生物喋呤对烫伤脓毒症大鼠一氧化氮合成的影响

目的：探讨生物喋呤BH4在金黄色葡萄球菌（简称金葡菌）脓毒症中的生物学效应，阐明BH4对一氧化氮（NO）诱生的调控作用。方法：76只Wistar大鼠随机分为正常对照组（n=10)、烫伤对照组（n=10)、烫伤后金葡菌感染组（n=40)和羟基嘧啶（DAHP）拮抗组（n=16)。无菌留取动物肝、肺组织采用RT－PCR方法检测三磷酸鸟苷环水解酶I（GTP－CHI）、诱生型一氧化氮合酶（iNOS)基因表达，同时测定组织中BH4和NO的水平。结果：烫伤后金葡菌感染组动物肝、肺组织中GTP－CHI基因表达明显上调，BH4产生显著增加，iNOS mRNA表达和NO的水平亦明显升高，DAHP组GTP－CHI基因表达上调和BH4合成NO的产生亦明显下降。结论：烫伤后金葡菌感染可诱导体内BH4的合成，BH4在基因和蛋白水平调控着iNOS所介导的NO大量生成，从而对金葡菌脓毒症的病理过程起促进作用。     

Significance of biopterin induction in rats with postburn Staphylococcus aureus sepsis

It has been demonstrated that biopterin, an essential cofactor of nitric oxide synthase (NOS), plays an important role in the pathogenesis of endotoxin-induced shock, yet its biological significance in gram-positive sepsis remains unclear. In this study, we adopted a rat model of postburn Staphylococcus aureus sepsis to investigate the potential role of biopterin in the pathogenesis of gram-positive sepsis. Wistar rats were inflicted with a 20% total body surface area (TBSA) full-thickness scald injury followed by S. aureus challenge, and then guanosine triphosphate-cyclohydrolase I (GTP-CHI) mRNA expression and biopterin levels in liver, kidneys, lungs, and heart were determined. We found that after S. aureus challenge, GTP-CHI gene expressions and biopterin levels were markedly upregulated in various tissues. Meanwhile, multiple organ dysfunction was induced by S. aureus challenge. It was shown that cardiac GTP-CHI mRNA expression and renal BH(4) levels were positively correlated with MB isoenzyme of creatine kinase (CK-MB) and creatinine (r = 0.892, P = 0.0012 and r = 0.9423, P = 0.0015, respectively). These results suggested that thermal injury combined with S. aureus challenge could induce de novo biosynthesis of biopterin, which might play a role in the development of multiple organ dysfunction syndrome secondary to postburn sepsis.     

烫伤后金黄色葡萄球菌感染致严重脓毒症大鼠模型的建立

目的初步建立烫伤后金黄色葡萄球菌(金葡菌)感染所致严重脓毒症的动物模型。方法雄性Wistar大鼠行20%总体表面积Ⅲ度烫伤,于伤后24小时经腹腔注射对数生长期的金葡菌菌液4ml/kg(浓度为8×10     

雷帕霉素对烫伤后金黄色葡萄球菌脓毒症大鼠白细胞介素10表达的影响

目的探讨脓毒症时应用雷帕霉素(RPM)干预对肝脏内源性白介素10(IL10)表达和急性肝损伤的影响。方法采用烫伤后金黄色葡萄球菌感染致严重脓毒症大鼠模型,50只大鼠随机分为正常对照组(n=5)、烫伤对照组(n=5)、烫伤脓毒症组(n=30)和RPM处理组(n=10)。采用逆转录多聚酶链式反应测肝组织IL10mRNA表达,并应用ELISA方法分别检测肝组织、血中IL10蛋白水平,同时观察肝功能指标的改变。结果与烫伤脓毒症组比较,RPM干预后0.5h肝组织中IL10mRNA表达和血中IL10蛋白水平明显升高(P<0.05),干预后2h则有不同程度的下降,但仍显著高于伤前水平(P<0.05或P<0.01)。同时,RPM干预组肝功能酶学指标明显改善。结论烫伤脓毒症早期应用RPM有助于保护IL10的内源性抗炎效应,从而减轻失控性炎症反应和急性肝损伤。     

JAK/STAT通路对烫伤脓毒症大鼠Toll样受体基因表达的调节作用

目的：探讨Janus激酶／信号转导和转录激活子（JAK／STAT）通路在烫伤脓毒症大鼠Toll样受体2（TLR2）基因表达调控中的意义。方法：Wistar大鼠38只随机分为正常对照组（n=6)、烫伤后金黄色葡萄球菌（金葡菌）感染组（n=12)、AG490拮抗组（n=20)和雷帕霉素（Rapamycin,RPM)拮抗组（n=10), 检测动物肝、肾、肺组织中TLR2和肿瘤坏死因子－α（TNF－α）基因表达的改变。结果：烫伤合并金葡菌攻击后0．5h和2h，动物肝、肾、肺组织中TLR2 mRNA表达显著增高（P＜0．05或P＜0．01）。RPM干预可有效抑制动脉肝、肾组织TLR2 mRNA表达，但对肺脏TLR2 mRNA表达无明显影响；而AG490拮抗组动物各组织中TLR2 mRNA表达与未干预组相比均无明显差异。烫伤合并金葡菌感染后2h大鼠肝、肺、肾组织TNF－α基因表达均显著升高（P均＜0．01）。给予RPM可明显抑制各组织中TNF－α mRNA表达（P＜0．05或P＜0．01），AG490拮抗组大鼠肝、肾组织中TNF－α表达亦均显著低于未拮抗组（P均＜0．01）。结论：烫伤后金葡菌感染可促进体内TLR2基因表达，STAT可能直接或通过其诱生的炎症介质参与了对TLR2 mRNA表达的调控。     

The potential role of Staphylococcal enterotoxin B in rats with postburn Staphylococcus aureus sepsis

Staphylococcal enterotoxin B (SEB) is an important member of the superantigen family, which exerts a number of pathological effects in the human, as well as susceptible animals. The present study was conducted to observe the time course and tissue distribution of SEB in postburn Staphylococcus aureus infection; meanwhile, the relationship between SEB and multiple organ dysfunction was also studied. Eighty-six male Wistar rats were randomly divided into four groups as follows: normal control group (n = 10); scald control group (n = 10); postburn sepsis group (n = 50) in which rats inflicted with 20% total body surface area (TBSA) III degrees scald followed by SEB-producing S. aureus challenge were further divided into 0.5-, 2-, 6-, 12-, and 24-h subgroups, with 10 rats in each subgroup; and SEB monoclonal antibody (MAb) treatment group (n = 16) in which a dose of 4 mg/kg SEB MAb was given intravenously just before S. aureus challenge, and the rats were further divided into 2- and 6-h subgroups. It was found that after thermal injury combined with S. aureus infection, SEB was widely distributed to the liver, kidneys, lungs, and heart, exacerbating the pathophysiology of multiple organ dysfunction induced by postburn sepsis. At the same time, the gene and protein expressions of tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) were also markedly upregulated in various tissues. Early treatment with SEB-specific MAb-MAb2D(1)-could markedly decrease SEB levels in plasma as well as in various tissues, and could significantly reduce the 6-h mortality rate (17.64% [3/17] vs. 55.6% [20/36], P = 0.02). These data suggested that neutralization of SEB is effective in ameliorating S. aureus sepsis and subsequent multiple organ damage, which might be attributed to its inhibitory effect on inflammatory mediator formation.     

丙酮酸乙酯对烫伤延迟复苏大鼠多器官功能及死亡率的影响

目的观察丙酮酸乙酯（EP）对烫伤延迟复苏动物多器官功能及死亡率的影响，探讨其保护作用的机制。方法采用雄性Wistar大鼠30％总体表面积Ⅲ度烫伤模型。实验分为两部分进行：①死亡率观察：130只大鼠按照随机数字表法分为假烫伤组（n=10）、烫伤组（n=60。伤后6h腹腔注射生理盐水40ml／kg进行复苏，然后按照不同时间点腹腔注射等量生理盐水）和EP组（n=60。伤后6h腹腔注射生理盐水40ml／kg进行复苏，按不同时间点腹腔注射EP液40mg／kg。每日2次．间隔12h。给药3d）。除假烫伤组外，各组又分为伤前2h（n=20）、伤后2h（n=20）和伤后12h（n=20）给药3个亚组。观察不同时间点各组动物7d死亡率。②器官功能观察：70只大鼠随机分为假烫伤组（n=10）、烫伤组（n=30）和EP组（n=30，伤后2h给药），并分别于伤后12、24和72h活杀，检测器官功能指标改变。结果与烫伤组相比，伤后12hEP组动物死亡率显著降低（35．0％比75．0％，P〈0．05）。伤后2hEP组血清丙氨酸转氨酶、天冬氨酸转氨酶、尿素氯、肌酐、肌酸激酶水平及肺组织髓过氧化物酶活性均明显下降（P〈0．05或P〈0．01）。结论EP能明显改善严重烫伤延迟复苏大鼠的预后，并对重要器官功能具有显著保护作用。     

烫伤脓毒症大鼠肾脏核转录因子-kB活化与肾损伤关系的研究

目的 研究烫伤脓毒症大鼠肾脏核转录因子-kB（NF-kB）活化与肾损伤的关系。方法采用30％总体表面积Ⅲ度烫伤加内毒素攻击制备烫伤脓毒症大鼠模型。54只Wistar大鼠随机分为正常对照组、烫伤脓毒症1、2、6、12和24h组，烫伤脓毒症1、2和6h＋NF-kB抑制剂吡咯烷二硫基甲酸酯（PDTC）组。采用凝胶电泳迁移率改变分析法（EMSA）检测肾组织NF-kB活性；采用酶联免疫吸附法检测血浆及肾组织中肿瘤坏死因子-α（TNF-α）含量的变化；采用自动生化分析仪检测血肌酐（SCr）和尿素氮（BUN）含量。结果肾组织NF-kB活性于烫伤脓毒症后1h明显增强并达到高峰（P〈0．01），PDTC可显著降低烫伤脓毒症后1h NF-kB的活性。烫伤脓毒症后1h和2h血浆及肾组织中TNF-α水平均明显增高（P均〈0．01），PDTC可显著降低伤后血浆TNF-α水平（P均〈0．01），对肾组织中TNF-α水平影响不明显。烫伤脓毒症后BUN及SCr含量均明显增高（P均〈0．01），PDTC对BUN和SCr含量均无显著影响。结论NF-kB抑制剂可降低烫伤脓毒症大鼠肾组织NF-kB活性，但对肾脏功能无明显保护作用。     

拮抗晚期糖基化终末产物受体对烫伤延迟复苏大鼠多器官功能及死亡率的影响

目的 观察拮抗晚期糖基化终末产物受体(RAGE)对烫伤延迟复苏动物多器官功能及死亡率的影响,并探讨其作用机制.方法 选取雄性Wistar大鼠,采用重度烫伤延迟复苏模型(30%总体表面积Ⅲ度烫伤).实验分为两部分.死亡率观察:130只大鼠被随机分为假手术组(n=10)、烫伤组(n=60)及RAGE抗体治疗组(n=60),观察伤后7 d内每日动物的存活率.器官功能观察:72只大鼠被随机分为假手术组(n=24)、烫伤组(n=24)及RAGE抗体治疗组(n=24),于伤后1、3、5和7 d各活杀6只动物,取血,用全自动生化分析仪测定肝、肾和心脏器官功能指标.结果 烫伤组伤后1～7 d,大鼠血中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、肌酐(cr)、尿素氮(BUN)及肌酸激酶同工酶(CK-MB)水平均显著高于假手术组(P<0.05或P<0.01),其中ALT、AST、Cr及BUN水平均于伤后3 d达峰值;给予RAGE抗体治疗可不同程度降低烫伤动物血中各指标水平,其中AST在伤后1～7 d显著下降,余指标在伤后1～5 d均明显改善(P<0.05或P<0.01).RAGE抗体治疗组伤后7 d内每日大鼠存活率显著高于烫伤组(P<0.05或P<0.01).结论 RAGE抗体干预能明显改善重度烫伤延迟复苏大鼠的预后,并对重要器官功能具有显著保护作用.     

泛素-蛋白酶体途径对烫伤脓毒症大鼠肠道炎症反应与屏障功能的作用研究

目的研究泛素-蛋白酶体途径对烫伤脓毒症大鼠肠组织核转录因子-κB（NF-κB）活化、肿瘤坏死因子-α（TNF-α）表达以及血浆二胺氧化酶（DAO）活性的作用。方法采用30％总体表面积（TBSA）Ⅲ度烫伤合并内毒素攻击大鼠为模型模拟临床烫伤哝毒症。60只Wistar大鼠随机分为正常对照组、烫伤哝毒症模型组、泛素-蛋白酶体抑制剂N-乙酰亮氨酰亮氨酰正亮氨酸（ALLN）组、NF-κB抑制剂吡咯烷二硫基甲酸酯（PDTC）组。采用凝胶电泳迁移率改变分析法（EMSA）分析肠组织NF—κB活性；采用酶联免疫吸附法（ELISA）检测肠组织TNF-α含量；采用分光光度法检测血浆DAO活性。结果各组肠组织NF—κB活性于伤后1h均明显增强，并达到高峰（P均〈0．01）．之后呈现下降趋势；两种抑制剂均可显著降低伤后1h和2hNF-κB的活性。ALLN可明显降低伤后1h肠组织中TNF—α含量（P〈0.01）。两种抑制剂对伤后1h和2h血浆I）AO活性均无明显影响。结论早期使用泛素-蛋白酶体抑制剂可降低烫伤脓毒症大鼠肠组织NF—κB活性．降低肠组织中炎症反应．但对肠组织屏障功能无保护作用。     

血必净注射液对烧伤延迟复苏大鼠器官功能及死亡率的影响

目的 观察血必净注射液对烧伤延迟复苏大鼠多器官功能损害和死亡率的影响。方法 采用大鼠30％总体表面积Ⅲ度烫伤模型。130只雄性Wistar大鼠按随机数字表法分为假伤组（n=10）、烫伤组（n=60，伤后6h腹腔内注射40ml／kg生理盐水）和血必净组（n=60，血必净注射液4ml／kg，每日2次）。除假伤组外，各组再根据不同给药时间点分为伤前2h（n=20）、伤后2h（n=20）和伤后12h（n=20）给药组。分别观察不同时间点各组动物7d的死亡率及伤后12h多器官功能改变。结果 与烫伤组相比，伤后12h血必净组动物死亡率显著降低（75．0％比40．0％。P〈0．05）；同时，血必净组伤后12h血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、尿素氮（BUN）、肌酐（Cr）及肌酸激酶（CK）水平均明显降低（P〈0．05或P〈0．01）。结论 血必净注射液能够明显降低严重烧伤延迟复苏大鼠的死亡率，并对重要器官具有保护作用。     

Peptidoglycan of Staphylococcus aureus causes inflammation and organ injury in the rat

OBJECTIVE: Previous studies have implicated a role of peptidoglycan in the pathophysiology of organ injury in sepsis. However, the systemic response to, and organ injury caused by, peptidoglycan have been scarcely studied in vivo. DESIGN: Prospective, randomized study. SETTING: University-based research laboratory. SUBJECTS: Fifty-seven anesthetized, male Wistar rats. INTERVENTIONS: After surgical preparation, anaesthetized rats were administered 3 mg/kg Staphylococcus aureus peptidoglycan (n = 9), 10 mg/kg S. aureus peptidoglycan (n = 14), or an equal volume of saline (sham, n = 12) in the jugular vein over a 10-min period. MEASUREMENTS AND MAIN RESULTS: Injection of low-dose peptidoglycan (3 mg/kg) had no measurable effects on the rats. In contrast, high-dose peptidoglycan (10 mg/kg) caused increased serum values of aspartate aminotransferase (p < or =.005), alanine aminotransferase (p < or =.001), gamma-glutamyltransferase, and bilirubin (p < or =.05) (indicators of liver injury/dysfunction) as well as a moderate, but significant, increase in serum creatinine and urea (p < or =.05) (indicators of renal dysfunction). Plasma analyses showed a substantial increase in plasma values of tumor necrosis factor-alpha, interleukin-6, and interleukin-10 (p < or =.05 for all vs. sham) at 1 and 3 hrs (enzyme-linked immunosorbent assay). This was accompanied by accumulation of messenger RNAs for tumor necrosis factor-alpha, interleukin-6, and interleukin-10 in both the liver and the lung (p < or =.05 for all cytokines vs. sham) (real-time polymerase chain reaction). Peptidoglycan also caused increased DNA binding of nuclear factor-kappaB (band-shift assays) and phosphorylation of c-Jun and Jun N-terminal kinase (Western blots). In the kidney, interleukin-6 messenger RNA was increased, whereas Toll-like receptor 4 messenger RNA was significantly decreased. CONCLUSIONS: These results demonstrate that injection of peptidoglycan alone causes organ injury/dysfunction, organ inflammation, and systemic inflammation in the rat, involving nuclear factor-kappaB and possibly activator protein 1. These data support the contention that peptidoglycan is a contributing factor in the pathophysiology of organ injury in sepsis.     

内毒素休克大鼠组织生物喋呤与高迁移率族蛋白B1表达的关系

目的　探讨生物喋呤 (BH4)对内毒素休克大鼠肝、肺、肾等多器官高迁移率族蛋白B1(HMGB1 )基因表达的影响及其可能机制。方法　采用内毒素休克模型 ,1 0 4只大鼠随机分为正常对照组(n =8)、内毒素休克组 (n =4 8)和BH4合成抑制剂— 2 ,4 二胺 6 羟基嘧啶 (DAHP)拮抗组 (n =4 8)。分别测定血浆BH4含量和肝、肺、肾组织HMGB1mRNA的表达水平。结果　与正常对照组比较 ,内毒素攻击后 2～ 2 4h大鼠血浆BH4含量显著升高 (P <0 0 1 )。同时 ,内毒素攻击后 2～ 6h大鼠肝、肺、肾组织HMGB1mRNA表达显著增强 ,并于 1 2～ 2 4h达峰值 (P <0 0 1 ) ,4 8h仍持续于较高水平。给予DAHP处理后 ,血浆BH4含量在 2、 6、 1 2h显著低于内毒素休克组 (P <0 0 5 ) ;动物肝、肾组织中HMGB1mRNA表达亦明显下调 (P <0 0 5 ) ,各时间点其水平均接近正常对照范围 :与内毒素休克组相比 ,DAHP组肺组织HMGB1mRNA表达峰值显著下降 (P <0 0 5 )。结论　生物喋呤对机体HMGBl的基因表达具有显著影响 ,它参与了内毒素休克时多种组织“晚期”炎性介质———HMGB1的诱生过程     

氧自由基对烫伤大鼠延迟复苏后肠上皮细胞凋亡的影响

目的：观察烧伤延迟复苏后肠粘膜上皮细胞凋亡的发生规律及与氧自由基损伤的关系。方法：１５０只雄性Ｗｉｓｔａｒ大鼠随机分为Ａ组（烫伤立即复苏组,ｎ＝６０）、Ｂ组（烫伤延迟复苏组,ｎ＝５０）、Ｃ组（Ｎ－乙酰半胱氨酸（ＮＡＣ）治疗组,ｎ＝２０）和Ｄ组（别嘌呤醇治疗组,ｎ＝２０）。３０％总体表面积（ＴＢＳＡ）Ⅲ度烫伤大鼠伤后６小时进行复苏。观察伤后肠粘膜上皮细胞凋亡发生规律,测定Ａ、Ｂ组伤后３、６、１２、２     

Pulmonary vascular permeability changes in an ovine model of methicillin-resistant Staphylococcus aureus sepsis

Introduction

Endothelial dysfunction is a hallmark of sepsis, associated with lung transvascular fluid flux and pulmonary dysfunction in septic patients. We tested the hypothesis that methicillin-resistant Staphylococcus aureus (MRSA) sepsis following smoke inhalation increases pulmonary transvascular fluid flux via excessive nitric oxide (NO) production.

Methods

Ewes were chronically instrumented, and randomised into either a control or MRSA sepsis (MRSA and smoke inhalation) group.

Results

Pulmonary function remained stable in the control group, whereas the MRSA sepsis group developed impaired gas exchange and significantly increased lung lymph flow, permeability index and bloodless wet-to-dry weight-ratio (W/D ratio). The plasma nitrate/nitrite (NOx) levels, lung inducible nitric oxide synthases (iNOS) and endothelial nitric oxide synthases (eNOS), vascular endothelial growth factor (VEGF) protein expressions and poly-(ADP)-ribose (PAR) were significantly increased by MRSA challenge.

Conclusions

These results provide evidence that excessive NO production may mediate pulmonary vascular hyperpermeability in MRSA sepsis via up regulation of reactive radicals and VEGF.     

Conservative treatment of scald burns is superior to early excision.

Early excision of deep burns has been advocated; however, it is difficult to clinically determine the depth of scald burns during the early postburn period. This prospective, randomized study was designed to determine whether early excision was superior to conservative treatment of scald injuries. Patients with scald injuries (which were not caused by grease) of clinically indeterminant depth were randomized to early (n = 12) or late (n = 12) excision; all patients with obvious superficial and full-thickness injuries were excluded. In the early excision group, all deep wounds were tangentially excised and grafted within 72 hours of admission, whereas in the late treatment group wounds were excised and grafted after 2 weeks had passed since injury. Area excised, postburn day of excision, percent graft take, operating-room time, blood replacement, incidence of infection, and length of hospital stay were compared. No patient experienced a significant wound infection or systemic sepsis. A significantly smaller area of excision was necessary for those patients who were treated with delayed surgery, and concomitant decreases in operating-room time and blood loss were observed. Notably, only one half of the patients who were randomized to the delayed excision group ultimately required surgical intervention to achieve wound closure. Graft take was comparable for both groups, as was length of hospital stay. Early clinical evaluation of scald injuries appears to be equivocal, and later evaluations reveal a less severe injury. Financial gains can be made when surgical excision of scald injuries is delayed until 2 weeks after injury because of a related reduction in hospital expenditures.     

烫伤后肠壁组织T淋巴细胞和浆细胞数量的变化

目的：了解烧伤后肠壁组织T淋巴细胞和IgA浆细胞数量的变化与伤后肠道细菌易位及肠源性脓毒症发生、发展的关系。方法：Wistar大鼠50只，随机分成对照组（l只）和烫伤组（40只）。烫伤组动物背部脱毛，将背部浸于沸水中12秒钟，造成40％体表面积Ⅲ度烫伤，分别于伤后第1、3、7和10日处死，留取标本；对照组动物不烫伤，于处理后第1日处死，留取标本。采用免疫组化方法分别测定回肠固有层和粘膜层CD3 、CD4 和CD8 淋巴细胞以及IgA浆细胞数量，并测定肠道细菌IgA包被率和肠道细菌易位率。结果：伤后肠壁组织中CD3 、CD4 T淋巴细胞和lgA浆细胞的数量明显减少，CD4 ／CD8 比值和肠道细菌IgA包被率亦明显降低，而肠道细菌易位率则明显升高。结论：肠壁组织中T淋巴细胞和IgA浆细胞数量减少、肠道细菌IgA包被率降低与肠道细菌易位率升高有密切关系，其在烧伤后肠源性脓毒症的发生和发展中可能具有重要意义。     

丙酮酸乙酯对烫伤延迟复苏大鼠细胞免疫功能的影响

目的观察丙酮酸乙酯(EP)对烫伤延迟复苏大鼠细胞免疫功能的影响,并探讨其作用机制。 方法采用大鼠30％总体表面积Ⅲ度烫伤模型.103只大鼠随机分为正常对照组(n=7)、假烫伤组(n=32)、 烫伤组(n=32,伤后6 h腹腔内注入40 ml／kg生理盐水)和EP(3.23 mg／ml)干预组(n=32.伤后6 h腹腔内 注入40 ml／kg EP液),分别于伤后1、3、5和7 d活杀,检测脾淋巴细胞增殖能力、白细胞介素-2(IL-2)生成 及白细胞介素-2受体(IL-2R)表达。结果烫伤延迟复苏后1~7 d,脾淋巴细胞丝裂原刺激的增殖反应明显 受抑制(P均<0.05)。烫伤后1~5 d IL-2生成明显减少(P均<0.05),且烫伤后1和3 d IL-2R的表达显 著降低(P均<0.05)。EP干预能够明显恢复烫伤后1~7 d脾淋巴细胞的增殖能力(P均<0.05),伤后1、3 和5 d,IL-2的生成显著增加,但对IL-2R的表达无影响(P均>0.05)。结论 EP能显著增加脾淋巴细胞的 增殖能力和IL-2的产生,从而有效改善烫伤延迟复苏后细胞免疫功能障碍。     

人参皂甙对烫伤脓毒症大鼠细胞免疫功能的影响

目的：探讨人参皂甙对烫伤脓毒症后细胞免疫功能的影响及其作用机制。方法：健康雄性SD大鼠66只，随机分为脓毒症组（24只）、人参皂甙组（24只）和对照组（18只）。将大鼠用沸水致背部30％总体表面积Ⅲ度烫伤，烫伤后12h腹腔注射内毒素（5mg／kg）予以“二次打击”，制成烫伤脓毒症模型。用流式细胞仪检测大鼠外周血中CD4^＋T细胞、CD8^＋T细胞、CD25^＋T细胞和CD4^＋CD25^＋调节性T细胞（Tr细胞）的细胞数。结果：“二次打击”后大鼠外周血中CD4^＋T细胞、CD25^＋T细胞比例显著下降，CD8^＋T细胞、CD4^＋CD25^＋Tr细胞比例显著升高；此过程随时间而加重，各时间点与对照组比较差异均有显著性（P均〈0．01）；用药后24h、72h占淋巴细胞百分比人参皂甙组CD8^＋T细胞、CD4^＋CD25^＋Tr细胞占淋巴细胞百分比显著低于脓毒症组（P均〈0．01），CD4^＋T细胞、CD25^＋T细胞比例显著高于脓毒症组（P均〈0．01）。结论：烫伤和内毒素“二次打击”后外周血中CD4^＋CD25^＋Tr细胞表达增强，人参皂甙可有效抑制其表达，显著改善烫伤脓毒症时细胞免疫功能障碍。