MiR-20a inhibits cutaneous squamous cell carcinoma metastasis and proliferation by directly targeting LIMK1

Background MicroRNA-20a (miR-20a) plays a key role in tumorigenesis and progression. But its function is reverse in different kinds of malignant tumor, and its role and mechanism in cutaneous squamous cell carcinoma (CSCC) remains unclear. Object To determine the miR-20a’s roles in CSCC and confirm whether LIMK1 is a direct target gene of miR-20a. Methods First miR-20a and LIMK1 expression levels were detected in six pairs of CSCC tissues and corresponding normal skin by qRT-PCR. Then MTT assays and colony formation assays were performed to evaluate the impact of miR-20a on cell proliferation. In addition, scratch migration assays and transwell invasion assays were performed to check miR-20a’s effect on cell metastasis. Since LIMK1 (LIM kinase-1) was predicted as a target gene of miR-20a, the changes of LIMK1 protein and mRNA were measured by western blot and qRT-RCR methods after miR-20a overexpression. Moreover the dual reporter gene assay was performed to confirm whether LIMK1 is a direct target gene of miR-20a. Finally LIMK1 mRNA and miR-20a in other 30 cases of CSCC pathological specimens were determined and a correlation analysis was evaluated. Results The miR-20a significantly low-expressed in CSCC tissues compared with that in matched normal tissues while LIMK1 has a relative higher expression. MiR-20a inhibited A431 and SCL-1 proliferation and metastasis. Both of LIMK1 protein and mRNA levels were downregulated after miR-20a overexpression. The dual reporter gene assays revealed that LIMK1 is a direct target gene of miR-20a. Furthermore, qRT-PCR results of LIMK1 mRNA and miR-20a in 30 cases of CSCC pathological specimens showed miR-20a is inversely correlated with LIMK1 expression. Conclusion Our study demonstrated that miR-20a is involved in the tumor inhibition of CSCC by directly targeting LIMK1 gene. This finding provides potential novel strategies for therapeutic interventions of CSCC.     

针灸治疗子宫脱垂疗效观察

目的观察针灸治疗Ⅰ度子宫脱垂的临床疗效。方法将60例Ⅰ度子宫脱垂患者随机分为治疗组和对照组,每组30例,对照组采用支持疗法和盆底肌肉锻炼,治疗组在对照组的基础上施以维道透刺关元、提托透刺子宫断续波电针配合温和灸百会治疗。治疗3个月后比较两组临床疗效及治疗前后PFDI-20短表评分。结果治疗组总有效率为90.0%,对照组为40.0%,两组比较差异具有统计学意义(P0.01)。治疗组治疗后PFDI-20短表各项评分与同组治疗前比较,差异均具有统计学意义(P0.05)。对照组治疗后PFDI-20、POPDI-6和CARDI-8与同组治疗前比较,差异均具有统计学意义(P0.05)。治疗组治疗后PFDI-20短表各项评分与对照组比较,差异均具有统计学意义(P0.01,P0.05)。结论透刺电针配合灸百会是一种治疗子宫脱垂的有效方法。     

电针早期干预对预防创伤后应激障碍临床观察

目的观察电针百会、大椎穴对经历重大创伤但尚未出现创伤后应激障碍(PTSD)的受试者的预防作用。方法 68例受试者随机分为电针组和西药组,共干预治疗2个月,在干预前后和干预后3个月、6个月采用埃森创伤问卷(ETI)、症状自评量表(SCL-90)等量表评定。结果干预前后和干预后3个月、6个月评分组内比较差异均有统计学意义(P0.05),总体上组间效应差异不显著(P0.05),但躯体化及抑郁两组因子电针组优于西药组(P0.05)。结论电针百会、大椎与药物干预对PTSD的预防作用相近,且电针组副反应小,依从性好。     

糖尿病视网膜病变23G和20G玻璃体手术

目的 对比观察23G和20G玻璃体手术治疗增生型糖尿病视网膜病变（PDR）的临床结果和并发症.方法 接受玻璃体切除手术治疗的PDR 52例（64只眼）纳入本回顾性对比研究.按其所接受的手术方式分为23G微创玻璃体切除手术组（23G组）和20G玻璃体切除手术组（20G组）,分别为32例（40只眼）和20例（24只眼）.手术后随访6个月,对比分析两组的最佳矫正视力,眼压及术中术后并发症情况.结果 两组术后1,3和6个月最佳矫正视力均比术前有显著提高（χ2=20.32,22.56,18.23,P＜0.01）.23G组术后第一天的眼压低于术前眼压（t=2.75,P＜0.01）.23G组的手术时间短于20G组（t=2.71,P=0.01）.除23G组有9只眼（22.5％）发生早期术后低眼压（与20G组比较,χ2 =4.56,P=0.03）,两组术中术后并发症情况无明显差异.结论 23G微创玻璃体切除手术治疗PDR的有效性与20G玻璃体切除手术基本相同,两者术中术后并发症情况差异无统计学意义.     

20-O-β-d-glucopyranosyl-20(S)-protopanaxadiol-fortified ginseng extract attenuates the development of atopic dermatitis-like symptoms in NC/Nga mice

Ethnopharmacological relevance

Ginseng and ginsenosides are frequently used in the treatment of chronic inflammatory diseases. Recently, 20-O-β-d-glucopyranosyl-20(S)-protopanaxadiol (GPD), the main metabolite of ginsenosides, was reported to have both anti-allergic and anti-pruritic effects. The immunomodulatory effects of GPD-fortified ginseng extract (GFGE) on atopic dermatitis (AD)-like symptoms in mice were investigated. This study was designed to investigate the preventive effect of GFGE on AD-like symptoms.

Materials and methods

The effects of orally administered GFGE on Dermatophagoides farinae body extract (DFE)-induced AD-like symptoms in NC/Nga mice were assessed by analyzing dermatitis score, ear thickness, scratching time, skin histological changes, and serum level of macrophage-derived chemokine (MDC). In addition, splenocytes were isolated from the mice and stimulated with anti-CD3 and anti-CD28 monoclonal antibodies to produce cytokines.

Results

Oral administration of GFGE significantly attenuated DFE-induced increases in dermatitis score, ear thickness, scratching time, and severity of skin lesions in NC/Nga mice. GFGE treatment also reduced level of MDC in serum, infiltration of eosinophils and mast cells in skin, and production of cytokines in splenocytes.

Conclusions

These results suggest that GFGE might ameliorate DFE-induced AD-like symptoms and be an alternative therapeutic agent for the prevention of AD.     

Anti-influenza virus activity of the ethanolic extract from Peperomia sui

Ethnopharmacological relevance

Peperomia sui Lin and Lu (Peperomia sui), a well-known Taiwanese folk medicine, has a broad range of biological effects, especially in treatment of upper respiratory tract diseases. However, no previous study has explored the activity of Peperomia sui against influenza virus infections. This study was carried out to evaluate the anti-influenza virus activity and the potential virucidal effect of the ethanolic extract of Peperomia sui (PSE).

Methods

The anti-H6N1 avian influenza viral activity of PSE against the influenza virus A/Chicken/TW/0518/2011 (H6N1) in chicken fibroblast DF-1 cells was evaluated by cell viability assay, hemagglutination assay, neuraminidase activity assay, indirect immunofluorescence assay and quantitative RT-PCR assay.

Results

PSE significantly increased the viability of cells that were infected by the H6N1 virus. PSE also suppressed the synthesis of viral nucleoprotein (NP), and inhibited the growth of the virus in DF-1 cells. Further, PSE inhibited the neuraminidase activity of H6N1 virus.

Conclusions

The findings of this study provide important information for the exploitation and utilization of Peperomia sui in treatment of influenza infection.     

雷公腾内酯与多柔比星诱导耐药白血病细胞凋亡协同作用及其机制的探讨

目的：以耐多柔比星（adriamycin,ADM）的人急性髓系白血病（acute myeloid leukemia,AML）耐药细胞株HL60/ADM为研究对象,探讨IC20浓度雷公腾内酯（triptolide,TPL）能否提高ADM诱导耐药白血病细胞凋亡及其与Nrf2通路的关系。方法：流式细胞仪检测空白对照组、IC20浓度TPL单药组、ADM单药组和TPL联合ADM组处理HL-60/ADM后细胞凋亡率;实时荧光定量PCR检测各个处理组作用后,Nrf2及其下游基因醌氧化还原酶（quinone oxidoreductase,NQO1）、谷胱甘肽还原酶（glutathione reductase,GSR）及血红素加氧酶1（heme oxygenase 1,HO-1）的表达水平变化;蛋白质印迹法检测各处理组作用后Nrf2蛋白表达变化。结果：TPL单药组细胞凋亡率为（5.28±0.80）%,与空白对照组的（7.09±0.46）%比较差异无统计学意义,P=0.226;但该浓度TPL可使ADM组细胞凋亡率由（19.55±1.70）%提高到（72.62±4.83）%,是ADM单药组的3.71倍,P〈0.001。空白对照组、TPL单药组、ADM单药组及双药联合组Nrf2mRNA表达水平分别为1、0.742±0.052、0.619±0.042和0.241±0.010,NQO1分别为1、0.363±0.075、0.228±0.053和0.050±0.034;GSR分别为1、0.268±0.042、0.231±0.106和0.038±0.017;HO-1分别为1、0.495±0.023、0.282±0.099和0.048±0.036;各用药组Nrf2及其下游基因NQO1、GSR及HO-1的mRNA表达水平较对照组均出现显著下调,P〈0.001;其中双药联合组下调程度最大。蛋白质印迹法结果显示,用药组及联合组Nrf2表达水平较对照组均有不同程度下调,其中联合组下调最为明显。结论：IC20浓度雷公腾内酯可显著提高ADM诱导耐药白血病细胞凋亡,其分子机制与下调Nrf2通路有关。     

20-羟-二十烷四烯酸在糖尿病心血管并发症中的作用

糖尿病是以高血糖为特征的代谢紊乱综合征,其心血管并发症是导致糖尿病患者致残、致死的主要原因.20-羟-二十烷四烯酸(20-hydroxyeicosatetraenoic acid,20-HETE)是近年来发现的花生四烯酸(Arachidonic acid,AA)第三条代谢通路,细胞色素P-450(Cytochrome P-450,CYP450)途径的活性代谢产物.现有研究表明其在调节肾功能和血管平滑肌紧张度中起到重要作用,但对20-HETE与糖尿病的关系研究甚少.本文对近年来国际上20-HETE与糖尿病心血管并发症的研究报道进行综述.     

Elevated CCR6+ CD4+ T lymphocytes in tissue compared with blood and induction of CCL20 during the asthmatic late response

CCR6 is expressed by multiple leucocyte subsets, including peripheral blood memory T cells, and mouse models implicate a role for this receptor in diverse inflammatory responses that include allergic airway disorders, inflammatory bowel disease and autoimmune encephalitis. In order to study the role of CCR6 in humans, we have investigated the patterns of CCR6 expression and function on T cells from the peripheral blood, skin, nose and lung, in health and in allergic disease. Results show that CCR6 was expressed consistently on a higher proportion of tissue versus peripheral blood-derived CD4+ T cells (P < 0.01). CCR6 was expressed predominantly on CD4+ compared with CD8+ cells in both blood- and tissue-derived T cells (P < 0.001). The number of cells showing CCR6 expression was not proportionally greater in peripheral blood or nasal mucosal T cells of subjects with symptomatic allergic rhinitis. CCR6+ cells demonstrated enhanced functional responses to CCL20 and CCL20 was increased in bronchoalveolar lavage fluid of asthmatics following endobronchial allergen provocation (P < 0.05). Thus, CCR6 may be important in the regulation of T cell recruitment to tissue and up-regulation of CCL20 expression may contribute to the recruitment and/or retention of effector T cells in allergic asthma.