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Copyright of Systems Engineering & Electronics is the property of Journal of Systems Engineering & Electronics Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Henan Agricultural Sciences is the property of Editorial Board of Journal of Henan Agricultural Sciences and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

To explore the mechanism of chitosan oligosaccharides(COS) in reducing atherosclerotic plaque formation from the perspective of protein glycosylation modification. Methods Totally 40 ApoE-/- mice were randomly divided into control group and COS group. The control group was given a high-fat diet for 12 weeks, and COS group was given a high-fat diet plus COS(gavage per day, 500 mg/kg) for 12 weeks. Serum lipid detection, HE staining and Oil red O staining were used to detect plaque formation. Lectin chip, liquid chromatography tandem-mass spectrometry and ELISA were used to detect potential changes of glycoprotein in serum. Cholesterol ester outflow and free cholesterol ester determination experiment were used to evaluate the effect of changes in scavenger receptor class B type Ⅰ(SRBI) protein glycosylation modification site on cholesterol effluence in macrophages. Results COS significantly reduced the level of TC and LDL-C(P＜0.05) in mice, but had no effect on the level of TG,HDL-C,ApoA1 and ApoB100. The intima thickness and plaque size of the aorta were significantly thinner and smaller(P＜0.05)in the COS group compared with the control group. The molecular weight of lens culinaris agglutinin(LCA)binding protein with the most obvious change is 80-90 ku, and SRBI was one of them. COS promoted the cholesterol outflow and inhibited the accumulation of free cholesterol ester in RAW264.7 cell(P＜0.05). Knockdown or glycosylation site mutation with SRBI inhibited cholesterol outflow caused by COS, and increased the accumulation of intracellular free cholesterol(P＜0.05). Conclusions COS promotes lipid efflux by increasing SRBI glycosylation and expression, thereby alleviating atherosclerotic plaque formation. [ABSTRACT FROM AUTHOR]

Copyright of Journal of Materials Science & Engineering (1673-2812) is the property of Journal of Materials Science & Engineering Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)