急性胰腺炎患者IL-6、TNFα水平测定及临床意义

目的研究急性胰腺炎患者IL-6、TNFα分泌情况及其临床意义。方法选择30例急性胰腺炎患者和28例健康对照,用生物学方法检测血浆中IL-6、TNFα的水平。结果急性胰腺炎患者血浆中IL-6、TNFα分别为(76．4±10．1)k u/L、60．7％±12．3％,均高于正常对照组(20．8±6．1)ku/L、12．4％±4．7％,随疾病的恢复逐渐趋于正常(28．5±9．1)ku/L、18．8％±6．4％。结论急性胰腺炎患者血浆中的IL-6、TNFα水平均高于正常组,说明二者参与这一炎症过程。     

Changes in plasma IL4, TNF�� and CRP in response to regular passive smoking at home among healthy school children in Khartoum, Sudan

Background

Regular exposure to tobacco smoke at home causes airway inflammation and altered cytokine regulation; however, there is variation between individuals of different countries.

Objective

To determine effects of passive smoking on plasma IL4, TNFá, and CRP in healthy male school-children in Khartoum.

Methods

A total of 135 male school-pupils (69 passive smokers and 66 non-smokers) were selected randomly from three primary schools for boys in Khartoum. Information about smoking history was collected from each pupil and his parents using a questionnaire. Plasma CRP, IL4 and TNFá were measured using commercially available ELISA kits.

Results

Plasma IL4 and TNFá in the passive smokers (mean ± SEM) is at 2.92 ± 0.93 and 19.78 ± 4.67 pg/ml respectively; whereas in the non-smokers . It is at 0.45 ± 0.28 and 5.05 ± 1.54 pg/ml respectively. The difference between the two groups is statistically significant (p <0.05). The mean plasma IL4 and TNFá were lowest with no exposure, higher with moderate exposure, and highest with heavy exposure (P < 0.05). Plasma CRP showed insignificant difference between the two groups.

Conclusion

Passive smoking causes significant rise in plasma TNFá and IL4 with a dose dependent effect among school-pupils in Khartoum.     

缺血再灌后淋巴液对正常大鼠白介素-8和肿瘤坏死因子的影响

目的 :观察缺血再灌后淋巴液对正常大鼠的影响 ,探讨多器官功能障碍产生的机理。方法 :从模型大鼠乳糜池内引流肠道淋巴液注入健康大鼠内 ,检测健康大鼠肠道淋巴液内白介素 8(IL 8)、肿瘤坏死因子 (TNFa)的含量。结果 :缺血再灌后淋巴液IL 8浓度比正常组 ,也比血浆IL 8高 ,注射缺血再灌后淋巴液后 3h、5h ,实验组血浆IL 8比注射前低 ,与对照组相近。缺血再灌后淋巴液TNFa浓度比血浆高 ,注射缺血再灌淋巴液后 3h血浆TNFa浓度较对照组高。结论 :缺血再灌后淋巴液内IL 8和TNFa较血浆高 ,注射缺血再灌后淋巴液的大鼠血浆TNFa含量明显增加。     

中波紫外线诱导HaCaT细胞凋亡与扇贝多肽的影响：肿瘤坏死因子α/肿瘤坏死因子受体1通路的研究

背景：扇贝多肽可以通过Fas通路及NF-κB通路发挥对中波紫外线照射后的人角质形成细胞株(HaCaT)的保护作用。 目的：观察中波紫外线辐射后HaCaT细胞的凋亡情况和细胞内肿瘤坏死因子α/肿瘤坏死因子受体1的活化情况,以及扇贝多肽的干预作用。 方法：实验以20 mJ/cm2中波紫外线辐照HaCaT细胞0.5 h建立细胞辐射损伤模型,药物低、中、高剂量组、阳性对照组、抑制剂组分别在造模前2 h加入1.42,2.84,5.69 mmol/L的扇贝多肽、5.68 mmol/L的维生素C及50 mg/L的抗肿瘤坏死因子α单克隆抗体。 结果与结论：中波紫外线辐照后,HaCaT细胞凋亡增多,肿瘤坏死因子α、肿瘤坏死因子受体1 mRNA及磷酸化JNK蛋白表达量增加;1.42,2.84,5.69 mmol/L的扇贝多肽均可降低中波紫外线辐照引起的细胞内肿瘤坏死因子α、肿瘤坏死因子受体1 mRNA及磷酸化JNK表达,抑制HaCaT细胞凋亡,以5.69 mmol/L扇贝多肽的作用效果最明显,与5.68 mmol/L维生素C的作用相当,且50 mg/L抗肿瘤坏死因子α单克隆抗体也可明显降低中波紫外线辐照引起的细胞内磷酸化JNK表达。说明扇贝多肽能抑制中波紫外线辐照引起的HaCaT细胞凋亡,其可以通过肿瘤坏死因子α/肿瘤坏死因子受体1通路发挥抗凋亡作用。     

The role of cytokines in UbD promoter regulation and Mallory-Denk body-like aggresomes

Mallory-Denk bodies (MDBs) are found in chronic liver diseases. Previous studies showed that diethyl-1,4-dihydro-2,4,6-trimethyl-3,5-pyridinedicarboxylate (DDC) induced formation of MDBs and the up regulation of UbD expression in mouse liver. UbD is a protein over expressed in hepatocellular carcinomas. It is a potential preneoplastic marker in the mouse. It is hypothesized that inflammatory cytokines play a critical role in UbD up regulation and MDB formation. TNFa and IFNg treatment of HCC cell line Hepa 1-6, induced the expression of UbD and the expression of genes coding for the immunoproteasome (LMP2, LMP7, and MECL-1 subunits). TNFa and IFNg induced the activity of the UbD promoter, using a luciferase assay. The cotreatment with TNFa and IFNg induced the activity of the UbD promoter through an Interferon Sequence Responsive Element (ISRE). In addition, long term treatment with TNFa and IFNg induced the formation of MDB-like aggresomes in Hepa 1-6 cells, which emphasizes the role of inflammation in the formation of MDBs leading to the formation of liver tumors, in the mouse. Identifying the mechanism that regulates gene expression of UbD supports the hypothesis that down regulation of UbD and the proinflammatory gene expression would prevent MDB and HCC formations. Previous studies indicate that S-adenosylmethionine or betaine prevented IFNg induced UbD and MDB formations.     

急黄汤抗大鼠急性肝衰竭的动态观察

目的:探讨急黄汤抗实验性急性大鼠肝衰竭的作用和机制。方法:以D-G1aN 900mg/kg剂量一次腹腔注射制成大鼠急性肝衰竭模型,治疗组造模前3d开始灌胃急黄汤清膏10mL/(kg·d),浓度为200％,于造模后24、48、72h,模型组及治疗组各取8只大鼠断头处死采血测定ALT、TB、PT、FP、TNFα,取肝组织作病检。结果:急黄汤在不同时相能明显降低急性肝衰竭大鼠ALT、TB、PT、FP、TNFα水平,改善肝组织病变,与模型组比较,P<0.05或P<0.01,有显著性差异。结论:急黄汤具有抗D-G1aN大鼠急性肝衰竭作用,可能与降低急性肝衰竭的重要介质TNFα及肝细胞损伤的标志物FP有关。     

静脉丙种球蛋白早期干预对急性病毒性心肌炎心肌酶、血清TNFα、IL-4及疗效观察

目的观察静脉丙种球蛋白对急性病毒性心肌炎心肌酶、血清TNFα及IL-4的影响及临床疗效。方法采用随机数字表法将92例患者随机分为2组即治疗与对照组,两组患者均嘱卧床休息,应用广谱抗生素,给予三磷酸腺苷,辅酶A,维生素C,维生素E,普通胰岛素,肌苷等常规治疗,合并心律失常者加用相应抗心律失常药物。治疗组在上述治疗的基础上加用静脉丙种球蛋白（蓉生静丙,2.5 g/瓶,成都生物制品研究所研制）,200 mg/kg·d,连用7 d。2周后进行疗效评定。结果两组患者在临床症状及ECG明显改善,TNFα、IL-4明显降低,差异有统计学意义（P〈0.05或P〈0.01）。结论早期应用静脉丙种球蛋白早期干预可明显降低CK、CK-MB、LDH1、LDH2,调节免疫系统,改善临床症状。     

重症急性胰腺炎急性期细胞因子及胰腺腺泡细胞凋亡的动态变化

目的 本研究通过重症急性胰腺炎（SAP）大鼠血清淀粉酶、TNFa、IL－6、胰腺腺泡细胞凋亡指数及胰腺组织学变化程度作用的动态观察，以进一步了解治疗SAP的作用机理。方法 用chetty法制做大鼠SAP模型，动态测定术后0h、24h、30h、36h各组血清TNFa、IL－6浓度，并取得胰组织做病理学检查；同时，应用TUNEL技术分析大鼠胰腺腺泡细胞凋亡的变化。结果 研究发现SAP组30、36h时血清TNFa、IL－6水平明显升高，腹水量明显增加，胰组织病变程度明显加重；胰腺腺泡细胞凋亡指数较SAP组胰腺腺泡细胞凋亡指数明显升高。结论 重症急性胰腺炎（SAP）胰酶及炎症介质的释放及胰腺腺泡细胞凋亡在其病情发展起一定的作用。