重组人生长激素治疗肝硬化低清蛋白血症

目的:观察重组人生长激素(rhGH)治疗肝硬化引起的低清(白)蛋白血症的临床疗效。方法:选择血清清蛋白低于30g·L-1的肝硬化病人46例,男性39例,女性7例,分为治疗组、对照组各23例。治疗组在常规保肝及对症治疗基础上,给予rhGH,4IU,皮下注射,每日1次,连续14d;对照组仅给予常规保肝及对症治疗,14d为一个疗程。检测2组病人治疗前及治疗结束d1和4wk后血清清蛋白及其他肝功能指标变化,并进行临床观察。结果:治疗组治疗前血清清蛋白(25±s3)g·L-1,治疗结束d1血清清蛋白(31±3)g·L-1(P<0.01),4wk后血清清蛋白(33±3)g·L-1(P<0.01);对照组治疗前血清清蛋白(25±3)g·L-1,治疗结束d1血清清蛋白(25±3)g·L-1,4wk后血清清蛋白(24.4±2.6)g·L-1(P>0.05),2组治疗结束d1及4wk后血清清蛋白相比,差异有非常显著意义(P<0.01)。治疗结束d1及4wk内治疗组比对照组病人精神状态、食欲、尿量、腹腔积液、肝功能等均明显改善且持续稳定,有显著差异(P<0.05)。无明显不良反应。结论:rhGH可以增加肝硬化病人的血清清蛋白的水平,改善营养状况,无明显不良反应。     

乌司他丁对原位肝移植术肺损伤的保护作用

目的:观察原位肝移植术(OLT)中肺损伤的程度,探讨乌司他丁(UTI)对OLT中肺损伤的保护作用.方法:40例择期行OLT手术患者随机分为UTI组和对照组各20例,UTI组(n=20)切皮后将UTI 100万单位加入100mL生理氯化钠溶液,持续静脉输注,之后每隔4 h重复使用.对照组(n=20)以等容量生理氯化钠溶液代替.于麻醉后切皮前、无肝前期120 min、无肝期30 min、新肝期10 min、新肝期60 min和术毕对肺顺应性、吸气阻力、呼气阻力、峰值压力和平台压力进行观察.结果:在新肝期10 min、新肝期60 min和术毕时,对照组的肺顺应性显著下降,吸气阻力、呼气阻力、峰值压力和平台压力显著升高(P<0.05).UTI组的吸气阻力、呼气阻力、峰值压力和平台压力值均明显低于对照组(P<0.05),而肺顺应性值明显高于对照组(P<0.05).结论:0LT过程造成肺损伤,UTI在OLT中对肺损伤有保护作用.     

田基黄提取物保肝作用的实验研究

目的:以D-半乳糖胺盐酸盐腹腔注射造成大鼠急性肝损伤模型,观察田基黄药材不同提取部位的肝保护作用,最终确定有效部位.方法:将SD大鼠给D-半乳糖胺盐酸盐造成急性肝损伤模型,腹腔注射田基黄不同溶剂的提取物,观察血清中的ALT、AST的变化,确定有效部位.结果:给予田基黄乙醇总提物和乙酸乙酯部位均可降低大鼠血清中的ALT、AST.结论:田基黄乙醇总提取物和乙酸乙酯部位具有明显的保肝作用.     

成年女性不同年龄组的肝代谢功能研究

目的:探讨健康成年女性不同年龄组肝代谢功能的差别.方法:用RP-HPLC检测49例18～34岁,46例35～50岁,18例51～60岁成年女性健康受试者的唾液咖啡因清除率(SCL).结果:18～34岁年龄组的SCL在正常值范围,18～34岁年龄组、35～50岁年龄组和51～60岁年龄组各组间比较,差别显著(P＜0.001).结论:女性随着年龄的增长,SCL下降,肝代谢功能减低.     

中老年脂肪肝患者96例血脂及血糖情况临床分析

目的探讨中老年超声诊断的脂肪肝与血脂、血糖的相关性。方法测定中老年脂肪肝患者96例(观察组)和中老年非脂肪肝健康查体者32例(对照组)的血脂、血糖并进行比较。结果观察组的总胆固醇、甘油三脂、血糖的平均值明显高于对照组。观察组合并甘油三脂、血糖的发病率高于对照组,差异显著(P<0.01)。单纯胆固醇增高与脂肪肝的发病率无明显关系。结论脂肪肝的发生与血脂、血糖的增高关系密切,应高度重视。     

Aryl hydrocarbon receptor-activating polychlorinated biphenyls and their hydroxylated metabolites induce cell proliferation in contact-inhibited rat liver epithelial cells.

Polychlorinated biphenyls (PCBs) exhibit tumor-promoting effects in experimental animals. We investigated effects of six model PCB congeners and hydroxylated PCB metabolites on proliferation of contact-inhibited rat liver epithelial WB-F344 cells. The 'dioxin-like' PCB congeners, PCB 126, PCB 105, and 4'-OH-PCB 79, a metabolite of the planar PCB 77 congener, induced cell proliferation in a concentration-dependent manner. In contrast, the 'non-dioxin-like' compounds that are not aryl hydrocarbon receptor (AhR) agonists, PCB 47, PCB 153, and 4-OH-PCB 187, an abundant noncoplanar PCB metabolite, had no effect on cell proliferation at concentrations up to 10 muM. The concentrations of dioxin-like PCBs leading to cell proliferation corresponded with the levels inducing the expression of cytochrome P450 1A1 mRNA, suggesting that the release from contact inhibition was associated with AhR activation. The effects of PCB 126 and PCB 153 on expression of proteins controlling G0/G1-S-phase transition and S-phase progression were compared. Only PCB 126 was found to upregulate cyclin A and D2 protein levels, and to increase both total cyclin-dependent kinase 2 (cdk2) and cyclin A/cdk2 complex activities. Despite the observed upregulation of cyclin D2, no increase in cdk4 activity was observed. The expression of cdk inhibitor p27Kip1 was not affected by either PCB 126 or PCB 153. These results suggest that dioxin-like PCBs can induce cell proliferation of contact-inhibited rat liver epithelial cells by increasing cyclin A protein levels, a process that then leads to upregulation of cyclin A/cdk2 activity and initiation of DNA replication. This mechanism could be involved in tumor-promoting effects of dioxin-like PCBs.     

Propylene oxide in blood and soluble nonprotein thiols in nasal mucosa and other tissues of male Fischer 344/N rats exposed to propylene oxide vapors--relevance of glutathione depletion for propylene oxide-induced rat nasal tumors.

High concentrations of propylene oxide (PO) induced inflammation in the respiratory nasal mucosa (RNM) of rodents. Concentrations > or =300 ppm caused nasal tumors. In order to investigate if glutathione depletion could be relevant for these effects, we determined in PO exposed male Fischer 344/N rats PO in blood and soluble nonprotein SH-groups (NPSH) in RNM and other tissues. Rats were exposed once (6 h) to PO concentrations between 0 and 750 ppm, and repeatedly for up to 20 days (6 h, 5 days/week) to concentrations between 0 and 500 ppm. At the end of the exposures, PO in blood and NPSH in tissues were determined. PO in blood was dependent on concentration and duration of exposure. After the 1-day exposures, NPSH depletion was most distinctive (RNM > liver > lung). Compared to controls, NPSH levels were 43% at 50 ppm PO in RNM and 16% at > or =300 ppm in both RNM and liver. Lung NPSH fell linearly to 20% at 750 ppm. After repeated exposures over 3 and 20 days to 5, 25, 50, 300, and 500 ppm, NPSH losses were less pronounced. At both time points, NPSH were 90%, 70%, 50%, 30%, and 30% of the control values in RNM. Liver NPSH decreased to 80% and 50% at 300 and 500 ppm, respectively. After 20 days, lung NPSH declined to 70% (300 ppm) and 50% (500 ppm). We conclude that continuous, severe perturbation of GSH in RNM following repeated high PO exposures may lead to inflammatory lesions and cell proliferation, critical steps on the path towards tumorigenicity.     

中正丹治疗肝胆气滞型胆囊功能性障碍68例临床观察

目的:观察中正丹治疗肝胆气滞型胆囊功能性障碍的疗效.方法:将131例患者随机分为两组,治疗组68例,用中正丹治疗,对照组63例,用西沙必利治疗,比较两组疗效.结果:两组总体疗效相当,治疗组在缓解疼痛、协调胆囊动力方面与对照组比较差异无显著性(P＞0.05),但在改善全身症状方面明显优于对照组(P＜0.05).治疗组未见副作用,对照组出现头晕、嗜睡、腹泻等副作用.结论:中正丹治疗肝胆气滞型胆囊功能性障碍疗效肯定,且副作用较西沙必利少,值得推广应用.     

中药穴位透入配合肝病治疗仪治疗脂肪肝的临床研究

目的:观察中药穴位透入配合肝病治疗仪治疗脂肪肝的临床疗效观察.方法:将82例随机分为两组,对照组34例,采用常规治疗;治疗组48例,在常规治疗基础上给予中药穴位透入配合肝病治疗仪进行治疗.结果:临床总显效率治疗组与对照组分别为52.08%和26.47%,总有效率分别为91.67%和64.70%,治疗组的总显效率和总有效率均明显优于对照组(P＜0.01或P＜0.05).两组治疗后的临床症状及血清AST、ALT、TC和TG浓度与治疗前比较,均有显著性改善或降低(P＜0.01),但治疗组治疗后与对照组治疗后比较,均有显著性差异(P＜0.01),治疗组治疗后B超检查正常肝脏增加率及中、重度脂肪肝减少率明显高于对照组治疗后,两组治疗后比较,均有显著性差异(P＜0.05).结论:中药穴位透入配合肝病治疗仪治疗脂肪肝可显著改善其主要临床症状和肝功能,降低血脂,明显优于常规治疗的疗效,有助于提高临床疗效.     

理气化痰祛瘀法对非酒精性脂肪肝大鼠血清FFA TNF-αIL-6的影响

目的:观察理气化痰祛瘀中药对高脂饮食诱导的脂肪肝大鼠血清游离脂肪酸(FFA)、肿瘤坏死因子α(TNF-α)、白细胞介素-6(IL-6)的影响,探讨其可能作用机理.方法:以高脂饮食喂养Wistar大鼠12周,建立大鼠非酒精性脂肪肝模型,以不同剂量的理气化痰祛瘀中药治疗8周,常规HE染色观察肝组织的病理改变,比色法检测血清FFA含量,放免法测定血清TNF-α、IL-6的含量.结果:模型组大鼠血清FFA、TNF-α、IL-6含量较正常组明显升高.理气化痰祛瘀法中药能明显改善肝细胞的脂肪变性情况(P＜0.05),显著降低血清中FFA、TNF-α、IL-6含量(P＜0.01,P＜0.05).结论:FFA、TNF-α、IL-6参与高脂饮食诱导的大鼠非酒精性脂肪肝的发生,理气化痰祛瘀法中药能显著降低大鼠血清FFA、TNF-α、IL-6水平,防止脂肪肝进一步发展.