依那西普抑制博来霉素诱导的小鼠肺纤维化

 目的：观察肿瘤坏死因子 α(TNF-α)拮抗剂依那西普对博来霉素诱导的肺纤维化小鼠的抑制纤维化作用,并探讨依那西普治疗肺纤维化的可能机制。方法：将45只SPF级雌性昆明小鼠随机分为3组：对照组（气管内雾化生理盐水）、纤维化组（气管内博来霉素3 mg/kg溶于100 μL生理盐水内雾化）和依那西普干预组（气管内雾化博来霉素后,4 mg/kg依那西普溶于100 μL生理盐水内腹腔注射,每3 d注射1次）。处理后第28 d收集样本,小鼠左肺置于10%中性甲醛固定,石蜡包埋切片后行HE与Masson染色;右肺碱水解法检测组织羟脯氨酸(HYP)的含量;酶联免疫法检测血清TNF-α和转化生长因子 β（TGF-β）的含量;提取肺组织总蛋白,Western blotting 检测磷酸化ERK1/2、JNK和p38的表达。结果：依那西普干预组肺组织病理损伤及气道上皮下胶原沉积较纤维化组减轻,肺叶炎症损伤评分和纤维化评分明显下降（均P<0.01）,肺组织HYP含量显著降低（P<0.05）,血清TNF-α 和TGF-β的浓度明显减少（均P<0.01）,肺组织ERK1/2、JNK和p38蛋白的磷酸化水平也显著下降（P<0.01,P<0.05,P<0.01）。结论：依那西普能显著下调TNF-α 和TGF-β的水平,从而抑制ERK1/2、JNK和p38的活化,缓解博来霉素诱导的小鼠肺纤维化病变。     

α7nAChR参与生理浓度糖皮质激素的抗炎作用*

 目的： 探讨α7烟碱型乙酰胆碱受体（α7nAChR）在生理浓度糖皮质激素（GCs）抗炎过程中的作用。方法: MTT法检测不同浓度氢化可的松对小胶质细胞BV-2活性的影响;在建立LPS刺激的BV-2细胞炎症模型基础上,实验分组如下：(1) 空白对照组;(2) LPS组;(3) GCs＋LPS组;(4) α7nAChR阻断剂甲基牛扁亭碱（MLA）＋GCs＋LPS组,ELISA法测定细胞上清中TNF-α和IL-1β的含量。结果: 2 000 和1 000 nmol/L 氢化可的松可分别使细胞存活率降低至(76.9±5.5)%和(90.8±7.3)%,表现出超生理剂量GCs的细胞损伤作用。LPS明显刺激BV-2细胞释放TNF-α和IL-1β,并呈现时间和剂量依赖性。生理浓度（500和250 nmol/L）的氢化可的松均可减少LPS诱导BV-2细胞释放TNF-α和IL-1β,10 nmol/L MLA预处理BV-2细胞能拮抗GCs抑制炎症因子释放的作用。结论: α7nAChR参与了生理浓度GCs的抗炎作用。     

经皮三叉神经电刺激减轻戊四氮诱导的大鼠癫痫发作并抑制海马内IL-1β和TNF-α的表达

 目的:探讨经皮三叉神经电刺激预处理对戊四氮（PTZ）诱发的急性癫痫大鼠的行为学及海马致痫细胞因子白细胞介素1β(IL-1β)及肿瘤坏死因子α(TNF-α)的影响。方法:动物随机分为对照组、致痫组（PTZ组）和经皮三叉神经电刺激组,分别给予7 d、14 d和28 d的假刺激和三叉神经电刺激预处理后,腹腔注射PTZ 建立急性癫痫动物模型,观察给药后大鼠癫痫行为学表现,并分别用免疫组织化学方法及ELISA方法对海马IL-1β、TNF-α进行检测。结果:经皮三叉神经电刺激可以明显减轻大鼠的痫性发作级别,减少癫痫发作持续的时间（P<0.05）, 且海马细胞因子IL-1β及TNF-α的表达明显少于PTZ组（P<0.05或P<0.01）。结论:经皮三叉神经电刺激预处理在PTZ 急性点燃癫痫大鼠模型中不仅具有抗惊厥作用, 还可以减少海马致痫细胞因子IL-1β及TNF-α的表达,可能为癫痫的防治带来新的策略。       

EGCG改善高浓度TNF-α对人皮肤创伤愈合中成纤维细胞的抑制作用

目的: 探讨高浓度肿瘤坏死因子α(TNF-α)对人皮肤创伤愈合中成纤维细胞的抑制作用以及表没食子儿茶素没食子酸酯(EGCG)的干预效应。方法: 体外培养原代人皮肤成纤维细胞,以10 μg/L TNF-α作用24 h或联合EGCG预处理干预,用细胞计数试剂盒观察细胞增殖,细胞划痕愈合实验观察成纤维细胞的迁移,Western blotting法研究I型胶原蛋白的表达。结果: TNF-α显著抑制皮肤成纤维细胞的增殖和迁移,EGCG呈浓度依赖性地改善TNF-α的增殖抑制作用,以EGCG(40 μmol/L)预处理后,TNF-α对细胞迁移的抑制作用也得到恢复。Western blotting发现TNF-α还能抑制I型胶原蛋白的表达,而加入EGCG(40 μmol/L)后其表达有显著恢复。结论: EGCG能显著改善高浓度TNF-α对人皮肤成纤维细胞增殖和迁移的抑制作用,并恢复I型胶原的表达,从而促进皮肤创口的愈合。     

TNF-α对HepG2细胞LXRα介导的胆固醇外流的影响及其分子机制

 目的:观察肿瘤坏死因子α（TNF-α）对肝X受体α（LXRα）启动子活性及其下游ATP结合盒转运蛋白（ABCA1和ABCG1）表达的影响,从而探讨TNF-α加速HepG2细胞内胆固醇积聚的分子机制。方法:构建LXRα基因的启动子表达载体,观察炎症因子TNF-α对LXRα启动子活性的影响,进一步将HepG2细胞分为对照组（control）、TNF-α组（20 μg/L）、高脂组（LDL,100 mg/L）及联合处理组（TNF-α 20 μg/L+ LDL 100 mg/L）。采用实时定量PCR和Western blotting检测LXRfα、ABCA1和 ABCG1的mRNA及蛋白的表达。［3H ］标记胆固醇,液体闪烁计数法检测胆固醇外流量。油红O染色和定量比色法分析细胞内胆固醇的含量。结果:成功构建LXRα启动子的萤火虫萤光素酶报告质粒,证明了该启动子有明显活性,TNF-α能明显抑制LXRα启动子的活性。进一步检测发现,和对照组相比,TNF-α下调了LXRα、ABCA1和ABCG1 mRNA与蛋白表达。高脂组胆固醇外流量增加,而TNF-α组胆固醇外流量明显降低。油红O染色显示,TNF-α使细胞内脂质染色明显增加。结论: TNF-α可通过抑制LXRα启动子活性从而抑制HepG2细胞内胆固醇外流导致肝细胞内脂质异常积聚。     

α-MSH对脂多糖诱导小鼠腹腔巨噬细胞SOCS-3mRNA表达的影响

目的:观察α-黑色素细胞刺激素(α-MSH)对脂多糖(LPS)诱导小鼠腹腔巨噬细胞SOCS-3mRNA表达及NO释放的影响,以探讨α-MSH拮抗LPS的作用机制。方法:用半定量逆转录多聚酶链反应(RT-PCR)的方法检测LPS诱导体外培养的小鼠腹腔巨噬细胞SOCS-3mRNA表达水平和给予α-MSH后对SOCS-3mRNA表达的影响;用Griess试剂检测单独给予LPS与同时给予α-MSH和LPS作用巨噬细胞后对NO生成量的影响。结果:未受LPS刺激的小鼠腹腔巨噬细胞表达低水平的SOCS-3。LPS组SOCS-3的表达和NO的生成显著高于对照组,而同时给予α-MSH和LPS培养,巨噬细胞的SOCS-3的表达明显低于LPS组,NO的生成则几乎完全阻断。结论:LPS在启动炎症的过程中可能也激活了SOCS介导的负调节机制;但SOCS可能不参与α-MSH的抗LPS作用。     

肝细胞核因子4α在实验性结肠炎中的表达及意义

 目的： 通过检测肝细胞核因子4α（HNF4α）在小鼠实验性结肠炎肠组织中表达水平,探讨其在溃疡性结肠炎（UC）发病过程中的作用及意义。方法： 分别采用2%和2.5%的葡聚糖硫酸钠（DSS）溶液诱导BALB/c小鼠急性结肠炎模型,以疾病活动指数（DAI）、组织学损伤及炎症细胞因子表达水平评价炎症严重程度。分析HNF4α表达水平与结肠炎严重程度及内皮型钙黏蛋白（E-CAD）、连接黏附分子1（JAM-1）和桥粒糖蛋白2（DSC-2）表达的相关性。结果： 与正常对照组相比,DSS处理组小鼠DAI、组织学损伤及炎症因子表达显著增高（P<0.05）,结肠黏膜中HNF4α蛋白及mRNA表达显著降低（P<0.01）。相关性分析结果提示HNF4α蛋白表达与DAI及组织学损伤程度呈负相关（P<0.01）,HNF4α mRNA表达与E-CAD、JAM-1和DSC-2 mRNA表达呈正相关（P<0.01）。结论： HNF4α表达水平与实验性结肠炎严重程度及细胞间连接蛋白表达密切相关,提示HNF4α低表达可削弱肠道黏膜屏障功能,从而促进UC的发生发展。     

巨噬细胞移动抑制因子经Rho激酶途径促进人胚肺成纤维细胞表型转化

 目的：观察重组巨噬细胞移动抑制因子（rMIF）对人胚肺成纤维细胞（MRC-5）表型转换的作用,探讨哮喘气道重塑的发生机制。方法：不同浓度的rMIF (25~100 μg/L)分别作用于MRC-5细胞24 h或48 h,RT-PCR法检测α-平滑肌肌动蛋白（α-SMA）  mRNA表达,Western blotting检测α-SMA蛋白合成;100 μg/L rMIF刺激MRC-5细胞48 h,刺激前0.5 h加入Rho拮抗剂Y27632,RT-PCR法检测α-SMA mRNA表达,Western blotting法检测α-SMA表达;100 μg/L rMIF分别刺激MRC-5 6 h、12 h、24 h或48 h,Western blotting检测磷酸化肌球蛋白磷酸酶目标亚单位1（p-MYP1）蛋白合成。结果：刺激MRC-5 24 h,不同浓度的rMIF对α-SMA mRNA转录未见显著影响（P>0.05）。刺激MRC-5细胞48 h,rMIF可呈剂量依赖地促进α-SMA mRNA （r=0.697,P<0.01）和蛋白（r=0.957,P<0.01）表达。Y27632预刺激后,显著抑制rMIF100 μg/L促进α-SMA mRNA和蛋白表达的作用（均P<0.01）。rMIF刺激6 h后,p-MYPT1表达显著增加（P<0.01）,12 h达到高峰（P<0.01）,24 h开始下降,但24 h和48 h其水平仍高于对照组（均P<0.01）。结论：rMIF通过Rho信号通路刺激成纤维细胞表型转化,可能在哮喘气道重塑的发病机制中发挥关键作用。     

大鼠背部脊柱两侧全层皮肤圆形创面增生性瘢痕愈合过程中臭氧的作用**☆

背景：预防硬膜外瘢痕的形成,可减少腰椎手术失败综合征的发生。臭氧应用于腰椎间盘突出症的治疗已取得较好的临床效果。 目的：观察臭氧对大鼠伤口瘢痕愈合过程的影响。 方法：外科切口法制备大鼠背部脊柱两侧圆形全层皮肤创面增生性瘢痕模型,分为3组,纯氧组及臭氧组分别注射纯氧及30~40 mg/L臭氧,总量均为5 mL,空白组不注射任何药物,每周2次,4周后取瘢痕/肉芽组织标本,利用苏木精-伊红染色及免疫组化方法,对比观察各组标本瘢痕/肉芽组织外观及肿瘤坏死因子α、碱性成纤维细胞生长因子表达的变化。 结果与结论：与空白组及纯氧组相比,臭氧组愈后瘢痕面积较小,上皮生成较多,炎性细胞浸润较少,胶原纤维较纤细,且断裂较多;臭氧组肿瘤坏死因子α阳性细胞数较低(P < 0.01),碱性成纤维细胞生长因子阳性细胞数较高(P < 0.01)。提示臭氧通过其抗炎作用,减少炎性细胞浸润,并可通过抑制成纤维细胞及巨噬细胞释放的肿瘤坏死因子α以及提高碱性成纤维细胞生长因子的表达,减少胶原的过度合成,从而起到抑制肉芽组织炎症及瘢痕组织增生的作用。关键词：臭氧;瘢痕;伤口愈合;肿瘤坏死因子α;碱性成纤维细胞生长因子 缩略语注释：TNF-α: tumor necrosis fact-alpha,肿瘤坏死因子α;bFGF: basic fibroblast growth factor,碱性成纤维细胞生长因子 doi:10.3969/j.issn.1673-8225.2012.15.012     

小鼠肾小管发育过程中纤维粘连蛋白与整合素α5的表达

背景：纤维粘连蛋白-整合素α5相互作用影响肾小管发育的体内研究较少。 目的：观察小鼠肾小管发育过程中纤维粘连蛋白及其受体整合素α5的表达。 方法：选取胚龄(E)12,14,16,18 d和生后日龄(P)1,3,7,14,21,28,40 d的小鼠。 结果与结论：免疫组织化学染色结果显示纤维粘连蛋白于E12 d时即表达于输尿管芽的基底膜处,随后表达于发育各个时期的肾小管基膜;整合素α5于E12 d时开始表达,表达部位是肾小管的上皮细胞。体视学测量结果显示纤维粘连蛋白表达的面密度值和整合素α5表达的体密度值都随肾脏的发育逐渐增大。Western blot结果显示纤维粘连蛋白和整合素α5蛋白的水平都随肾脏的发育逐渐增加。可见纤维粘连蛋白和整合素α5在小鼠肾小管的发育和成熟过程中的表达具有一定的时空性,对肾小管的发育起一定的作用。     

Analysis of gene expression profiles in rat hippocampus following treatment with nicotine and an alpha7 nAChR selective agonist

The nicotinic acetylcholine receptors (nAChRs) play critical roles in neuronal transmission and modulation. Among the diverse nAChRs, the alpha7 subtype has been considered as a potential therapeutic target for treating cognitive deficits associated with neuropsychiatric and neurodegenerative diseases. Although a number of mechanisms including neurotransmitter and biochemical effects linking alpha7 nAChR activation and cognitive function are beginning to be described, the underlying molecular processes especially following repeated administration remain unclear. To address this, we have performed gene expression analysis in rats treated with nicotine and a selective alpha7 nAChR agonist, PNU-282987. Our results showed significant overlap in gene expression changes induced by PNU-282987 and nicotine, suggesting convergent pathways triggered by these compounds. Treatment with nicotine also resulted in regulation of a number of genes that were not regulated by PNU-282987, consistent with the interaction of nicotine with other nAChRs beyond the alpha7 subtype. Interestingly, these gene expression changes were observed 24 h post-dose, suggesting that both nicotine and PNU-282987 cause protracted changes in gene expression. Overall, our results identify gene expression changes that may contribute to further defining the roles of nAChR activation in cognitive function.     

Cells and tissue interactions with glycated collagen and their relevance to delayed diabetic wound healing

Dermal accumulation of advanced glycation end products (AGEs) has increasingly been implicated as the underlying cause of delayed diabetic wound healing. Devising an in vitro model to adequately mimic glycated tissues will facilitate investigation into the mechanism of glycation in conjunction with exploration of new approaches or improvement of current therapies for treating diabetic chronic wounds. Collagen matrices were artificially glycated and the presence of AGEs was demonstrated by immunostaining. Both the mechanical properties of the collagen matrices and their interactions with fibroblasts (morphology, attachment, proliferation, and migration) were altered after glycation, moreover, there was evidence of impairment on extracellular matrix (ECM) remodeling as well as inhibition of cell-induced material contraction. The actin cytoskeletons of the fibroblasts residing in the glycated collagen matrices were reorganized. In vivo mice full-thickness dermal wound models implanted with glycated collagen matrices showed delayed wound healing response. Thus, the glycated collagen matrix is an adequate in vitro model to mimic glycated tissues and could serve as a facile experimental tool to investigate the mechanism of glycation in conjunction with exploration of new approaches or improvement of current therapies for treating diabetic wounds.     

Expression of Thrombomodulin and Consequences of Thrombomodulin Deficiency during Healing of Cutaneous Wounds

Thrombomodulin is a cell surface anticoagulant that is expressed by endothelial cells and epidermal keratinocytes. Using immunohistochemistry, we examined thrombomodulin expression during healing of partial-thickness wounds in human skin and full-thickness wounds in mouse skin. We also examined thrombomodulin expression and wound healing in heterozygous thrombomodulin-deficient mice, compound heterozygous mice that have <1% of normal thrombomodulin anticoagulant activity, and chimeric mice derived from homozygous thrombomodulin-deficient embryonic stem cells. In both human and murine wounds, thrombomodulin was absent in keratinocytes at the leading edge of the neoepidermis, but it was expressed strongly by stratifying keratinocytes within the neoepidermis. No differences in rate or extent of reepithelialization were observed between wild-type and thrombomodulin-deficient mice. In chimeric mice, both thrombomodulin-positive and thrombomodulin-negative keratinocytes were detected within the neoepidermis. Compared with wild-type mice, heterozygous and compound heterozygous thrombomodulin-deficient mice exhibited foci of increased collagen deposition in the wound matrix. These findings demonstrate that expression of thrombomodulin in keratinocytes is regulated during cutaneous wound healing. Severe deficiency of thrombomodulin anticoagulant activity does not appear to alter reepithelialization but may influence collagen production by fibroblasts in the wound matrix.     

富血小板纤维蛋白联合姜黄素纳米颗粒水凝胶促糖尿病小鼠创面愈合

背景:糖尿病难愈性创面目前仍缺乏十分理想的治疗手段,探索促进糖尿病创面愈合的方法意义重大。目的:观察富血小板纤维蛋白联合姜黄素纳米颗粒水凝胶对糖尿病小鼠创面愈合的影响。方法:分别制备富血小板纤维蛋白与姜黄素纳米颗粒水凝胶。从100只成年C57BL/6J小鼠中随机取20只作为正常对照(A组),另外80只建立糖尿病模型。在建模成功的72只小鼠背部制作直径1 cm的圆形全层皮肤损伤创面,随机分4组处理:B组涂抹生理盐水,C组涂抹富血小板纤维蛋白与游离姜黄素溶液,D组涂抹富血小板纤维蛋白与姜黄素纳米颗粒溶液,E组涂抹富血小板纤维蛋白与姜黄素纳米颗粒水凝胶,每组18只。A组小鼠背部制作直径1 cm的圆形全层皮肤损伤创面,涂抹生理盐水。于创面造模当日即开始给药,之后隔日分别给予上述对应药物,直至伤后12 d。处理后第3,9,12天,观察创面愈合及创缘组织病理组织学变化。结果与结论:(1)处理后第12天,A、C、D、E组创面基本愈合完全,B组创面未完全愈合,E组创面愈合率高于B、C、D组(P <0.05);(2)处理后第3天苏木精-伊红染色显示,E组创面愈合情况好于B、C、D组,炎细胞浸润及肉...     

可乐定通过激活胆碱能抗炎通路抑制肺损伤小鼠炎性反应

目的:探讨可乐定对肺损伤小鼠炎性反应的影响及其作用机制。方法:以脂多糖(lipopolysac charide,LPS)诱导的肺损伤小鼠为模型,静脉注射可乐定,取左肺上叶组织,检测肺湿干重比(W/D)和总肺含水量(TLW),ELISA试剂盒检测炎性因子IL-1β、IL-6和TNF-α的含量,RT-PCR和Western blot检测α7烟碱型乙酰胆碱受体(α7nAChR)、高迁移率族蛋白B1(HMGB1)表达的变化;鼻内吸入法将α7nAChR基因RNA干扰慢病毒载体导入肺损伤模型小鼠肺内,或者静脉注射HMGB1外源性蛋白,检测炎性因子和HMGB1的变化。结果:可乐定可减轻LPS诱导的小鼠肺损伤,并通过降低细胞因子IL-6、IL-10和TNF-α水平从而抑制LPS诱导的炎性反应;可乐定促进α7nAChR表达从而激活胆碱能抗炎通路,并抑制HMGB1的表达。结论:可乐定对肺损伤小鼠具有抗炎作用,这可能与激活胆碱能抗炎通路,抑制HMGB1的表达有关。     

The peritoneal macrophage inflammatory profile in cirrhosis depends on the alcoholic or hepatitis C viral etiology and is related to ERK phosphorylation

Background

Continuous diabetes-associated complications are a major source of immune system exhaustion and an increased incidence of infection. Diabetes can cause poor circulation in the feet, increasing the likelihood of ulcers forming when the skin is damaged and slowing the healing of the ulcers. Whey proteins (WPs) enhance immunity during childhood and have a protective effect on some immune disorders. Therefore, in this study, we investigated the effects of camel WP on the healing and closure of diabetic wounds in a streptozotocin (STZ)-induced type I diabetic mouse model.

Results

Diabetic mice exhibited delayed wound closure characterized by a significant decrease in an anti-inflammatory cytokine (namely, IL-10) and a prolonged elevation of the levels of inflammatory cytokines (TNF-??, IL-1?? and IL-6) in wound tissue. Moreover, aberrant expression of chemokines that regulate wound healing (MIP-1??, MIP-2, KC and CX3CL1) and growth factors (TGF-??) were observed in the wound tissue of diabetic mice compared with control nondiabetic mice. Interestingly, compared with untreated diabetic mice, supplementation with WP significantly accelerated the closure of diabetic wounds by limiting inflammatory stimuli via the restoration of normal IL-10, TNF-??, IL-1?? and IL-6 levels. Most importantly, the supplementation of diabetic mice with WP significantly modulated the expression of MIP-1??, MIP-2, KC, CX3CL1 and TGF-?? in wound tissue compared with untreated diabetic mice.

Conclusion

Our data demonstrate the benefits of WP supplementation for improving the healing and closure of diabetic wounds and restoring the immune response in diabetic mice.     

Accelerated wound closure in neutrophil-depleted mice

The infiltration of neutrophils into injured tissue is known to protect wounds from invading pathogens. However, more recent studies suggest that neutrophils might inhibit the wound repair process. To investigate the role of neutrophils in wounds, mice were neutrophil-depleted by injection with rabbit anti-mouse neutrophil serum. Remarkably, epidermal healing, measured by wound closure, proceeded significantly faster in neutropenic than control mice (77.7+14.2% vs. 41.2+0.9%, P<0.02 at day 2). Dermal healing was not affected by neutrophil depletion, as neither collagen deposition nor wound-breaking strength was significantly different between neutropenic and control mice. As the delayed repair of diabetic individuals exhibits robust inflammation, the effect of neutrophil depletion on diabetic wound healing was investigated. Similar to the observations in wild-type mice, wound closure was accelerated by nearly 50% in neutropenic, diabetic mice. The results suggest that although neutrophils may provide protection against infection, they may retard wound closure.     

臭氧气浴对深Ⅱ度烧伤大鼠创面病理变化及组织细胞因子表达的影响

目的:探讨臭氧气浴干预对大鼠深Ⅱ度烧伤创面的病理变化及局部组织中细胞因子血小板源性生长因子(PDGF)、转化生长因子β_3(TGF-β_3)和肿瘤坏死因子α(TNF-α)表达的影响。方法:取80只雄性清洁级SD大鼠,随机分为臭氧气浴实验组和常规换药对照组各40只。建立背部深Ⅱ度烧伤模型,伤后3 d、7 d、14 d和21d,2组创面分别取材检测。创面常规换药,对照组的创面以生理盐水清洗和碘伏油纱包扎,隔日换药1次;臭氧气浴实验组在换药前将大鼠放入清洁泡沫盒内,打开臭氧发生器开关,以输出浓度为50 mg/L的臭氧熏蒸创面20min,关闭开关,再行创面常规换药,隔日1次,直至愈合。各时点每组大鼠创面打开时取1次创面中心组织标本,然后实验组行生理盐水棉球轻拭创面和臭氧气熏蒸,对照组仅用生理盐水棉球轻拭创面后再分别取材1次。标本行HE染色组织学观察和免疫组化染色半定量观察,结合图像数据分析及ELISA法检测2组创面组织中细胞因子PDGF、TGF-β_3和TNF-α含量。结果:创面大体观察可见,臭氧气浴实验组的创面平整,边缘清晰,炎性反应轻,肿胀和渗出程度均较对照组弱,创面愈合率高于常规换药对照组,2组比较差异有统计学意义。显微镜下观察HE染色组织可见臭氧气浴实验组的创面各时点炎性反应程度比常规换药对照组轻,而新生毛细血管、成纤维细胞和上皮细胞增生数量明显优于常规换药对照组。与对照组比较,臭氧气浴实验组各时点烧伤大鼠的创面组织匀浆上清液中PDGF和TGF-β_3表达量均高于常规换药对照组,而TNF-α表达量明显低于对照组,2组比较差异均有统计学意义。结论:臭氧气浴疗法干预大鼠深Ⅱ度烧伤创面,能改善局部病理变化,促进与创面愈合相关的细胞因子PDGF和TGF-β_3表达,同时减轻炎性介质TNF-α的表达。