[Research advances on the role and mechanism of microRNA in hypertrophic scar].

Hypertrophic scar (HS) affects the function and beauty of patients, and brings a heavy psychological burden to patients. However, the specific pathogenesis mechanism of HS in molecular biology level is not yet clear, and this disease is still one of the clinical diseases difficult to prevent and cure. MicroRNA (miR) is a family of single-stranded endogenous noncoding RNAs that can regulate gene expression. The abnormal transcription of miR in hypertrophic scar fibroblasts can affect the transduction and expression of downstream signal pathway or protein, and the exploration of miR and its downstream signal pathway and protein helps deeply understand the occurrence and development mechanism of scar hyperplasia. This article summarized and analyzed how miR and multiple signal pathways involve in the formation and development of HS in recent years, and further outlined the interaction between miR and target genes in HS.

Effect of hematoporphyrin monomethyl ether-mediated PDT on the mitochondria of canine breast cancer cells.

Hematoporphyrin monomethyl ether (HMME) is a promising porphyrin-related photosensitize for photodynamic therapy (PDT). There still remains unknown changes regarding the mitochondrial in canine breast cancer cells treated with HMME-PDT. The aim of this study is to investigate the effect of HMME-PDT on structure and dysfunction of mitochondrial in cancer cells. The experimental approach included an initial study on the uptake of HMME using microscopic observation of the HMME-treated cells, optimization of the PDT-induced cell death by the MTT assay. These cells were then treated with HMME and a He-Ne laser at the wavelength of 632.8 nm following our optimized condition. Examination of mitochondrial changes by observing the stained cells under light microscope, mitochjondrial membrane potential flow cytometry, measuring the Ca(2+), SOD/GSH activity, ATPase and MDA contents for the mitochondria functions. The kinetics of HMME uptake in CHMm cells was determined and its cytocolic instead of nuclear distribution was demonstrated. The dose of 16mM HMME-PDT combined with 2.8 J/cm(2) laser irradiation was had the maximal impact on cell viability. This treatment resulted in structural changes in mitochondria that were accompanied with the loss of mitochjondrial membrane potential. As a result, HMME-PDT increased mitochondrial ROS, inhibited the enzymatic activities of mitochondrial SOD and GSH-Px, abolished mitochondrial ability in the uptake and release of calcium, and decreased mitochondrial ATPase activity. The combination of these abnormalities led to accumulation of ROS in mitochondrial to high levels, which in turn contributed to HMME-PDT-induced damages of mitochondrial structure and mitochondrial dysfunction.

[Determination of captopril in plasma and urine by high-performance liquid chromatography with column switching].

A rapid and sensitive column-switching high performance liquid chromatographic procedures was described for determination of captopril in plasma and urine. p-Bromophenacyl bromide, a derivatizing reagent, was added to the plasma and urine samples to form an adduct which showed ultraviolet absorbing properties. After that, the urine sample was injected directly and for plasma the protein was removed with 6% of perchloride before injection. The column-switching system was equipped with a pre-column of 5 cm x 0.5 cm ID, packed with mu Boundapak C18, 37-50 microns, and an analytical column of 15 cm x 0.5 cm ID, packed with YWG-C18, 10 microns. After washing out the impures from pre-column with 0.2% acetic acid the retained substances were eluted into analytical column with acetonitrile-water-acetic acid (35:65:0.4). Captopril was detected at 260 nm. The method was linear within 20-1000 ng/ml for plasma and 10-200 micrograms/ml for urine. The recovery averaged 103.2% and 99.5% for plasma and urine, respectively. The coefficient variations were all less than 10%.