血清25-羟维生素D3、IL-33与支气管哮喘病情程度及肺功能的相关性研究

目的研究血清25-(OH)D3、IL-33与支气管哮喘病情程度及肺功能的相关性。方法选取64例支气管哮喘患者作为研究对象(哮喘组),同期选取70例健康体检者作为健康组。比较健康组与哮喘组25-(OH)D3及IL-33水平,分析25-(OH)D3、IL-33与哮喘患者肺功能指标的相关性。结果哮喘组25-(OH)D3水平显著低于健康组,IL-33水平显著高于健康组(P0.05);在哮喘组中,轻度患者25-(OH)D3、FVC、FEV1、FEV1%pre及PEF水平均明显高于中度和重度患者,IL-33水平明显低于中度和重度患者(P0.05);25-(OH)D3与肺功能指标呈正相关,IL-33与肺功能指标呈负相关(P0.05)。结论支气管哮喘患者的血清25-(OH)D3与肺功能指标呈正相关,IL-33与肺功能指标呈负相关,通过检测患者血清25-(OH)D3及IL-33水平可有效评估其肺功能指标及病情程度。     

COPD急性加重期hsCRP、TNF-α及IL-6的表达及相关性分析

目的 分析高教C反应蛋白(CRP)、肿瘤坏死因子(TNF-α)、白细胞介素-6(IL-6)在慢性阻塞性肺病(COVD)急性加重期的表达及相关性,探讨它们在COPD急性加重期(AECOPD)的作用及意义.方法 分别测定36例健康人群、32稳定期组和28例急性加重期患者血清hsCRP、TNF-α、IL-6水平,数据用SPSS12.0软件分析.结果 对照组hsCRP、TNF-α、IL-6的血清浓度值明显低于稳定期组和急性加重期组hsCRP、TNF-α、IL-6血清浓度值,差异十分显著(P<0.05).稳定期组和急性加重期组hsCRP、TNF-α、IL-6血清浓度升高存在相关性(P<0.05).结论 hsCRP、TNF-α、IL-6在慢性阻塞性肺病急性加重期(AECOPD)患者血清中明显增高且存在明显相关.提示三者可能参与AECOPD的发病过程,并在AECOPD的诊断和预后预测中具有潜在价值.     

COPD急性加重期hsCRP、TNF-α及IL-6的表达及相关性分析

目的分析高敏C反应蛋白（CRP）、肿瘤坏死因子（TNF-α）、白细胞介素-6（IL-6）在慢性阻塞性肺病（COPD）急性加重期的表达及相关性,探讨它们在COPD急性加重期（AECOPD）的作用及意义。方法分别测定36例健康人群、32稳定期组和28例急性加重期患者血清hsCRP、TNF-α、IL-6水平,数据用SPSS12.0软件分析。结果对照组hsCRP、TNF-α、IL-6的血清浓度值明显低于稳定期组和急性加重期组hsCRP、TNF-α、IL-6血清浓度值,差异十分显著（P〈0.05）。稳定期组和急性加重期组hsCRP、TNF-α、IL-6血清浓度升高存在相关性（P〈0.05）。结论 hsCRP、TNF-α、IL-6在慢性阻塞性肺病急性加重期（AECOPD）患者血清中明显增高且存在明显相关。提示三者可能参与AECOPD的发病过程,并在AECOPD的诊断和预后预测中具有潜在价值。     

IL-8、IL-1β、TNF-α水平在COPD发病中意义的探讨

目的:检测慢性阻塞性肺疾病(COPD)患者诱导痰液和血清中白细胞介素-8(IL-8),白细胞介素-1β(IL-1β),肿瘤坏死因子-α(TNF-α)水平,探讨细胞因子在COPD发病中的作用.方法:选取符合COPD诊断标准的患者88例、健康对照者96例,采用放射免疫分析COPD急发期(AECOPD)、缓解期患者、健康对照组的诱导痰和血清IL-8、IL-1β、TNF-α水平,并比较AECOPD患者血清中IL-8,IL-1β,TNF-α水平与肺功能FEV1.0的相关性.结果:健康吸烟组和AECOPD与COPD稳定期患者诱导痰中IL-8分别为(2.72±1.39)μg/L、(5.76±3.87)μg/L、(3.52±2.18)μg/L,IL-1β分别为(2.67±1.38)μg/L、(3.95±2.16)μg/L、(2.98±1.37)μg/L,TNF-α分别为(74.28±24.83)pmol/L、(148.32±32.74)pmol/L、(95.62±17.35)pmol/L;血中IL-8分别为(1.37±2.62)μg/L、(4.26±3.16)μg/L、(2.66±1.54)μg/L,IL-1β分别为(1.78±1.26)μg/L、(3.69±3.52)μg/L、(2.42±1.87)μg/L,TNF-α分别为(46.53±31.77)pmol/L、(102.92±72.68)pmol/L、(59.62±33.87)pmol/L;三组比较差异具有统计学意义.且痰液和血清中IL-8,IL-1β,TNF-α水平高低与第一秒用力呼气容积(FEV1.0)呈显著负相关.结论:IL-8,IL-1β,TNF-α等细胞因子在COPD的发病及急性加重中起重要作用,而且与机体的系统性炎症反应有密切关系.     

1α,25-二羟基维生素D;通过TLR4信号通路抑制川崎病血清诱导的THP-1细胞炎症因子表达

目的:研究1α,25-二羟基维生素D₃[1,25-(OH)₂D₃]是否通过调控巨噬细胞Toll样受体4(TLR4)信号通路的活化影响川崎病炎症反应的发生。方法:收集襄阳市第一人民医院收治的73例川崎病患儿血清,另收集急性上呼吸道感染患儿(感染组)和儿保科体检儿童(对照组)的血清各30例,利用试剂盒检测各组25-羟基维生素D₃[25-(OH)D₃]水平的变化,并绘制受试者工作特征(ROC)曲线,确定诊断截断点。体外细胞实验,利用采集的血清诱导THP-1巨噬细胞构建川崎病固有免疫模型,实验分组为:15%正常血清组、15%川崎病血清组及15%川崎病血清+1,25-(OH)₂D₃(1 nmol/L、10 nmol/L和100 nmol/L)组[1,25-(OH)2D3均于血清刺激前加入]。加入血清刺激24h后,利用RT-qPCR检测TLR4、白细胞介素1β(IL-1β)和肿瘤坏死因子α(TNF-α)的mRNA表达水平,ELISA检测细胞培养上清液中TNF-α的含量;Western blot检测TLR4和p-P65的蛋白水平;免疫荧光技术检测TLR4蛋白的表达。结果:川崎病患儿体内白细胞数、中性粒细胞数、血小板数、丙氨酸转氨酶及C-反应蛋白均较感染组显著升高(P<0.05)。与对照组及感染组相比,川崎病患儿血清25-(OH)D₃水平显著降低(P<0.01),诊断截断点为27.55μg/L,ROC曲线下面积为0.922,预测的灵敏度为93.3%,特异度为75.0%。体外细胞实验显示,与正常血清组相比,川崎病血清可显著促进巨噬细胞TLR4、IL-1β和TNF-α的mRNA表达(P<0.05),增加巨噬细胞分泌TNF-α的含量(P<0.05);1,25-(OH)2D3预保护抑制血清诱导的炎症因子产生。川崎病血清显著提高巨噬细胞TLR4和p-P65蛋白水平(P<0.05),而1,25-(OH)₂D₃可显著抑制这一作用(P<0.05)。结论:川崎病患儿体内25-(OH)D₃水平显著降低,而补充1,25-(OH)₂D₃可通过调节TLR4信号通路来抑制川崎病血清诱导的THP-1细胞炎症反应。     

1α，25-二羟基维生素D3通过TLR4信号通路抑制川崎病血清诱导的THP-1细胞炎症因子表达

目的:研究1α,25-二羟基维生素D3[1,25-(OH)2D3]是否通过调控巨噬细胞Toll样受体4(TLR4)信号通路的活化影响川崎病炎症反应的发生。方法:收集襄阳市第一人民医院收治的73例川崎病患儿血清,另收集急性上呼吸道感染患儿(感染组)和儿保科体检儿童(对照组)的血清各30例,利用试剂盒检测各组25-羟基维生素D3[25-(OH)D3]水平的变化,并绘制受试者工作特征(ROC)曲线,确定诊断截断点。体外细胞实验,利用采集的血清诱导THP-1巨噬细胞构建川崎病固有免疫模型,实验分组为:15%正常血清组、15%川崎病血清组及15%川崎病血清+1,25-(OH)2D3(1 nmol/L、10 nmol/L和100 nmol/L)组[1,25-(OH)2D3均于血清刺激前加入]。加入血清刺激24h后,利用RT-qPCR检测TLR4、白细胞介素1β(IL-1β)和肿瘤坏死因子α(TNF-α)的mRNA表达水平,ELISA检测细胞培养上清液中TNF-α的含量;Western blot检测TLR4和p-P65的蛋白水平;免疫荧光技术检测TLR4蛋白的表达。结果:川崎病患儿体内白细胞数、中性...     

TNF-α、IL-8与老年急性冠状动脉综合征关系的研究

目的:观察老年冠心病不同类型患者中肿瘤坏死因子α(TNF-α)、白细胞介素-8(IL-8)水平变化及其相互之间的关系,进一步探讨急性冠状动脉综合征临床识别和预测的炎症指标。方法:采用放射免疫分析观察了42例ACS、43例SCHD患者和30例老年健康人血清TNF-α、IL-8水平。结果:ACS患者和稳定性冠心病(SCHD)患者TNF-α和IL-8水平均显著高于对照组(P<0.05,P<0.01);ACS组TNF-α及IL-8含量虽然略高于SCHD组,但无统计学意义(P>0.05)。结论:TNF-α、IL-8等可能是导致ACS发生的危险因素,提示可能与急性冠脉综合征的发生有关,是动脉粥样硬化斑块不稳定的重要标志。     

GRO-α和HNP1-3在AECOPD患者中的表达及临床意义

目的分析GRO-α和HNP1-3在AECOPD患者中的表达及临床意义。方法选择本院2016年10月至2019年9月收治的100例AECOPD患者作为AECOPD组,同时选取同一时间段来我院体检的82例健康体检者作为健康组和82例COPD稳定期患者作为COPD稳定期组。采用回顾性分析法分析所有研究对象的各项临床资料,比较各组研究者的GRO-α和HNP1-3水平及肺功能指标;分析AECOPD组患者的GRO-α和HNP1-3水平与肺功能指标的相关性。结果 AECOPD组患者的GRO-α、HNP1-3水平显著高于COPD稳定期组和健康组,差异具有统计学意义(P0.05);AECOPD组患者的肺功能指标显著低于COPD稳定期组和健康组,差异具有统计学意义(P0.05);AECOPD组患者的GRO-α和HNP1-3水平与FEV1、FVC、FEV1/FVC呈负相关(P0.05)。结论血清中的GRO-α和HNP1-3水平随着患者的病情严重程度而升高,与肺功能指标FEV1、FVC、FEV1/FVC呈负相关。GRO-α和HNP1-3水平的检测在AECOPD患者病情严重程度的判断中具有重要的价值。     

白细胞介素-8、肿瘤坏死因子-α检测在慢性阻塞性肺疾病患者病情评估中的应用

目的:白细胞介素-8(Interleukin-8,IL-8)、肿瘤坏死因子-α(Tumor necrosis factor,TNF-α)检测在慢性阻塞性肺疾病患者病情评估中的应用.方法:选自2019年1月至2020年11月期间于我院就诊的92例慢性阻塞性肺疾病患者为此次研究对象,设为研究组;另外选取92例同期在我院体检健康者,设为对照组.对比两组患者血清以及痰液中IL-8、TNF-α水平以及不同疾病类型患者IL-8、TNF-α水平.结果:研究组患者炎性因子IL-8、TNF-α水平明显高于对照组(P<0.05);研究组患者痰液IL-8、TNF-α水平显著高于对照组(P<0.05).急性期患者血清IL-8、TNF-α水平明显高于缓解期患者(P<0.05).结论:在慢性阻塞性肺疾病患者病情评估中应用IL-8、TNF-α检测,可作为慢性阻塞性肺疾病患者患者诊断和疗效判断的指标,对指导临床治疗有重要意义.     

结直肠癌患者TNF-α、IL-6、 IL-8水平与临床分期的关系与研究

目的 从血清TNF-α、IL-6、IL-8的角度探讨结直肠癌患者的免疫功能与临床分期的关系.方法 采集我院收治126例已经病理学诊断为结直肠癌且未进行任何治疗的患者(肿瘤组)、40例健康志愿者(正常组)的血清和60例既往采集的慢性肠炎患者(良性疾病组)的血清,用ELISA检测所有样本血清TNF-α、IL-6、IL-8的水平,并采用国际通用TNM分期法对结直肠癌患者进行临床分期,利用SPSS对结果进行统计学分析.结果 结直肠癌患者血清中TNF-α、IL-6、IL-8的水平均高于正常组,但其他免疫相关细胞因子水平相同.临床Ⅰ期和正常组中TNF-α、IL-6、IL-8的水平无差异,临床Ⅱ期和正常组比较,TNF-α、IL-6、IL-8的水平有所提高,临床Ⅲ期、Ⅳ期和正常组比较,TNF-α、IL-6、IL-8的水平显著上升.TNF-α、IL-6、IL-8的水平均随病理进程的加重表达量呈上升的趋势.结论 TNF-α、IL-6、IL-8参与了结直肠癌发生发展的过程并且为结直肠癌发病的重要炎症基础,检测其在血清中的水平有利于了解结直肠癌的病理进程和为结直肠癌的治疗和预后提供参考.     

西洛司特对COPD患者炎症水平的调节作用

目的:探讨西洛司特对慢性阻塞性肺疾病(COPD)患者外周血IL-4、IL-8、TNF-α的调节作用和临床疗效.方法:70例COPD稳定期患者随机分为治疗组和对照组,每组各35例,治疗组服用西洛司特片(葛兰素史克公司)15mg bid,对照组服用安慰剂1片bid,共6个月为一疗程.结果:治疗前,两组IL-4、IL-8、T...     

Immunomodulatory effects of vitamin D in peripheral blood monocyte-derived macrophages from patients with rheumatoid arthritis

1,25-Dihydroxyvitamin D (1,25(OH)₂D₃), the active form of vitamin D, modulates both innate and adaptive immune responses. Emerging epidemiological data has also demonstrated disease-modifying and immunomodulatory effects of vitamin D in a wide range of human autoimmune diseases, including rheumatoid arthritis (RA). To evaluate in vitro effects of 1,25(OH) ₂D₃ in primary cultures of peripheral blood monocyte-derived macrophages of RA patients, monocyte/macrophages, isolated from peripheral blood mononuclear cells of RA patients and healthy subjects by exploiting their ability to adhere to plastic, were treated with increasing concentrations of 1,25(OH)₂D₃ for 48 h. TNF-α, IL-1 α, IL-1β, IL-6 and RANKL production was determined by ELISA and nitric oxide (NO) release using the Griess method. Immunocytochemistry analysis was also performed to evaluate alterations in transmembrane TNF-α expression after 1,25(OH) ₂D₃ treatment. A significant dose-dependent decrease in TNF-α and RANKL production by cultured RA macrophages after 1,25(OH)₂D₃ treatment was found, whereas a significant reduction in normal cells was observed only at higher concentrations. IL-1 α, IL-1β and IL-6 levels were reduced by 1,25(OH) ₂D₃ at higher concentrations in all cell populations. TNF-α immunostaining was less intense in treated cells compared with untreated. 1,25(OH) ₂D₃ significantly reduced NO levels regardless of the concentration used. Vitamin D downregulated proinflammatory mediators in monocyte-derived macrophages, and RA cells appeared more sensitive than normal cells. These effects further provide a rationale for the therapeutic value of vitamin D supplementation in the treatment for RA.     

1,25-Dihydroxyvitamin D3 modulates T cell differentiation and impacts on the production of cytokines from Chinese Han patients with early rheumatoid arthritis

To study the effects of 1,25-dihydroxyvitamin D₃ (1,25(OH)₂D₃) on the differentiation of T cells and the levels of cytokines in patients with early rheumatoid arthritis (eRA). The levels of Th1, Th2, Th17, and Treg cells were detected with BDFACS Calibur flow cytometer. The expression of IFN-ɤ, TNF-α, IL-2, IL-4, IL-6, IL-10, IL-17, and IL-22 was examined in 54 patients with eRA using a cytometric bead array (CBA). After 72 h of incubation of PBMCs from eRA patients with 1,25(OH)₂D₃, the levels of IFN-ɤ, TNF-α, IL-2, IL-6, and IL-17 significantly decreased compared to those of the control. 1,25(OH)₂D₃ had no significantly impact on the levels of IL-4, IL-10, and IL-22. The proportion of Th17 and the ratio of Th17/Treg significantly decreased in 1,25(OH)₂D₃-treated groups compared to those of the control. 1,25(OH)₂D₃ had no significantly impact on the proportion of Th1, Th2, Treg, and the ratio of Th1/Th2. Although no statistically significant difference was observed, proportion of Th1 was decreased after 1,25(OH)₂D₃ treatment compared with anti-CD3/CD28 only. The present study demonstrated that 1,25(OH)₂D₃ inhibited the synthesis of specific cytokines: Th1 (IFN-ɤ) and Th17 (IL-17, IL-22, IL-6, TNF-α) might upregulated Th2 cytokine (IL-4), which indicated the possible immunoregulatory roles and bone-sparing effects of 1,25(OH)₂D₃ in eRA through modulation of the Th1 and Th17 cytokine balance.

     

Inhibition of production and function of interleukin-6 by 1,25-dihydroxyvitamin D3

1,25-Dihydroxyvitamin D3 (1,25-(OH)2D3) has been shown to interfere with immunoglobulin production and lymphocyte proliferation in vitro. These lymphocyte functions are influenced by interleukin (IL)-6 produced by antigen presenting cells. Hence, the ability of 1,25-(OH)2D3 to interfere with the production and function of IL-6 was investigated. 1,25-(OH)2D3 and the analogue MC 903 inhibited IL-6 production by LPS-stimulated human mononuclear cells. The precursor 25-OH D3 was ineffective. Likewise, 1,25-(OH)2D3 but not 25-OH D3 inhibited rIL-6-driven as well as rIL-1 alpha/beta-driven proliferation of murine thymocytes. This effect of 1,25-(OH)2D3 was partially or totally overcome by larger concentrations of rIL-6 as well as by rIL-2 and ionomycin. Consistently, the production of IL-6 and IL-2 in rIL-1 driven thymocyte cultures were found to be reduced by 1,25-(OH)2D3. Inhibition of production and function of IL-6 may therefore be involved in 1,25-(OH)2D3-mediated regulation of lymphocyte functions in vitro.     

Thymosin α1 plus routine treatment inhibit inflammatory reaction and improve the quality of life in AECOPD patients

Abstract

Context: Thymosin α1 (Tα1) is considered to be a promising immunomodulatory drug and could balance immunity and tolerance in immune tolerance and autoimmunity.

Objective: To explore the efficacy of Tα1 plus routine complex treatment in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD).

Methods: Eighty-four AECOPD patients were enrolled and randomized into an experimental group and a control group. All patients received the routine treatment. Additionally, the experimental group received subcutaneous injections of Tα1 while the control group received placebo. Four weeks later, the curative effect of treatment and immune function of both groups were analyzed.

Results: Partial pressures of oxygen (PaO₂), PaCO₂, and pulmonary function of the experimental group improved after treatment compared to that recorded prior to treatment and that observed for the control group (p?<?0.01, both). The CD4⁺ T cell count, serum interferon (IFN)-γ levels, and the ratios of CD4⁺/CD8⁺ and IFN-γ/interleukin (IL)-4 increased in both groups (p?<?0.01), while the CD8⁺ T cell count and levels of IL-4, IL-8, and leukotrienes B4 (LTB4) decreased as expected (p?<?0.01). Meanwhile, the above-mentioned indices of the experimental group improved significantly compared to the indices of the control group (p?<?0.05 or 0.01).

Conclusions: Tα1 plus routine treatment could improve the immune function of AECOPD patients and inhibit the inflammatory reaction, thus reducing the recurrence of chronic obstructive pulmonary disease (COPD).     

1 alpha,25-Dihydroxyvitamin D3 and a novel vitamin D analogue MC 903 are potent inhibitors of human interleukin 1 in vitro

1 alpha,25-dihydroxycholecalciferol (1,25(OH)2D3) inhibits the lymphocyte growth hormone, interleukin 2. Since its production is dependent upon interleukin 1 (IL-1) produced by antigen-presenting cells, we tested five vitamin D3 analogues for effects on the production and function of human natural and recombinant IL-1. The production was not affected, but 1,25(OH)2D3 (greater than 10(-11) M) and a synthetic derivative MC 903 (greater than = 10(-10) M) inhibited the proliferation of mouse thymocytes to IL-1. The vitamins failed to affect the cytotoxic activity of tumor necrosis factor. 1,25(OH)2D3 may play a physiological immunomodulatory role as a selective inhibitor of the function of IL-1, and MC 903 may prove clinically useful in this regard because of its limited calcium metabolic activity.     

1 alpha,25-dihydroxyvitamin D3 suppresses interleukin-1beta-induced interleukin-8 production in human whole blood: an involvement of erythrocytes in the inhibition

Interleukin (IL)-8, which is involved in inflammatory responses, is produced by a variety of cell types, monocytes/macrophages and neutrophils, in response to inflammatory stimuli including lipopolysaccharide, IL-1, and tumor necrosis factor alpha. Here we report the inhibitory effects of 1alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3) on IL-8 production in human whole blood culture. 1,25(OH)2D3 inhibited only the late phase of the biphasic IL-8 production in lipopolysaccharide-stimulated human whole blood. It also effectively inhibited IL-8 production induced by IL-lbeta compared with that induced by tumor necrosis factor alpha. IL-8 mRNA expression in IL-lbeta-stimulated whole blood was found to require de novo protein synthesis. Although monocytes were found to be mainly responsible for IL-1beta-induced IL-8 production in whole blood, 1,25(OH)2D3 inhibited IL-8 production by isolated mononuclear cells only marginally. The inhibitory effect of 1,25(OH)2D3 on mononuclear cells was restored by adding erythrocytes. These results suggest that erythrocytes play a role in mediating the inhibitory effects of 1,25(OH)2D3 on IL-8 production in IL-1beta-stimulated whole blood.     

1,25（OH）2D3对甲状旁腺素诱导的肾小管上皮细胞转分化和TGF-β1的表达的影响

目的:探讨1,25(OH)2D3对甲状旁腺素(PTH)诱导的肾小管上皮细胞转分化和转化生长因子-β1(TGF-β1)表达的影响。方法:人肾小管上皮细胞(HK-2细胞)培养在含50 mL/L FCS的DMEM/F12培养液中。对照组:加入等体积含50 mL/L FCS的DMEM/F12培养液;PTH刺激组:加入终浓度为10-10 mol/L PTH的含50 mL/L FCS的DMEM/F12培养液;PTH+1,25(OH)2D3干预组:加入10-10 mol/L PTH,同时加入不同浓度(10-10、10-9、10-8、10-7 mol/L)的1,25(OH)2D3。刺激HK-2细胞48 h。半定量RT-PCR法检测细胞中α-平滑肌肌动蛋白(α-SMA)和TGF-β1的基因表达;Western blot法检测细胞中α-SMA和TGF-β1的蛋白表达;免疫细胞化学法检测细胞中α-SMA的表达;ELISA法检测细胞培养上清液中TGF-β1的含量。结果:半定量RT-PCR结果显示,对照组HK-2细胞中几乎无α-SMA的mRNA表达,仅有少量的TGF-β1 mRNA表达;PTH刺激组α-SMA和TGF-β1mRNA表达量与对照组比较明显增加;PTH+1,25(OH)2D3干预组表达量比PTH刺激组显著降低,且随着1,25(OH)2D3浓度的升高呈一定的剂量依赖性(P<0.05)。Western blot结果显示,对照组HK-2细胞中无α-SMA的蛋白表达,仅有少量的TGF-β1蛋白表达;10-10 mol/L的PTH能够明显诱导HK-2细胞中α-SMA的蛋白表达,增加TGF-β1的蛋白表达量;PTH+1,25(OH)2D3干预组,α-SMA和TGF-β1的蛋白表达量比PTH刺激组显著降低(P<0.05)。免疫细胞化学法结果显示,对照组几乎无α-SMA阳性表达的细胞,PTH刺激组可见大量细胞α-SMA表达阳性;PTH+1,25(OH)2D3干预组α-SMA表达阳性的细胞数明显低于PTH刺激组(P<0.05)。ELISA结果显示,对照组细胞上清液中可检测到少量的TGF-β1,PTH刺激组含量显著升高,PTH+1,25(OH)2D3干预组与PTH刺激组比较含量明显降低(P<0.05)。结论:1,25(OH)2D3能够部分拮抗PTH诱导的HK-2细胞转分化和TGF-β1的表达。