧化物酶(GSH-Px)、超氧化物歧化酶(SOD)的水平,分析不同组别患者血清中上述各指标水平的变化.结果 A组和B组患者血清中的ROS、MDA水平均高于健康成人组.A组患者血清中的ROS、MDA水平显著高于B组患者(JP<0.05);而GSH-Px、SOD水平显著低于B组患者(P<0.05).结论 糖尿病患者及下肢血管病变患者体内存在着氧化应激,糖尿病伴下肢血管病变患者较糖尿病不伴下肢血管病变患者自由基水平升高更明显.     

胃炎灵胶囊对慢性萎缩性胃炎模型大鼠氧化-抗氧化平衡的影响

[目的]观察胃炎灵胶囊对慢性萎缩性胃炎(CAG)模型大鼠氧化-抗氧化平衡的影响。[方法]设立空白对照组,并采用综合法复制CAG动物模型32只,随机分为4组,即模型组、胃炎灵大剂量组、胃炎灵小剂量组、维酶素组,每组8只。治疗后分别对各组大鼠胃组织谷胱甘肽-过氧化物酶(GSH-Px)、一氧化氮(NO),胃组织及血清超氧化物歧化酶(SOD)活性、丙二醛(MDA)水平进行检测。[结果]与空白组比较,模型组大鼠胃组织GSH-Px、SOD活性下降(P<0.01),MDA、NO水平升高(P<0.01);血清SOD活性下降(P<0.01),MDA水平升高(P<0.01);与模型组比较,胃炎灵胶囊可提高胃组织GSH-Px、SOD活性(P<0.05,<0.01),降低MDA、NO水平(P<0.01,<0.05),提高血清SOD活性(P<0.05),降低MDA水平(P<0.05),且以胃炎灵胶囊大剂量组作用显著。[结论]胃炎灵胶囊具有提高抗氧化酶活性,减轻自由基损伤和抑制脂质过氧化物反应的作用。     

前列舒通胶囊联合α-硫辛酸对中老年2型糖尿病勃起功能障碍患者血清同型半胱氨酸、一氧化氮及氧化应激产物的影响

目的探讨前列舒通胶囊联合α-硫辛酸对老年2型糖尿病勃起功能障碍患者血清同型半胱氨酸(Hcy)、一氧化氮(NO)及氧化应激产物的影响。方法中老年2型糖尿病勃起功能障碍患者54例,随机分为对照组和实验组,每组27例,分别给予相应的药物治疗。治疗结束后,对所有患者的血清Hcy、NO及氧化应激产物相关指标进行检测。结果治疗后,与对照组比较,实验组患者血清Hcy水平较低(P0.05),血清NO、一氧化氮合酶(NOS)水平较高(P0.05),血清超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)水平较高,血清丙二醛(MDA)水平较低(P0.05),血清内皮素(ET)-1水平较低(P0.05),IEF-5评分较高(P0.05)。结论前列舒通胶囊联合α-硫辛酸能够显著降低2型糖尿病勃起功能障碍患者血清Hcy、MDA以及ET-1水平,提高血清NO、NOS、SOD以及GSH-Px水平,减轻氧化应激反应,提高治疗效果。     

Melatonin inhibits lipid peroxidation and stimulates the antioxidant status of diabetic rats

Although melatonin has been established as a free radical scavenger and antioxidant, its effects in diabetes have not been thoroughly investigated. The purpose of this study, therefore, was to investigate the effects of melatonin administration on lipid peroxidation and antioxidant status in streptozotocin (STZ)-induced diabetes in rats. Concentrations of malondialdehyde (MDA) and reduced glutathione (GSH) in erythrocytes and activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were compared in 3 groups of 10 rats each [control non-diabetic rats (group I), untreated diabetic rats (group II) and diabetic rats treated with melatonin (group III)]. In the study groups, diabetes developed 3 days after intraperitoneal (i.p.) administration of a single 60-mg/kg dose of STZ. Thereafter, while the rats in group II received no treatment, the rats in group III began to receive a 10-mg/kg i.p. dose of melatonin per day. After 6 wk, the rats in groups II and III had significantly lower body weights and significantly higher blood glucose levels than the rats of group I (P<0.001 and P<0.001, respectively). There were no significant differences in body weight or blood glucose levels between groups II and III. MDA levels in untreated diabetic rats were higher than those in control group rats and in diabetic rats treated with melatonin (P<0.01 and P<0.05, respectively). However, MDA levels in diabetic rats treated with melatonin were not different from those of the control group. The GSH, GSH-Px and SOD levels of untreated diabetic rats were significantly lower than those of the control group (P<0.02, P<0.002 and P<0.05, respectively). In group III, however, melatonin prevented decreases in the thiol antioxidant and the associated enzymes, and so these levels were not significantly different from those in the control group. These results confirm the presence of oxidative stress in STZ-induced experimental diabetes and indicate the beneficial free radical-scavenging and antioxidant properties of melatonin.     

Melatonin ameliorates chronic renal failure-induced oxidative organ damage in rats

Chronic renal failure (CRF) is associated with oxidative stress that promotes production of reactive oxygen species (ROS). Melatonin, the chief secretory product of the pineal gland, was recently found to be a potent free radical scavenger and antioxidant. The aim of this study was to examine the role of melatonin in protecting the aorta, heart, corpus cavernosum, lung, diaphragm, and kidney tissues against oxidative damage in a rat model of CRF, which was induced by five of six nephrectomy. Male Wistar albino rats were randomly assigned to either the CRF group or the sham-operated control group, which had received saline or melatonin (10 mg/kg, i.p.) for 4 wk. CRF was evaluated by serum blood urea nitrogen (BUN) level and creatinine measurements. Aorta and corporeal tissues were used for contractility studies, or stored along with heart, lung, diaphragm, and kidney tissues for the measurement of malondialdehyde (MDA, an index of lipid peroxidation), protein carbonylation (PC, an index for protein oxidation), and glutathione (GSH) levels (a key antioxidant). Plasma MDA, PC, and GSH levels and erythrocytic superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status in CRF. In the CRF group, the contraction and the relaxation of aorta and corpus cavernosum samples decreased significantly compared with controls (P < 0.05-0.001). Melatonin treatment of the CRF group restored these responses. In the CRF group, there were significant increases in tissue MDA and PC levels in all tissues with marked reductions in GSH levels compared with controls (P < 0.05-0.001). In the plasma, while MDA and PC levels increased, GSH, SOD, CAT, and GSH-Px activities were reduced. Melatonin treatment reversed these effects as well. In this study, the increase in MDA and PC levels and the concomitant decrease in GSH levels of tissues and plasma and also SOD, CAT, GSH-Px activities of plasma demonstrate the role of oxidative mechanisms in CRF-induced tissue damage, and melatonin, via its free radical scavenging and antioxidant properties, ameliorates oxidative organ injury. CRF-induced dysfunction of the aorta and corpus cavernosum of rats was reversed by melatonin treatment. Thus, supplementing CRF patients with adjuvant therapy of melatonin may have some benefit.     

2型糖尿病对阻塞性睡眠呼吸暂停患者血清GSH—Px、MDA水平的影响

目的探讨2型糖尿病（T2DM）对OSAHS患者体内谷胱甘肽过氧化物酶（GSH—Px）、丙二醛（MDA）水平的影响。方法选取正常对照组42例,OSAHS组49例,OSAHS合并T2DM患者39例,记录其姓名、性别、年龄、身高、体质量、体质量指数、腰臀比,进行多导联睡眠检测,测定血清GSH—Px活力,MDA含量。结果OSAHS组、0sAHS合并T2DM组与正常对照组之间相互比较,性别、年龄、BMI、腰臀比的差异无统计学意义（P值〉0．05）。与正常对照组相比,OSAHS组和OSAHS合并T2DM组的GSH—Px活性明显下降,MDA含量明显增高,差异有统计学意义（P值〈0．05）,与OSAHS组相比,OSAHS合并T2DM组的GSH—Px活性下降,MDA含量增高,差异有统计学意义（P值〈0．05）。结论OSAHS患者体内存在过氧化损伤,OSAHS患者如合并T2DM,则体内过氧化损伤进一步加重。     

Comparative analysis of the protective effects of melatonin and vitamin E on streptozocin-induced diabetes mellitus

There is a clearly documented link between diabetic complications and lipid peroxidation. Hyperglycemia causes a reduction in levels of protective endogenous antioxidants and increases generation of free radicals. The present study was carried out to compare the protective effects of melatonin and vitamin E against streptozocin (STZ)-induced diabetes in rats. Melatonin was administered s.c. (100 microg/kg) whereas vitamin E was given i.p. (100 mg/kg) after induction of diabetes with STZ (60 mg/kg). Plasma total cholesterol, triglyceride and low density lipoprotein (LDL) levels were increased in STZ group while both melatonin and vitamin E injection caused a significant decrease in the levels of all these parameters. The lipid lowering effect of melatonin was greater than that of vitamin E. Melatonin caused a significant decrease in brain, liver and kidney tissue malondialdehyde (MDA) levels which were increased because of STZ-induced diabetes. Vitamin E also reduced elevated MDA concentrations in diabetic rat tissues, but the effect of melatonin was more potent than that of vitamin E. Furthermore, treatment of diabetic rats with melatonin increased brain and kidney glutathione peroxidase (GSH-Px) activity to the levels below that of control rats. Vitamin E was found to be less effective on GSH-Px activity levels in brain and kidney than melatonin whereas it was more potent than melatonin in liver. In summary, melatonin prevents many diabetic complications by reducing oxidative stress and protects organisms from oxidative damage and dyslipidemia. Considering the much lower molar concentration of melatonin compared with vitamin E, melatonin seems to be a more potent antioxidant, especially in the brain and kidney.     

缺碘与高碘大鼠甲状腺抗氧化能力的实验研究

目的 研究缺碘与高碘对鼠甲状腺抗氧化能力的影响,探讨自由基对甲状腺的损伤作用。方法 将Wistar大鼠随机分为3组：适碘组（NI）、高碘组（HI）、低碘组（LI）,观察喂养12周、24周大鼠甲状腺及全身抗氧化能力的改变。结果 低碘组大鼠血清超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）与同期适碘对照组比较无明显变化,丙二醛（MDA）在实验的第24周显著升高;甲状腺组织匀浆SOD、GSH-Px和MDA在12周和24周均明显升高;甲状腺生物膜SOD和MDA在12周和24周均明显高于同期适碘对照组。高碘组血清、组织匀浆及甲状腺生物膜SOD、GSH-Px和MDA在实验过程中均无明显改变。结论 碘缺乏可导致Wistar大鼠甲状腺组织过氧化损伤;而碘过多在本实验期间未表现出对甲状腺的明显损伤作用。     

L-精氨酸对糖尿病大鼠肝、心肌及膈肌线粒体自由基损伤的保护作用

目的探讨L-精氨酸(L-Arg)对糖尿病大鼠肝脏、心肌及膈肌线粒体自由基损伤的保护作用. 方法给大鼠腹腔注射四氧嘧啶制备糖尿病模型,随机分为糖尿病组、L-Arg治疗组及正常对照组;用药4 w末测定三组大鼠肝脏、心肌及膈肌细胞线粒体中Mn-SOD、GSH-Px活性和MDA含量及膈肌线粒体内GSH含量.结果糖尿病组较正常组,大鼠肝、心肌、膈肌线粒体内GSH-Px活性显著降低(P＜0.01,P＜0.05,P＜0.001),MDA含量显著升高(P＜0.01,P＜0.05,P＜0.01),肝、膈肌线粒体Mn-SOD活性(均P＜0.01)及膈肌线粒体GSH含量(P＜0.05)也明显降低;与模型组比较,L-Arg可显著增加糖尿病大鼠肝、心肌、膈肌线粒体GSH-Px活性(P＜0.05,P＜0.05,P＜0.001)及肝、膈肌线粒体Mn-SOD活性(均P＜0.001),并使膈肌线粒体MDA含量显著降低(P＜0.01),而GSH含量明显升高(P＜0.001). 结论糖尿病大鼠肝、心肌、膈肌线粒体内自由基生成增多;L-Arg可通过提高肝、心肌、膈肌细胞线粒体中自由基清除酶的活性来加速自由基的清除,提高机体的抗氧化能力,从而保护机体功能免受氧化损伤.     

桃叶珊瑚苷对糖尿病大鼠线粒体的抗氧化作用

目的 研究桃叶珊瑚苷对链脲佐菌素(STZ)诱导的糖尿病大鼠血糖和线粒体抗氧化能力的影响. 方法 通过STZ腹腔注射建立糖尿病大鼠模型,将其随机分为糖尿病组、STZ低剂量组和STZ高剂量组,并与空白对照组比较.观察桃叶珊瑚苷治疗前后糖尿病大鼠的形态、体质量、血糖、线粒体内脂质过氧化和抗氧化体系的变化. 结果 与空白对照组比较,糖尿病大鼠血糖、MDA显著升高,CAT、GSH-Px、SOD活力显著下降;桃叶珊瑚苷治疗后血糖、MDA显著降低,CAT、GSH-Px、SOD活力显著升高. 结论 桃叶珊瑚苷能显著降低糖尿病大鼠的血糖值,改善线粒体的抗氧化水平,是一种潜在的防治糖尿病药物.     

法舒地尔治疗冠状动脉慢血流的疗效及对氧化应激的影响

目的 探讨盐酸法舒地尔对冠状动脉慢血流（coronary slow flow,CSF）患者的治疗作用及对血浆中机体氧化应激指标丙二醛（MDA）、晚期糖基化终产物（AGEs）、超氧物歧化酶（SOD）、谷胱甘肽转移酶（GST）水平的影响。 方法 选择因胸痛住院行冠状动脉造影检查显示结果正常但存在着CSF现象的患者82例,随机分为法舒地尔组与常规治疗组,每组患者均为41例。常规治疗组给予拜阿司匹林、阿托伐他汀、硝酸酯类等常规治疗;法舒地尔组在常规治疗基础上给予盐酸法舒地尔治疗。观察治疗前、后2周两组患者心绞痛疗效、冠状动脉血流速度TIMI计帧以及血浆MDA、AGEs、SOD和GST水平的变化。 结果 法舒地尔组治疗后患者心绞痛疗效总有效率为88%,常规治疗组为66%,差异有统计学意义（P<0.05）。法舒地尔组治疗后患者冠状动脉血流TIMI计帧显著低于治疗前及常规治疗组治疗后（均P<0.01）。两组治疗前MDA、AGEs、SOD、GST水平的比较差异均无统计学意义。法舒地尔组与常规治疗组治疗后血浆MDA、AGEs水平均显著低于本组治疗前（均P<0.01）。法舒地尔组与常规治疗组治疗后血浆SOD、GST水平均显著高于本组治疗前（均P<0.01）。法舒地尔组治疗后血浆MDA、AGEs水平均较常规治疗组治疗后显著下降（均P<0.01）。法舒地尔组治疗后血浆SOD、GST水平均较常规治疗组治疗后显著升高（均P<0.01）。 结论 法舒地尔治疗CSF的疗效优于常规治疗组,法舒地尔可能通过抑制机体氧化应激反应的机制发挥作用。     

The effects of vitamin D supplementation on lipid profiles and oxidative indices among diabetic nephropathy patients with marginal vitamin D status

AimsDiabetic nephropathy is one of the major microvascular complications of type 2 diabetes which insufficient vitamin D might -have a role in it's incidence. This study evaluated the effects of vitamin D supplementation on lipid profiles and oxidative/anti-oxidative indices in marginal vitamin D status patients with diabetic nephropathy.MethodsFor the current paralleled, randomized, double-blinded, placebo-controlled clinical trial, 50 diabetic nephropathy patients with marginal serum vitamin D were selected. Intervention group received 1,25-dihydroxycholecalciferol (50000 IU/week, n = 25), and placebo group (n = 25) received an identical placebo, for 8 weeks. Lipid profiles (LDL, HDL, TG and TC) and oxidative/anti-oxidative markers (TAC, SOD, CAT, GPX and MDA) were measured.ResultsVitamin D supplementation significantly increased vitamin D status in the intervention group, compared to the control group (P = 0.001). The reductions in the serum levels of TG, LDL and TC were significant (P = 0.04, P = 0.006 and P = 0.02, respectively) in the intervention group. The changes in oxidative/anti-oxidative markers and HDL levels were not significant after intervention.ConclusionIn conclusion, vitamin D supplementation for 8 weeks among diabetic nephropathy patients has beneficial effects on serum vitamin D status and dyslipidemia.