Background
The efficacy of pulsed dye laser combined (PDL) and UltraPulse fractional CO2 in treatment of hypertrophic scars is well documented. The present study investigates the efficacy of moist exposed burn ointment (MEBO)/moist exposed burn therapy (MEBT) in postlaser wound management.
Methods
Sixty‐one patients with immature, red hypertrophic scars were enrolled in this clinical trial. Patients were randomly divided into two groups: (a) the MEBO treatment group (n = 30) and (b) the control group (n = 31) treated with chlortetracycline hydrochloride ointment. Demographic data such as age, gender, and cause of scars were recorded. A visual analogue score (VAS) was collected to measure pain at 1, 6, 24, 72 hours, and 7 days post‐treatment. The Vancouver Scar Scale (VSS) was used to determine the response of the scars before and 3 months after the treatment. The wound healing time and pigmentation scores were also recorded.
Results
No significant differences were found in age, gender, and etiology of the scars in the two groups. The VAS scores in MEBO group were significantly lower than the control group within the first 3 days after treatment. The wound healing time of the MEBO group was significantly shorter than the control group. For both groups, VSS scores were significantly decreased and the scar markedly improved. However, the VSS scores were significantly lower in the MEBO group compared with the control group 3 months after treatment and pigmentation formation was dramatically lower in MEBO group compared with the control.
Conclusion
MEBT/MEBO treatment reduced the post‐treatment pain, shortened the wound healing duration, promoted the overall scar condition, and reduced the incidence of pigmentation.
Aspongopus chinensis Dallas is used as a traditional Chinese medicine. In China, clinical evidence suggests that it has anticancer activity. However, the anticancer active components are not fully elucidated. In the present study, we purified an anticancer active component (named CHP) from A. chinensis. To gain a comprehensive insight into the protein components, shotgun proteomic analysis was conducted. The anticancer active protein band was cut from the sodium dodecyl sulphate-polyacrylamide gel electrophoresis gel and digested with trypsin to generate peptide mixture. The peptide fragments were then analysed by liquid chromatography tandem mass spectrometry; 18 proteins were identified. In addition, we evaluated the effects of CHP on the proliferation and apoptosis of two human gastric cancer cell lines (SGC-7901 and BGC-823). The cultured cells were treated with CHP at concentrations of 20, 30, and 40 μg/mL. Inhibition of cell growth was determined by the MTT assay. Hoechst 33258 staining was adopted to detect apoptosis morphologically. Apoptotic cells were quantified by Annexin V-FITC/propidium iodide staining and flow cytometry. Tumour growth was assessed by subcutaneous inoculation of 4T1 cells into BALB/c mice. There was a concentration- and time-dependent decrease in the proliferation of both cell lines at CHP concentrations of 20–40 μg/mL. Apoptotic characteristics, such as karyopyknotic pyknic hyperfluorescence bolus and nuclear fragmentation, were observed in both the cell lines by Hoechst 33258 staining. Flow cytometry showed that CHP induced significant (P < 0.01) concentration-dependent apoptosis of SGC-7901 cells. In vivo assay showed that CHP can partially inhibit tumour growth derived from 4T1 cells in vivo. The present study is the first to report that CHP in A. chinensis inhibits the proliferation of cancer cell lines via the suppression of cancer cell proliferation and acceleration of apoptosis.
The insecticide acetamiprid is used to control noxious agricultural pests. However, it can cause mammalian toxicity. We evaluated the reproductive toxicity of acetamiprid in adult male Sprague Dawley rats. Rats were given oral acetamiprid alone or with vitamin E for 35 days. Rat plasma testosterone concentration and sperm quality decreased significantly as the levels of luteinizing hormone (LH) increased after exposure. At the same time, acetamiprid increased malondialdehyde and nitric oxide (NO) levels of Leydig cells. Further analysis showed that acetamiprid reduced the adenosine triphosphate (ATP) and cyclic adenosine monophosphate (cAMP) production of Leydig cells, but the expression of luteinizing hormone/choriogonadotropin receptor (LHCGR) and the activity of adenylyl cyclase were not changed. Acetamiprid exposure also significantly diminished protein levels of steroidogenic acute regulatory protein (STAR), hydroxy-delta-5-steroid dehydrogenase, 3 beta- and steroid delta-isomerase cluster (HSD3B), and cytochrome P450, family 11, subfamily a, polypeptide 1 (CYP11A1), and testicular mRNA levels, which are cAMP-dependent proteins that are essential for steroidogenesis. Electron microscopy indicated mitochondrial membrane damage in the Leydig cells of the testes of exposed rats. Vitamin E ameliorated the impairment of acetamiprid on Leydig cells. Our results indicate that acetamiprid causes oxidative stress and mitochondrial damage in Leydig cells and inhibits the synthesis of testicular ATP and cAMP. Acetamiprid disrupts subsequent testosterone biosynthesis by decreasing the rate of conversion of cholesterol to testosterone and by preventing cholesterol from entering the mitochondria within the Leydig cells. These effects caused reproductive damage to the rats.
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