纸片型1-MCP处理对采后安溪油柿果实活性氧代谢和细胞膜 透性的影响

研究了纸片型 1-甲基环丙烯（1-MCP）处理对采后安溪油柿果实活性氧代谢和细胞膜透性的影响。采后安溪 油柿果实经 1.35 μL/L 纸片型 1-MCP 处理 12 h 后,在(20±1) ℃、相对湿度 85%条件下贮藏。结果表明,与对照果实相 比,纸片型 1-MCP 处理能有效提高采后安溪油柿果实的超氧化物歧化酶（SOD）、过氧化物酶（POD）、过氧化氢酶（CAT） 和抗坏血酸过氧化物酶（APX）等活性氧清除酶活性,保持较高的还原型抗坏血酸（AsA）和还原型谷胱甘肽（GSH） 等内源抗氧化物质的含量;降低超氧阴离子自由基（O2 ? ? ）产生速率和膜脂过氧化产物丙二醛（MDA）含量的积累;延 缓采后安溪油柿果实细胞膜透性增加。因此,1.35 μL/L 纸片型 1-MCP 处理能有效提高采后安溪油柿果实的活性氧清除 能力,降低活性氧积累和抑制膜脂过氧化作用,从而延缓采后安溪油柿果实衰老,延长果实保鲜期。     

1-MCP延缓采后台湾青枣果实衰老及其与能量代谢的关系

研究1-甲基环丙烯(1-MCP)处理对采后‘中青’台湾青枣果实贮藏品质与烟酰胺腺嘌呤二核苷酸激酶(NADK)活性、烟酰胺腺嘌呤二核苷酸(NAD)、烟酰胺腺嘌呤二核苷酸磷酸(NADP)、还原型烟酰胺腺嘌呤二核苷酸(NADH)、还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)、能量物质[三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、一磷酸腺苷(AMP)]及能荷(EC)的关系。采后台湾青枣果实用1.8μL/L的1-MCP处理12 h后在(15±1)℃下贮藏,定期测定能量物质、NAD、NADP、NADH和NADPH含量、NADK活性及细胞膜透性,并在贮藏前后测定果实品质指标和腐烂率。结果表明:1-MCP处理保持‘中青’台湾青枣果实较高的ATP、NADP、NADPH含量,NADK活性和能荷值,较低的NAD和NADH含量,延缓贮藏期间细胞膜透性的增加;保持较高的果实硬度、可溶性固形物(TSS)、有机酸(TA)和维生素C含量,延缓果皮叶绿素含量下降,降低腐烂率。据此认为,1-MCP处理延缓采后台湾青枣果实衰老降低腐烂率可能与细胞保持较高的能荷水平有关。     

安喜布处理对台湾青枣果实果皮活性氧代谢和细胞膜透性的影响

安喜布(AnsiP-S,纸片型1-MCP缓释剂)是一种新型的保鲜剂.该文探讨有效1-MCP浓度为1.8μL/L的安喜布处理对采后‘中青’台湾青枣(Ziziphus mauritiana Lamk.cv.Zhongqing)果实果皮活性氧代谢和细胞膜透性的影响.结果表明:安喜布处理能保持较高的采后台湾青枣果实果皮超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和抗坏血酸过氧化物酶(APX)等活性氧清除酶活性和还原型抗坏血酸(AsA)、还原型谷胱甘肽(GSH)等内源抗氧化物质含量,降低果皮超氧自由基(O2-.)产生速率和膜脂过氧化产物丙二醛(MDA)含量,延缓果皮细胞膜相对渗透率升高,保持较高果实好果率.     

Marine Bromophenol Derivative 3,4-Dibromo-5-(2-bromo-3,4-dihydroxy-6-isopropoxymethyl benzyl)benzene-1,2-diol Protects Hepatocytes from Lipid-Induced Cell Damage and Insulin Resistance via PTP1B Inhibition

3,4-Dibromo-5-(2-bromo-3,4-dihydroxy-6-isopropoxymethyl benzyl)benzene-1,2-diol (HPN) is a bromophenol derivative from the marine red alga Rhodomela confervoides. We have previously found that HPN exerted an anti-hyperglycemic property in db/db mouse model. In the present study, we found that HPN could protect HepG2 cells against palmitate (PA)-induced cell death. Data also showed that HPN inhibited cell death mainly by blocking the cell apoptosis. Further studies demonstrated that HPN (especially at 1.0 μM) significantly restored insulin-stimulated tyrosine phosphorylation of IR and IRS1/2, and inhibited the PTP1B expression level in HepG2 cells. Furthermore, the expression of Akt was activated by HPN, and glucose uptake was significantly increased in PA-treated HepG2 cells. Our results suggest that HPN could protect hepatocytes from lipid-induced cell damage and insulin resistance via PTP1B inhibition. Thus, HPN can be considered to have potential for the development of anti-diabetic agent that could protect both hepatic cell mass and function.