溃疡性结肠炎大鼠肠黏膜PPAR γ的表达

目的 :观察溃疡性结肠炎 (ulcerativecolitis,UC)大鼠肠黏膜中过氧化物酶体增殖物激活受体γ(PPARγ)的表达。方法 :采用免疫组化法检测了10只UC大鼠 (UC组 )和10只正常对照组大鼠结肠黏膜中PPARγ的表达情况。结果 :UC组和对照组大鼠结肠上皮PPARγ阳性细胞分别为 (11.7±3.46)个和 (81.8±15.73)个 ,UC大鼠结肠上皮PPARγ的表达明显低于对照组(P<0.001)。结论 :UC大鼠结肠黏膜上皮PPARγ的表达明显下降 ,其可能与UC的发病有关     

Pharmacological effects of Chinese herb aconite (Fuzi) on cardiovascular system

Fuzi (aconite, Radix Aconiti praeparata), a widely used Chinese herb, plays a significant role in the cardiovascular system. This is mainly reflected by Fuzi's cardiotonic effect, its protective effect on myocardial cells, and its effect on heart rate and rhythm, blood pressure, and hemodynamics. In this article, the pharmacological effects and the corresponding mechanisms of Fuzi (aconite) and its active components on cardiovascular system are reviewed.     

切除修复交叉互补基因1调控卵巢癌耐药株A2780/顺铂迁移及侵袭的作用

目的探讨切除修复交叉互补基因1(ERCC1)调节卵巢癌耐药株A2780/顺铂(DDP)细胞迁移及侵袭能力的作用及其机制。方法根据细胞对顺铂的耐药性,分为普通组A2780、顺铂耐药组A2780/DDP。细胞计数试剂盒(CCK-8)检测A2780、A2780/DDP细胞活性及顺铂耐药性。Transwell细胞迁移、侵袭实验检测A2780、A2780/DDP细胞的迁移和侵袭能力。蛋白质印迹法(Western blot)检测A2780、A2780/DDP细胞中ERCC1、上皮表型E-钙黏蛋白(E-cadherin)及间质表型波形蛋白(Vimentin)的表达。小干扰RNA(siRNA)-ERCC1转染A2780/DDP中ERCC1表达后,Transwell细胞迁移、侵袭实验检测细胞迁移和侵袭能力的改变,Western blot检测细胞中ERCC1、E-cadherin及Vimentin表达的改变。两组间比较采用Student’s-t检验。结果A2780/DDP的半抑制浓度(IC50)值为17.66 mg/L,A2780的IC50值为2.236 mg/L,A2780/DDP较A2780的IC50提高了7.898倍。A2780/DDP细胞的迁移和侵袭能力明显高于非耐药株,且A2780/DDP中ERCC1和间质表型Vimentin的表达明显高于非耐药株A2780,而上皮表型E-cadhetin表达明显低于A2780。干扰A2780/DDP中ERCC1表达后,细胞的迁移和侵袭能力明显低于对照组,且细胞中ERCC1和间质表型Vimentin的表达低于对照组,而上皮表型E-cadhetin表达高于对照组。结果差异均有统计学意义。结论A2780/DDP中高表达的ERCC1通过促进细胞发生上皮-间充质转化增强细胞的迁移及侵袭的能力。     

反复感染手足口病患儿的预防和治疗

目的探讨消毒隔离结合免疫及营养治疗在预防和治疗反复感染手足口病患儿中的作用。 方法收集初次就诊的手足口病患儿共400例，利用随机数字表将患者分为治疗组与对照组各200例，治疗组患儿定期给予消毒隔离健康教育及营养随访，再次患病后给予个体化营养支持治疗。对照组患儿仅在感染手足口病后给予常规治疗。比较两组患儿手足口病再发率和重症率等指标。 结果治疗组患儿平均退热时间为（1.7 ± 1.1）d、皮疹消退时间为（4.0 ± 1.3）d、平均住院天数为（5.6 ± 2.4）d、抗菌药物使用率为19%（38/200）、激素使用率为8%（16/200），均显著低于对照组，差异具有统计学意义（t = 10.028、8.677、8.353、20.650、11.312，P = 0.015、0.032、0.001、0.004、0.011）。治疗组患儿1年内再发率、重症率和并发症发生率分别为12%（24/200）、1%（2/200）和5%（10/200），显著低于对照组患儿，差异均有统计学意义（χ² = 9.21、0.88、7.24，P = 0.010、0.002、0.007）。 结论健康教育、营养随访及个体化营养支持治疗可降低手足口病的再发率及重症率，改善临床结局。     

Impact of extracted urinary proteins and advanced glycation end product on autophagy pathway in renal tubular epithelial cells

Objective To investigate the effect of urinary proteins extracted from minimal change nephritic syndrome (MCNS) and advanced glycation end products (AGEs) on autophagy activity in renal tubular epithelial cells (TECs). Methods Kidney tissue specimens of patients with MCNS and DN were obtained from the kidney pathology library of the Affiliated Hospital of Guangdong Medical College. The kidney tissue from patients with hematuria and proven to be minimal change by pathology examination were used as control. The expression of LC3-Ⅱ in kidney was examined by immune histochemistry in vivo. Expression of LC3-Ⅱ was also studied after exposing HK-2 cells to 8 g/L urinary proteins and 100 mg/L AGE-BSA respectively. LC3-Ⅱ turnover was examined after exposure to urinary proteins in presence of Lysosomal inhibitors leupeptin (200 mg/L) or chloroquine(10μmol/L) by western blot assay. In addition, the autophagosome or autolysosome formation was assessed after transfecting a tandem mRFP-GFP tagged LC3 (tfLC3) plasmid into HK-2 cells. Finally, the production of neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1) were measured by ELISA after exposure of cells to autophagy enhancer rapamycin (10 μmol/L) and autophagy inhibitor chloroquine (10 μmol/L) in addition to urinary proteins. Results (1)In comparison with the control group, the expression of LC3-Ⅱ was significantly increased in TECs from patients with MCNS and DN(P＜0.01). (2)The expression of LC3-Ⅱwas enlarged after exposed to urinary proteins(P＜0.01), and further increased after leupeptin (autophagy inhibitor) addition. (3) Exposure to urinary proteins increased the autophogosomes and autolysosomes when observed by transfection of tfLC3 plasmid(P＜0.01). (4)The expression of LC3-Ⅱ was also elevated after treatment with AGE-BSA(P＜0.01), but no further increase after chloroquine (autophagy inhibitor) addition. (5) Only the autophogosome formation(P＜0.01), but not autolysosome formation, was found increased by transfection of tfLC3 plasmid after exposure to AGE-BSA. (6) Pre-treatment of HK-2 cells with autophagy enhancer rapamycin reduced the productions of neutrophil gelatinase-associated lipocalin (NGAL) and kidney injury molecule-1 (KIM-1), while blocking autophagy with autophagy inhibitor chloroquine exerted an opposite effect. Conclusions Autophagy was activated by urinary proteins, but inactivated by AGE-BSA. Autophagy activation may play a key role in protecting TECs in the progression of primary and secondary kidney diseases.     

Autophagy-related proteins LC3 and Beclin-1 impact the efficacy of chemoradiation on esophageal squamous cell carcinoma

Autophagy is a bulk protein and organelle degradation process essential for cellular maintenance, cell viability and development. This study investigated the prognostic role of LC3 and Beclin-1, two autophagy-related proteins, in patients with locally advanced esophageal squamous cell carcinoma (ESCC) treated with definitive chemoradiation.     

Correction to: Search of anti-allodynic compounds from Plantaginis Semen,a crude drug ingredient of Kampo formula “Goshajinkigan”

Journal of Natural Medicines - The article Search of anti-allodynic compounds from Plantaginis Semen, a crude drug ingredient of Kampo formula “Goshajinkigan”.     

参芪柴芍枳附汤辅治代谢性心脑血管疾病疗效观察

目的:观察参芪柴芍枳附汤辅治心脑血管疾病的疗效。方法:150例分为4个治疗组及1个对照组各30例,4个治疗组分别为糖尿病(消渴)+冠心病(胸痹)、糖尿病(消渴)+椎基底动脉供血不足(眩晕)、糖尿病(消渴)+脑梗死(中风)、糖尿病(消渴)+抑郁症(郁证),对照组为糖尿病(消渴)。对照组根据指南予以常规西医治疗。治疗组在常规西医治疗基础上加用参芪柴芍枳附汤口服,疗程15天。结果:各治疗组空腹血糖控制、中医临床症状及西医疗效均优于对照组(P<0.05)。结论:参芪柴芍枳附汤能改善心脑血管疾病临床症状。