川陈皮素对糖尿病肾病大鼠AMPK和eNOS表达的影响研究

【摘要】目的 观察川陈皮素对糖尿病肾病大鼠的治疗作用，并从腺苷酸蛋白活化激酶（AMPK）和内皮型一氧化氮酶（eNOS）途径探讨其作用机理。方法 采用高脂高糖饲料喂养+链脲佐菌素（STZ）腹腔注射复制2型糖尿病肾脏损害大鼠模型，模型构建成功后，将其随机分为正常组、模型组、贝那普利干预组以及川陈皮素低、中和高剂量治疗组（n=20）。实验中密切监测大鼠一般情况，治疗期结束后收集尿液检测24h蛋白尿，收集血液检测肾功能指标、抗氧化指标，收集肾脏观察肾脏病理学，同时检测肾脏组织中AMPK及eNOS蛋白和mRNA的表达结果。结果 正常组肾小球正常，无明显病理特征；模型组出现肾小球增大，系膜和肾间质纤维组织增生；贝那普利组和川陈皮素三个剂量组相较于模型组明显减轻。与正常组相比，模型组24h尿蛋白定量、UREA、CREA和MDA明显升高(P＜005)；SOD和GSH明显降低(P＜005)，与模型组相比，贝那普利和川陈皮素三个剂量组24h尿蛋白定量、UREA、CREA和MDA明显降低(P＜005)，SOD和GSH明显升高(P＜005)。与正常组相比，模型组p AMPK、AMPK和eNOS蛋白和mRNA表达均明显降低(P＜005)；与模型组相比，贝那普利组和川陈皮素低、中和高剂量组AMPK和eNOS蛋白和mRNA表达明显升高(P＜005)。结论 川陈皮素可保护肾功能，提高血清和肾脏抗氧化指标，同时增加AMPK和eNOS蛋白和mRNA表达，最终保护糖尿病肾脏损害。     

良性前列腺增生与前列腺慢性炎症的相关性研究进展

良性前列腺增生（BPH）是老年男性常见的泌尿系统疾病，其发病与前列腺慢性炎症之间存在显著相关。感染因子、尿液返流、代谢综合征、衰老过程和自身免疫应答在内的几种刺激，通过相应分子途径引起前列腺免疫细胞的组织定位和组成成分发生广泛改变，从而导致免疫系统失调，之后引发的组织损伤和缓慢愈合，导致了BPH发生和进展。本文通过总结良性前列腺增生与前列腺慢性炎症的相关性的临床研究结果，前列腺免疫细胞在病理生理机制层面与前两者之间的内在联系，以及抗炎药物对BPH-LUTS的干预作用，以其为BPH-LUTS的药物研发提供参考。     

A KRT1 gene mutation related to epidermolytic ichthyosis in a Chinese family

We report a Chinese family with members affected by epidermolytic ichthyosis (EI), caused by KRT gene mutations. The proband was a 14‐year‐old boy who had simultaneous appearance of nephroblastoma and epidermolytic ichthyosis (EI). Both the patient and his mother exhibited the specific clinical and pathological manifestations of EI. We analysed all exons and flanking sequences of the KRT1 and KRT10 genes using PCR, and found that the proband and his mother had a G>C transition at nucleotide position 1432 in exon 7 of KRT1, resulting in an amino acid substitution of glutamate (GAA) to glutamine (CAA) at codon 478 (E478Q). The KRT10 gene had no mutations.     

奥扎格雷联合低分子肝素钙治疗脑血栓的临床研究

目的：对应用低分子肝素钙与奥扎格雷联合对患有脑血栓疾病的患者实施治疗的临床效果进行研究。方法整群选择在该院2012年12月—2014年12月就诊的患有脑血栓疾病的患者86例，随机分为对照组和治疗组，每组43例。采用奥扎格雷对对照组患者实施治疗；采用低分子肝素钙与奥扎格雷联合对治疗组患者实施治疗。对比神经功能缺损评分在药物治疗前后的变化幅度、脑神经功能恢复正常时间和脑血栓药物治疗计划实施总时间、脑血栓疾病药物治疗效果、用药期间的不良反应人数。结果治疗组患者神经功能缺损评分在药物治疗前后的变化幅度明显大于对照组；脑神经功能恢复正常时间（9.66±2.41）d和脑血栓药物治疗计划实施总时间（13.28±2.14）d明显短于对照组（13.62±3.47）、（17.39±3.20）d；脑血栓疾病药物治疗效果（总有效率90.6%）明显优于对照组（总有效率69.8%）；用药期间的不良反应人数（1例）明显少于对照组（8例）。结论应用低分子肝素钙与奥扎格雷联合对患有脑血栓疾病的患者实施治疗的临床效果非常明显。     

Specific alterations in plasma proteins during depressed,manic, and euthymic states of bipolar disorder

Bipolar disorder (BD) is a common psychiatric mood disorder affecting more than 1-2% of the general population of different European countries. Unfortunately, there is no objective laboratory-based test to aid BD diagnosis or monitor its progression, and little is known about the molecular basis of BD. Here, we performed a comparative proteomic study to identify differentially expressed plasma proteins in various BD mood states (depressed BD, manic BD, and euthymic BD) relative to healthy controls. A total of 10 euthymic BD, 20 depressed BD, 15 manic BD, and 20 demographically matched healthy control subjects were recruited. Seven high-abundance proteins were immunodepleted in plasma samples from the 4 experimental groups, which were then subjected to proteome-wide expression profiling by two-dimensional electrophoresis and matrix-assisted laser desorption/ionization-time-of-flight/time-of-flight tandem mass spectrometry. Proteomic results were validated by immunoblotting and bioinformatically analyzed using MetaCore. From a total of 32 proteins identified with 1.5-fold changes in expression compared with healthy controls, 16 proteins were perturbed in BD independent of mood state, while 16 proteins were specifically associated with particular BD mood states. Two mood-independent differential proteins, apolipoprotein (Apo) A1 and Apo L1, suggest that BD pathophysiology may be associated with early perturbations in lipid metabolism. Moreover, down-regulation of one mood-dependent protein, carbonic anhydrase 1 (CA-1), suggests it may be involved in the pathophysiology of depressive episodes in BD. Thus, BD pathophysiology may be associated with early perturbations in lipid metabolism that are independent of mood state, while CA-1 may be involved in the pathophysiology of depressive episodes.