生命周期结束产品再生模式选择分析

本文认为,对生命周期结束的产品进行再造、翻新、再生是逆向物流的主要内容,也是企业管理的重要组成部分,对供应链具有重要意义。文章提出,影响再生模式选择的因素主要有两个:一是生命周期结束的产品是否适合拆解;二是再生处理的执行是否外包。这两个因素密切相关,决定着再生的四种可供选择的模式,即再生不拆解外包(低成本选择)、再生并拆解外包(折中的再生方式)、企业再生不拆解(控制物料和创建新的市场)、企业再生并拆解(通过循环供应链创造独特的价值),这四种模式都是可行的选择。外包必须在合乎环境要求的情况下进行,外包具有前期成本相对较低的优势,但也有风险。企业独自或积极参与再生,是企业发展的新思路。企业独自或积极参与再生并拆解,从竞争角度看是一种高风险的选择,要求企业固定资产投资较高并能引发企业发展战略的重大转移,这种选择一旦成功,企业将获得丰厚回报,减少或消除对原材料和市场的依赖性,减少环境风险,保证用户最终得到既经济又环保的新颖产品。

Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease

AIM To determine if manipulation of dietary advanced glycation end product(AGE), intake affects nonalcoholic fatty liver disease(NAFLD) progression and whether these effects are mediated via RAGE. METHODS Male C57Bl6 mice were fed a high fat, high fructose, high cholesterol(HFHC) diet for 33 wk and compared with animals on normal chow. A third group were given a HFHC diet that was high in AGEs. Another group was given a HFHC diet that was marinated in vinegar to prevent the formation of AGEs. In a second experiment, RAGE KO animals were fed a HFHC diet or a high AGE HFHC diet and compared with wildtype controls. Hepatic biochemistry, histology, picrosirius red morphometry and hepatic mR NA were determined. RESULTS Long-term consumption of the HFHC diet generated significant steatohepatitis and fibrosis after 33 wk. In this model, hepatic 4-hydroxynonenal content(a marker of chronic oxidative stress), hepatocyte ballooning, picrosirius red staining, α-smooth muscle actin and collagen type 1A gene expression were all significantly increased. Increasing the AGE content of the HFHC diet by baking further increased these markers of liver damage, but this was abrogated by pre-marination in acetic acid. In response to the HFHC diet, RAGE-/-animals developed NASH of similar severity to RAGE+/+ animals but were protected from the additional harmful effects of the high AGE containing diet. Studies in isolated Kupffer cells showed that AGEs increase cell proliferation and oxidative stress, providing a likely mechanism through which these compounds contribute to liver injury. CONCLUSION In the HFHC model of NAFLD, manipulation of dietary AGEs modulates liver injury, inflammation, and liver fibrosis via a RAGE dependent pathway. This suggests that pharmacological and dietary strategies targeting the AGE/RAGE pathway could slow the progression of NAFLD.

Generation of glyceraldehyde-derived advanced glycation end-products in pancreatic cancer cells and the potential of tumor promotion

AIM To determine the possibility that diabetes mellitus promotes pancreatic ductal adenocarcinoma via glyceraldehyde(GA)-derived advanced glycation-end products(GA-AGEs).METHODS PANC-1,a human pancreatic cancer cell line,was treated with 1-4 mmol/L GA for 24 h. The cell viability and intracellular GA-AGEs were measured by WST-8 assay and slot blotting. Moreover,immunostaining of PANC-1 cells with an anti-GA-AGE antibody was performed. Western blotting(WB) was used to analyze the molecular weight of GA-AGEs. Heat shock proteins 90α,90β,70,27 and cleaved caspase-3 were analyzed by WB. In addition,PANC-1 cells were treated with GA-AGEs-bovine serum albumin(GA-AGEs-BSA),as a model of extracellular GA-AGEs,and proliferation of PANC-1 cells was measured.RESULTS In PANC-1 cells,GA induced the production of GA-AGEs and cell death in a dose-dependent manner. PANC-1 cell viability was approximately 40% with a 2 mmol/L GA treatment and decreased to almost 0% with a 4 mmol/L GA treatment(each significant difference was P < 0.01). Cells treated with 2 and 4 mmol/L GA produced 6.4 and 21.2 μg/mg protein of GA-AGEs,respectively(P <0.05 and P < 0.01). The dose-dependent production of some high-molecular-weight(HMW) complexes of HSP90β,HSP70,and HSP27 was observed following administration of GA. We considered HMW complexes to be dimers and trimers with GA-AGEs-mediated aggregation. Cleaved caspase-3 could not be detected with WB. Furthermore,10 and 20 μg/m L GA-AGEs-BSA was 27% and 34% greater than that of control cells,respectively(P < 0.05 and P < 0.01).CONCLUSION Although intracellular GA-AGEs induce pancreatic cancer cell death,their secretion and release may promote the proliferation of other pancreatic cancer cells.

Effects of atorvastatin on progression of diabetic nephropathy and local RAGE and soluble RAGE expressions in rats

Objective:Advanced glycation end-products (AGEs) exert inflammatory and oxidative stress insults to produce diabetic nephropathy mainly through the receptor for AGEs (RAGE).This study aimed to assess the effect of atorvastatin on diabetic nephropathy via soluble RAGE (sRAGE) and RAGE expressions in the rat kidney.Methods:Thirty-two male Sprague-Dawley rats were divided into four groups based on the presence or absence of streptozotocin-induced diabetes with or without atorvastatin treatment (10 mg/kg for 24 weeks).Serum sRAGE and glycated albumin (GA) levels were measured with enzyme-linked immunosorbent assay (ELISA) and improved bromocresol purple methods.Renal AGEs,RAGE,endogenous secretory RAGE (esRAGE),and sRAGE were determined with reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting.Results:Mesangial expansion and microalbuminuria were aggravated in diabetic rats,and improved with atorvastatin treatment.Serum sRAGE levels were lower in diabetic than in normal rats.After atorvastatin treatment,serum and renal sRAGE levels were up-regulated,while renal RAGE expression was decreased in diabetic rats,associated with a reduction in accumulation of AGEs,though renal esRAGE mRNA expression was not significantly increased.Conclusions:Atorvastatin exerted a beneficial effect on diabetic nephropathy with reduced AGE accumulation,down-regulating RAGE expression and up-regulating sRAGE in the kidney.

Ursane derivatives isolated from leaves of Hylocereus undatus inhibit glycation at multiple stages

The present study was designed to evaluate the therapeutic potential of bioactive compounds from chloroform extract of the leaves of Hylocereus undatus in the formation of advanced glycation end products(AGEs) in vitro. Bioactivity-guided fractionation of chloroform extract from Hylocereus undatus afforded two novel 12-ursen-type triterpenes, 3β, 16α, 23-trihydroxy-urs-12-en-28-oic acid(1) and 3β, 6β, 19α, 22α-tetrahydroxy-urs-12-en-28-oic acid(2), as well as four known triterpenes 2α, 3β, 23-tetrahydroxy-urs-11-en-28-oic acid(3), 3β-acetoxy-28-hydroxyolean-12-ene(4), 3β, 16α-dihidroxyolean-12-ene(5) and 3β-acetoxy-olean-12-ene(6). Our results revealed that triterpenes 1–3 were able to inhibit the formation of AGEs in all tested assays. The data indicated that the triterpenes had inhibitory activity at the múltiple stages of glycation and that there might be a high potential for decreasing protein oxidation and protein glycation that can enhance glycative stress in diabetic complications.