Effect of isoflurane on proliferation and Na+,K+-ATPase activity of alveolar type II cells injured by hydrogen peroxide

The influence of isoflurane (Iso) on proliferation and Na+,K+-ATPase activity of alveolar type II cells (ATII cells) injured by hydrogen peroxide (H2O2) was investigated. ATII cells isolated and purified from adult Sprague-Dawley rats were randomly divided into six groups: control group, 0.28 mM Iso group, 2.8 mM Iso group, 75 microM H2O2 group, 75 microM H2O2 + 0.28 mM Iso group, and 75 microM H2O2 + 2.8 mM Iso group. After primary culture for 32 hours, the proliferation of ATII cells was detected by MTT assay, and after culture for 24 hours the activity of Na+,K+-ATPase and lactate dehydrogenase (LDH) in the cells, and malonaldehyde (MDA) content of the culture medium, were measured by colorimetry. It was found that 0.28 mM and 2.8 mM Iso had no effect on the proliferation of ATII cells (p > 0.05), but 75 microM H2O2 inhibited their proliferation (p < 0.05) compared with untreated controls; 0.28 mM and 2.8 mM Iso significantly decreased Na+,K+-ATPase activity of ATII cells compared with untreated control cells (p < 0.05), and 75 microM H2O2 markedly decreased Na+,K+-ATPase activity of ATII cells (p < 0.01) with untreated control cells. 0.28 mM and 2.8 mM Iso aggravated the decrease of Na+,K+-ATPase activity induced by H2O2. Iso had no effect on LDH activity and MDA content of the culture medium of normal ATII cells, but significantly increased LDH activity and MDA content of the culture medium of ATII cells injured by H2O2. These findings suggest that Iso itself may decrease the activity of Na+,K+-ATPase of ATII cells in vitro and further damage the cells' function under peroxidation conditions, but has no effect on the proliferation of ATII cells.     

PMN apoptosis and its relationship with the lung injury after chest impact trauma

Background Polymorphonuclear neutrophil (PMN), one of the most important inflammatory cells, functions throughout the initiation, progression and resolution of inflammation. This study aimed at investigating the relationship between PMN apoptosis and the lung injury after chest impact trauma. Methods PMNs were purified from rabbits subjected to the chest impact trauma and their apoptosis, necrosis, survival and respiratory burst were detected by flow cytometry. Meanwhile, lactate dehydrogenase and (LDH) ［Ca2+］i were measured. Results The delayed apoptosis of PMNs in bronchoalveolar lavage fluid was observed from 2 hours to 12 hours after trauma, and viable cells increased. Respiratory burst of PMNs in bronchoalveolar lavage fluid was increased significantly from 2 hours with the peak at 8 hours. Meanwhile, lactate dehydrogenase in bronchoalveolar lavage fluid was higher than that in control (P&lt;0.05) from 4 hours to 24 hours, and intracellular free Ca2+ in PMN was increased temporarilly. Conclusions Retention of PMN in tissues and the abnormality in apoptotic pathway inevitably generate persistent activation of PMN and excessive release of toxic substances, resulting in tissue injury. The temporary increase of intracellular free Ca2+ may be responsible for the delayed apoptosis of PMN.     

APE1表达增强与多发性骨髓瘤细胞对马法兰耐药的关系研究

目的：探讨脱嘌呤/脱嘧啶核酸内切酶（apurinic/apyrimidinic endonucle ase,APE1）在多发性骨髓瘤（multiple myeloma,MM）细胞中的表达及其与马法兰耐药的关系.方法：采用双荧光抗体免疫标记法结合激光共聚焦显微镜和免疫细胞化学观察KM3细胞、32例MM患者和10例正常自愿者骨髓标本APE1蛋白定位及表达,并通过免疫细胞化学和Western blot检测0～15 μmol/L马法兰作用KM3细胞1～2 d后APE1表达的变化.结果：APE1和CD38蛋白在MM细胞存在共表达,APE1蛋白表达尤以细胞核周围表达明显;APE1阳性表达在正常对照组、MM初治组和MM复发或难治组间依次增高,P＜0.05;马法兰可诱导KM3细胞APE1表达增强,并与其作用时间及剂量成正比.结论：APE1蛋白表达强度与MM疗效有关,且马发兰作用可诱导其表达增强,提示APE1基因表达增强可能在MM对马发兰耐药中起一定作用.     

浅谈药品价格政策与医药市场秩序的关系

目的探讨我国药品价格政策与医药市场秩序的关系。方法结合当前我国医药市场秩序,分析我国药品价格政策存在的问题。结果与结论我国的药品价格政策是导致当前医药市场秩序混乱的重要因素之一;我国的药品价格政策制订必须适合国情,价格实行政府管制。     

CD80, but not CD86 were up-regulated on the spleen-derived dendritic cells from OVA-sensitized and challenged BALB/c mice

Allergen-specific CD4+ T-helper (Th) 2 cells are involved in the induction and effector phase of allergic asthma. It is well established that T cells activation requires interaction of T cell receptor (TCR) and MHC-peptide complex, as well as costimulatory signal delivered by antigen presenting cells (APCs). There is increasing evidence that CD80 (B7.1) and CD86 (B7.2), as the most important costimulatory molecules, are involved in the allergic immune responses. In the present study, we investigated the CD80 and CD86 expression of spleen-derived dendritic cells (DCs) in a murine model of allergic asthma. We first established a murine model of ovalbumin (OVA)-allergic asthma that showed unique histological characteristic of allergic inflammation in the lung, high serum OVA-specific IgE level, high numbers of eosinophils in the bronchoalveolar lavage (BAL) and high production of Type 2 cytokines in the splenic T cells. In this model, we found that CD80 were significantly upregulated on the spleen-derived DCs from OVA-sensitized and challenged mice compared with that from PBS-treated or non-treated mice, while CD86 is not different among three groups. Furthermore, we demonstrated that Th2 immune responses were elicited by these DCs with high expression of CD80, even to nai;ve T cells from non-treated mice. Our results suggest that DCs in the spleen of allergic mice, via upregulation of CD80 might play a pivotal role in the maintenance and amplification of allergic immune response, namely Th2 immune response.     

Protective effect of nerve growth factor on neurons after traumatic brain injury

The protective effect of nerve growth factor (NGF) on neurons after traumatic brain injury (TBI) was investigated. A brain trauma model of fluid-percussion in rats was established, and 7s NGF was infused continuously in its cerebral ventricle. The activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT), and [Ca2+]i overloading in brain tissues was observed after giving exogenous NGF postinjury. We found that the activity of SOD, GSH-Px, and CAT was markedly higher in NGF-treated group than in the simple trauma group (P < 0.01). Although the level of [Ca2+]i in the NGF-treated group increased, the value was significantly lower than that in the simple trauma and control groups (P < 0.01). These findings suggest that exogenous NGF can (a) increase the activity of the major antioxidant enzymes in brain tissues and attenuate the injuries to neurons induced by oxygen-free radicals, (b) reduce the severe overload of [Ca2+]i and stabilize its homeostasis, and (c) provide clear protective effects on neurons after traumatic brain injury.     

癌细胞mtDNA限制性片段长度多态性分析

目的探讨人癌细胞ｍｔＤＮＡ与正常细胞ｍｔＤＮＡ一级结构的差异。方法采用一步法制备包括肺腺癌ＳＰＣ－Ａ－Ａ、ＰＬＡ－８０１Ｄ、Ａ５４９、Ａ５３１,肝细胞癌ＳＭＭＣ－７７２１,膀胱上皮癌ＥＪ共６个癌细胞系ｍｔＤＮＡ;用ＰｖｕⅡ、ＸｈｏⅠ、ＰｓｔⅠ、ＥｃｏＲⅠ、ＢｓｔＥⅡ、ＨｉｎｄⅢ、ＨｐａⅠ、Ｂｃ１Ⅰ、ＥｃｏＲⅤ、ＳｃａⅠ和ＸｂａⅠ共１１种限制性内切酶对所得ｍｔＤＮＡ进行ＲＦＬＰ分析;并用ＰＣＲ－ＲＦＬＰ方法分析了癌细胞ｍｔＤＮＡ非编码区结构变化。结果６个癌细胞系其ｍｔＤＮＡ基因编码区的３２个酶切位点均无变异,而有３个癌细胞系在其ｍｔＤＮＡ非编码区第１６２７６位核苷酸处出现了ＥｃｏＲⅤ新的酶切位点。结论提示癌细胞ｍｔＤＮＡ基因编码区一级结构相当稳定,而主要的核苷酸变异可能位于其ｍｔＤＮＡ非编码区。     

急性心肌梗塞表观粘度、全血粘弹性和泵功能关系初探

采用Low Shear—30流变仪,对急性心肌梗塞(AMI)和心绞痛(AP)各10例,在切变率(γ)范围0.376～128.5s~(-1)下测其表观粘度(ηa),并测定全血粘弹性参数(粘性分量η′、弹性分量η″、弹性模量G′和损失模量G″)和心脏泵功能参数,同时与正常人(NS)11例对照。结果:AMI组在高、中和低切变率下的ηa和上述粘弹性参数均高于AP组和NS组(P<0.05～0.01),泵功能参数(EF、SV、CO、LVET、PEP/LVET、HI和Cl)却低于AP组和NS组(P<0.05～0.01)。本文研究提示AMI的泵功能受损与其血液流变特性异常有关;纠正血液流变特性异常的方法或措施有利于AMI的治疗。     

Bcl-2、Bax在NHE-1抑制导致的大鼠肺动脉平滑肌细胞凋亡中的作用

目的:探讨Bcl-2、Bax蛋白表达在Na⁺/H⁺交换器-1(NHE-1)抑制而诱导大鼠肺动脉平滑肌细胞(PASMC)凋亡中的作用。方法: 荧光指示剂(Fura-2/AM)测定法检测转染NHE-1特异性核酶基因的大鼠PASMC内Ca²⁺(i)变化;RT-PCR方法检测细胞内bcl-2和baxmRNA表达变化, 免疫组化法检测细胞内Bcl-2和Bax蛋白表达变化。 结果:转染NHE-1特异性核酶基因后, 大鼠PASMC内i显著升高, bcl-2mRNA及蛋白表达显著降低, baxmRNA和蛋白表达显著增加。结论: NHE-1抑制诱导的PASMC凋亡与i增加、bcl-2表达降低及bax表达增加有关。