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Objective: To explore the role of microRNA (miRNA, miR) -16 in the development of coronary atheromatous plaques and to study possible mechanism involved in the process. Methods: Coronary artery tissues were obtained from 16 patients undergoing coronary artery bypass grafting,and the coronary artery plaques were divided into fibrous plaques and atheromatous plaques based on pathological examination. The expression level of miR-16 in coronary fibrous plaques and atheromatous plaques was detected by miRNAs array. The in vitro model of oxidized low density lipoprotein (oxLDL)-induced foam cells from macrophages was established, the transformation as well as apoptosis of foam cells were detected by TUNEL assay, cell counting and Western blotting. The release of inflammatory cytokines [interleukin (IL)-6, IL-8, monocyte chemoattractant protein (MCP)-1 and matrix metalloproteinase (MMP)-9] in the culture supernatant of form cell was tested by enzyme-linked immunosorbent assay(ELISA), and expression of miR-16 was tested by miRNAs array. Finally, miR-16 was transfected into macrophages and the apoptosis of foam cell as well as the release of inflammatory factors were detected. Results: Compared with fibrous plaques of coronary artery, the expression of miR-16 in coronary atheromatous plaques detected by miRNAs assay increased by 1.75 folds. In vitro model of oxLDL-induced foam cells showed that oxLDL might promote the transfer of macrophages into foam cells and induce foam cells apoptosis and stimulate the release of inflammatory factors (such as IL-6, IL-8, MCP-1 and MMP-9). Macrophages transfected with miR-16 could further induce the apoptosis of foam cells and secretion of inflammatory factors. Conclusions: oxLDL could induce the apoptosis of foam cells, release of inflammatory factors and up-regulate miR-16 expression, and the high expression of miR-16 could further enhance foam cell apoptosis and inflammatory response, further promote the progression of atherosclerosis. miR-16 might serve as a potential target for inhibiting artherosclerosis.

Four typical pretreatment methods of dilute acid, hydrothermal treatment, ionic liquid and steam blasting were used to treat licorice residue. The effects of different pretreatment methods on sugar production and structure of licorice residue were compared by high performance liquid chromatography, scanning electron microscope, fourier transform infrared spectrometer and X-ray diffraction analysis. The results showed that ionic liquid pretreatment had obvious effect on cellulose in licorice residue, and the contents of glucose, xylose and xylodisaccharide in the enzymatic hydrolysate were the highest, and the enzymolysis rate reached 77. 08% ± 2. 12%, which was 2. 05 times than that of untreated enzymatic hydrolysis rate. Hydrothermal pretreatment had obvious effects on hemicellulose licorice residue, and the contents of xylose, arabinose and xylodisaccharide in the pretreatment solution were the highest. The enzymatic hydrolysis efficiency of hemicellulum was the highest, reaching 82. 37% ± 1. 13%, which was 8. 90 times than that of untreated enzymolysis. Steam blasting pretreatment had obvious effect on licorice residue lignin, and the glucose yield in the pretreatment solution was the highest. The structural analysis results were consistent with the component analysis results. Compared with other pretreatment, the lignocellulose structure of licorice residue was effectively broken in the ionic liquid pretreatment process, which was more conducive to the further high-value utilization of licorice residue. [ABSTRACT FROM AUTHOR]

Objective: To investigate the effect of spearmint oil on emphysema-like changes and the expression of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta(IL-1beta), matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-9) in lipopolysaccharide (LPS) treated rats., Method: Emphysematous changes model was induced by intratracheal instillation of LPS once a week for up to 8 weeks in rats. Rats were divided into control, dexamethasone (0.3 mg x kg(-1)), and spearmint oil (10, 30,100 mg x kg(-1)) groups. Each group was treated with saline, dexamethasone, and spearmint of oil respectively for 4 weeks. Then total and different white blood cell counts in bronchoalveolar lavage fluid(BALF) were carried out. The pathologic changes of lung tissue such as alveolar structure, airway inflammation, and goblet cell metaplasia were observed by HE and AB-PAS staining. Expression of TNF-alpha, IL-1beta, TIMP-1 and MMP-9 were measured., Result: Both spearmint and dexamethasone decreased the destruction of pulmonary alveolus. The total and different white blood cell counts in BALF including neutrophile and lymphocyte of spearmint oil 100 mg x kg(-1) and dexamethasone group were significantly reduced, and the goblet cell metaplasia was also inhibited. Dexamethasone had inhibitory effect on the expression of TNF-alpha, IL-1beta, TIMP-1 and MMP-9. Spearmint oil 30, 100 mg x kg(-1) significantly reduced TNF-alpha and IL-1beta respectively. Spearmint oil 10, 30 and 100 mg x kg(-1) had no effect on the expression of TIMP-1, but could decrease the expression of MMP-9 significantly in lung tissues., Conclusion: Spearmint oil has protective effect on rats with emphysematous changes, since it improves alveolar destruction, pulmonary inflammation, and goblet cell metaplasia. The mechanism may include reducing TNF-alpha, IL-1beta content and inhibiting overexpression of matrix metalloproteinase-9 in lung tissues.