大鼠输精管注射HFMC后输精管内pH值的观察

本实验选用生育力正常成年雄性ＳＤ大鼠２５只，随机分为５组，行一侧输精管ＨＦＭＣ注射术，剂量为１０％ＨＦＭＣ２０μｌ，沉淀剂２０μｌ；另一侧输精管注射生理盐水４０μｌ对照，于注射时和注射后１、３、６、９和１２月分别测定双侧输精管ｐＨ值，其结果为注射ＨＦＭＣ侧输精管ｐＨ明显降低，为５．１８－５．８２，生理盐水对照侧为７．０４－７．６４，并随推移，注射ＨＦＭＣ侧输精管ｐＨ值逐渐升高，于术后１２月基本恢复     

微波辐射对大鼠附睾细胞形态及组织化学的影响

作者应用光镜、透射电镜及酶组织化学技术,动态观察了微波辐射后大鼠附睾形态、组织内多种酶(SDH、ICDH、MDH、LDH、G-6-PD、G-6-Pase、CCO、AcP、β-GA、AIP、ATPase)活性的变化。结果表明,微波辐射能引起大鼠附睾组织水贮积性病理改变,附睾上皮与有氧氧化有关的酶(SDH、ICDH、MDH、CCO、ATPase及G-6-Pase)活性降低,而无氧酵解酶(LDH)、戊糖旁路酶(G-6-PD)及溶酶体酶(β-GA、AcP)活性升高,提示微波辐射所致附睾损伤是由于血管扩张、瘀血及毛细血管内皮损伤造成的缺氧所致。但从实验结果可见,在微波辐射停止后28天内,上述各种酶可恢复或趋于恢复。     

Oxidative damage of dust storm fine particles instillation on lungs, hearts and livers of rats

The purpose of this study was to investigate the effects of dust storm fine particles (PM_2.5) on oxidative damage in lungs, hearts and livers of rats. Wistar rats were randomly divided into treated groups using PM_2.5 at different concentration (1.5, 7.5, 37.5 mg/kg) and control groups using saline. After a single intratracheal instillation 24 h, rats were sacrificed and activities of Cu,Zn-superoxide dismutase (SOD), levels of glutathione (GSH) and thiobarbituric acid reactive substances (TBARS) were investigated in these three organs of rats. Results show that dust storm PM_2.5 and normal weather PM_2.5 from both Baotou city and Wuwei city caused a dose-dependent decrease of SOD activities and GSH contents in lungs and livers, and a dose-dependent increase of TBARS levels in lungs, hearts and livers of rats as compared to their respective controls. Though the effects induced by normal weather PM_2.5 slightly heavier than dust storm PM_2.5 in both Baotou city and Wuwei city on each examined index, no significant difference was found. Furthermore, no significant difference was observed between the effects induced by dust storm PM_2.5 from Baotou city and that from Wuwei city, or between the effects induced by normal weather PM_2.5 from Baotou city and that from Wuwei city. These results lead to conclusions that both dust storm PM_2.5 and normal weather PM_2.5 could lead to oxidative damage of different disagrees in lungs, hearts and livers, suggesting that the dust storm PM_2.5 whose airborne mass concentrations were much higher should be more harmful. Its toxic effects might be attributed to oxidative damage mediated by pro-oxidant/antioxidant imbalance or excess free radicals. Further work is required to understand the toxicological role of dust storm PM_2.5 on multiple or even all organs in mammals.     

Isolation and structures of novel fungal metabolites as chemokine receptor (CCR2) antagonists

The chemokine receptor, CCR2, is predominantly expressed on monocytes/macrophages, and on a subset of memory T cells. It binds to several CC type chemokines of the monocyte chemoattractant protein (MCP) family of which MCP-1 exhibits the highest affinity. CCR2/MCP-1 expression/association in monocyte/macrophage/T cells has been associated with inflammatory processes such as rheumatoid arthritis, multiple sclerosis and atherosclerosis. Neutralization of CCR2 with either a peptide or receptor antagonist results in the prevention of joint swelling in rodent models of arthritis. In this paper, bioassay-guided discovery of CCR2 receptor antagonists derived from natural product extracts are reported. These antagonists belong to two main classes exemplified by bisthiodiketopiperazines and cytochalasins. Six compounds, including emestrin, two new emestrin analogs, and chaetomin represent the first group of compounds. These compounds inhibited the binding of MCP-1 to CCR2 (CHO membrane) with IC50 values of 0.8 to 9 microM and exhibited good activity in a whole cell assay using MCP-1 and human monocytes with IC50's ranging from 4-9 microM. Cytochalasins A and B represented the second group and inhibited the binding activity with IC50 values of 5 and 188 microM, respectively. This is the first report of natural product antagonists of the CCR2 receptor.     

Protein oxidation and DNA-protein crosslink induced by sulfur dioxide in lungs, livers, and hearts from mice

In this article, protein oxidative damage and DNA-protein crosslinks (DPC) induced by sulfur dioxide (SO(2)) in lungs, livers, and hearts of mice were studied. The protein carbonyl (PCO) content was measured using spectrophotometric DNPH assay to reflect the degree of protein oxidative damage, and the DPC coefficient was measured by using a KCl-sodium dodecyl sulfate (SDS) assay to show the degree of DNA damage in lungs, livers, and hearts from mice exposed to SO(2) at various concentrations (0, 14, 28, and 56 mg-m(- 3)) for 6 h per day for 7 days. The results indicate that SO(2) caused an increase of PCO and DPC level in all organs tested from mice in a concentration-dependent manner. The concentration-response relationships in all organs tested of both female and male mice could be fitted well with monolinear regression equations. The adjusted coefficient R squared of all equations is more than 0.9. These results lead to a conclusion that SO(2) may cause an increase of protein oxidation damage and DNA-protein crosslinking in lungs, livers, and hearts from mice. The rank order of absolute increase in PCO contents and DPC coefficient in three organs from mice compared with controls was lung > liver > heart. Our results also indicated the regulation of PCO and that of DPC induced by SO(2) were conformed to each other; this implies that the protein oxidative damage may be associated with the emergence of DPC.     

基质金属蛋白酶-9和基质金属蛋白酶组织抑制剂-1在高原地区慢性肺心病发病机制中的作用

目的探讨基质金属蛋白酶。9（MMP-9）及其基质金属蛋白酶组织抑制剂-1（TIMP-1）在高原慢性肺心病（HACCP）发病机制中的作用。方法选择高原肺心病急性加重期患者56例（A组）、缓解期患者51例（B组）和健康对照组40例（c组）,采用双抗体夹心酶联免疫吸附法（ELISA）测定诱导痰上清液中MMP-9、TIMP-1表达,并分析其与呼吸功能的关系。结果A组诱导痰中MMP-9、TIMP-1和MMP-9／TIMP-1比值[分别为（976．33±201．65）．g／ml、（624．35±151．22）ng／ml、（1．55±0．16）]显著高于B组[分别为（426．74±123．14）ng／ml、（326．404-112．21）ng／ml、（1．31±0．14）,t值为8．367～17．202,P〈0．01]和C组[分别为（142．55±66．11）ng／ml、（121．78±62．26）ng／ml、（1．14±0．11）,t值为13．642—25．832,P〈0．01];B组显著高于c组（t值为6．827～14．233,P〈0．01）。A、B组诱导痰上清液中MMP-9、TIMP-1、MMP-9／TIMP-1比值与诱导痰中性粒细胞、PaCO：均呈显著正相关（r=0．304～0．743,P〈0．01或P〈0．05）,与FEVl％、Pa02均呈显著负相关（r=-0．314～-0．689,P〈0．01或P〈0．05）。结论MMP-9、TIMP-1和MMP-9／TIMP-1比值失衡在HACCP发病机制中起了一定作用,并与中性粒细胞、PaCO：呈显著正相关,与FEV。％、PaO2呈显著负相关。     

2型糖尿病患者心率变异性时域指标与糖尿病视网膜病变的关系

目的：探讨2型糖尿病视网膜病变与心率变异性（HRV）的关系。方法：比较2型糖尿病患者无视网膜病变、背景性视网膜病变和增殖性视网膜病变的心率变异性时域指标。结果：增殖性视网膜病变2型糖尿病患者的心率变异性时域指标高于其他两组。结论：增殖性视网膜病变2型糖尿病患者的心率变异性时域指标明显下降,两者有相关性。