中药灌肠联合尤卓尔治疗婴儿湿疹60例

目的：观察中药灌肠联合尤卓尔治疗婴儿湿疹的疗效、复发情况和不良反应,推广治疗婴儿湿疹的中药给药新途径。方法治疗组采用中药灌肠（2ml/kɡ,qd）联合尤卓尔（外用,日二次）;对照组单独采用尤卓尔（外用,日二次）治疗。结果与对照组比较,治疗组（中药灌肠联合尤卓尔）治疗婴儿湿疹疗效好（P ＜0.05）、复发率低（P＜0.05）,且无明显不良反应（P〉0.05）。结论中药灌肠联合尤卓尔治疗婴儿湿疹安全、高效、不易复发,适于临床推广。     

经动脉药盒化疗治疗转移性黑色素瘤病人的护理

[目的]总结经动脉药盒化疗治疗转移性黑色素瘤病人的护理。[方法]对10例转移性黑色素瘤病人行动脉药盒植入术,利用动脉药盒进行化疗,并做好治疗前、中、后的护理。[结果]10例病人中1例出现化疗药物外渗终止治疗,其余均能按计划完成治疗。[结论]掌握动脉药盒植入后的护理操作方法是行动脉灌注化疗的关键,有利于治疗的顺利进行。     

葡萄糖对丁酸钠诱导的结肠癌细胞增殖抑制和凋亡效应的调节作用及其可能机制

目的:探讨葡萄糖对丁酸钠诱导的结肠癌细胞增殖抑制和凋亡效应的影响,并探讨其可能机制。方法:用MTT法检测细胞存活率。细胞凋亡用TUNEL法检测。用RT-PCR法检测葡萄糖转运蛋白1(GLUT1)、单羧酸载体1(MCT1)的mRNA表达水平。结果:低浓度葡萄糖诱导HT-29细胞系凋亡、调节其增殖,且葡萄糖能够明显抵制丁酸钠诱导凋亡和增殖抑制作用,同时对GLUT1 mRNA、MCT1 mRNA也有一定抑制作用。结论:葡萄糖浓度变化能够明显影响丁酸钠的诱导凋亡和增殖抑制作用,这种影响可能与细胞内葡萄糖和丁酸钠的浓度有关。     

Remodeling gut microbiota by Clostridium butyricum (C.butyricum) attenuates intestinal injury in burned mice

BackgroundThe dysbiosis of gastrointestinal microbiome is an important reason for burn-induced intestinal injury. Clostridium butyricum (C.butyricum) and its production butyrate are beneficial for the homeostasis of intestinal microflora and suppression of inflammatory response.PurposeThe roles of C.butyricum and butyrate in burn-induced intestinal injury were explored. The effects of oral administration of C.butyricum on intestinal injury were observed in burned mice.Materials and methodsThe skin surface of mice was exposed to 95 °C water to induce a burn injury. Then the intestinal microbiome structure, abundance of C.butyricum and level of butyrate were respectively observed. The correction between intestinal permeability indicated by FITC dextran level and abundance of C.butyricum or level of butyrate was analyzed. C.butyricum was cultured and orally administrated to burned mice. The levels of butyrate, FITC dextran and pro-inflammatory cytokines, including interleukin 6 (IL-6) and tumor necrosis factor α (TNF-α) were respectively measured.ResultsBurn injury altered the intestinal microbiome structure of mice, and especially decreased the abundance of C.butyricum and level of butyrate. Both the abundance of C.butyricum and the level of butyrate were negatively correlated with the intestinal permeability. Oral administration of C.butyricum increased the level of butyrate, decreased levels of TNF-α and IL-6, and suppressed intestinal damage in burn-injured mice.ConclusionOral administration of C.butyricum significantly alleviated the intestinal damage induced by burn injury. The therapeutic effects of C.butyricum and butyrate on burn injury should be further explored, which deserves further investigation.     

Is butyrate the link between diet,intestinal microbiota and obesity‐related metabolic diseases?

It is increasingly recognized that there is a connection between diet, intestinal microbiota, intestinal barrier function and the low‐grade inflammation that characterizes the progression from obesity to metabolic disturbances, making dietary strategies to modulate the intestinal environment relevant. In this context, the ability of some Gram‐positive anaerobic bacteria to produce the short‐chain fatty acid butyrate is interesting. A lower abundance of butyrate‐producing bacteria has been associated with metabolic risk in humans, and recent studies suggest that butyrate might have an anti‐inflammatory potential that can alleviate obesity‐related metabolic complications, possibly due to its ability to enhance the intestinal barrier function. Here, we review and discuss the potential of butyrate as an anti‐inflammatory mediator in metabolic diseases, and the potential for dietary interventions increasing the intestinal availability of butyrate.     

Butyrate reduces the frequency of micronuclei in human colon carcinoma cells in vitro

Butyrate, formed by bacterial fermentation of plant foods, has been shown to protect human colon cells from selected genotoxic substances. The mechanism for this effect could be the enhancement of toxicological defence leading to an increased detoxification of genotoxic risk factors and thus to a reduction of DNA and chromosome damage. Previous protective properties of butyrate against DNA damage induction in colon cells were demonstrated using the comet assay. In the present study the effect of butyrate on chromosome damage induced by ferric nitrilotriacetate (Fe-NTA) and hydrogen peroxide (H₂O₂) (suggested to be putative risk factors of colorectal carcinogenesis) was investigated using the cytokinesis-block micronucleus (CBMN) test. It was possible to reveal that pre-treatment of HT29 colon carcinoma cells with butyrate (2 and 4 mM) for 15 min caused a reduction of micronuclei induced with H₂O₂ (75 μM; p < 0.01) and Fe-NTA (500 and 1000 μM; p < 0.05). The decrease in the level of Fe-NTA- and H₂O₂-induced micronuclei was also confirmed in most of the corresponding variants of 24 h pre-treatment of cells with butyrate. The results obtained demonstrate for the first time protective properties of butyrate against chromosome damage induced by H₂O₂ and Fe-NTA in human colon carcinoma cells.