AIM: To investigate whether two kinds of in vitro prepared advanced glycation end products (AGE), Glu-BSA and Gal-BSA, could induce proinflammatory mediators IL-1beta and TNF-alpha, as well as oxidative stress and nitric oxide (NO), in astrocytes, thus contributing to brain injury. METHODS: Radioimmunoassay and RT-PCR technique were used to detect two cytokines' level and existence of receptor for AGE (RAGE). DTNB reaction was used to measure reduced glutathione (GSH) level. NO content was assayed using Griess reagent provided by Promega. RESULTS: Enhanced protein levels of both cytokines in supernatants and cell lysates of astroglia cultures were detected after treated with AGE-BSA 1 g/L, especially Gal-BSA, for 72 h. The increases were also in a concentration-dependent manner. Changes in protein levels might be attributed to changes in transcriptional levels documented by semi-quantitative RT-PCR. Both AGE-BSA could also reduce astrocytic GSH and induce NO release. RAGE was detected in astrocytes. CONCLUSION: Enhanced levels of astrocytic proinflammatory mediators IL-1beta and TNF-alpha, and oxidative stress caused by AGE might contribute to, at least partially, the detrimental effects of AGE in neuronal disorders and aging brain.
AIM: To investigate whether two kinds of in vitro prepared advanced glycation end products (AGE), Glu-BSA and Gal-BSA, could induce proinflammatory mediators IL-1beta and TNF-alpha, as well as oxidative stress and nitric oxide (NO), in astrocytes, thus contributing to brain injury. METHODS: Radioimmunoassay and RT-PCR technique were used to detect two cytokines' level and existence of receptor for AGE (RAGE). DTNB reaction was used to measure reduced glutathione (GSH) level. NO content was assayed using Griess reagent provided by Promega. RESULTS: Enhanced protein levels of both cytokines in supernatants and cell lysates of astroglia cultures were detected after treated with AGE-BSA 1 g/L, especially Gal-BSA, for 72 h. The increases were also in a concentration-dependent manner. Changes in protein levels might be attributed to changes in transcriptional levels documented by semi-quantitative RT-PCR. Both AGE-BSA could also reduce astrocytic GSH and induce NO release. RAGE was detected in astrocytes. CONCLUSION: Enhanced levels of astrocytic proinflammatory mediators IL-1beta and TNF-alpha, and oxidative stress caused by AGE might contribute to, at least partially, the detrimental effects of AGE in neuronal disorders and aging brain.
Authors: Michaele B Manigrasso; Piul Rabbani; Lander Egaña-Gorroño; Nosirudeen Quadri; Laura Frye; Boyan Zhou; Sergey Reverdatto; Lisa S Ramirez; Stephen Dansereau; Jinhong Pan; Huilin Li; Vivette D D'Agati; Ravichandran Ramasamy; Robert J DeVita; Alexander Shekhtman; Ann Marie Schmidt Journal: Sci Transl Med Date: 2021-11-24 Impact factor: 17.956
Authors: Rosan Barbosa de Matos; Suzana Braga-de-Souza; Bruno Pena Seara Pitanga; Victor Diógenes Amaral da Silva; Erica Etelvina Viana de Jesus; Alexandre Morales Pinheiro; Maria de Fátima Dias Costa; Ramon dos Santos El-Bacha; Cátia Suse de Oliveira Ribeiro; Silvia Lima Costa Journal: Korean J Parasitol Date: 2014-12-23 Impact factor: 1.341
Authors: Gurdip Daffu; Carmen Hurtado del Pozo; Karen M O'Shea; Radha Ananthakrishnan; Ravichandran Ramasamy; Ann Marie Schmidt Journal: Int J Mol Sci Date: 2013-10-01 Impact factor: 5.923