Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2012
Tunicamycin inhibits diabetes.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Shaabani Namir, Honke Nadine, Lang Philipp A, Görg Boris, Proksch Peter, Gailus Nicole, Gotoh Tomomi, Häussinger Dieter, Lang Karl S
Аннотация
BACKGROUND: Autoimmune diseases are characterized by a breakdown of immunologic tolerance, and this breakdown can lead to life-threatening or lifelong disorders. Moreover; drugs that are used to treat these diseases are few in number and are associated with many serious adverse effects.
METHODS: We used the rat insulin promoter-glycoprotein mouse model to analyze the role of tunicamycin in the process of autoimmune diabetes; the P14 mouse model to analyze the effect of tunicamycin on CD8(+) T cells; chop knockout mice to analyze the role of tunicamycin on an endoplasmic reticulum stress model; and fluorescence-activated cell sorting, quantitative real-time polymerase chain reaction, and histologic methods.
RESULTS: We found that a single dose of tunicamycin reduced the activation and pancreatic infiltration of CD8(+) T cells. This activity delayed the incidence of virus-induced diabetes and improved survival rates.
CONCLUSION: Tunicamycin may offer therapeutic opportunities for T cell-mediated autoimmune diseases such as diabetes.
METHODS: We used the rat insulin promoter-glycoprotein mouse model to analyze the role of tunicamycin in the process of autoimmune diabetes; the P14 mouse model to analyze the effect of tunicamycin on CD8(+) T cells; chop knockout mice to analyze the role of tunicamycin on an endoplasmic reticulum stress model; and fluorescence-activated cell sorting, quantitative real-time polymerase chain reaction, and histologic methods.
RESULTS: We found that a single dose of tunicamycin reduced the activation and pancreatic infiltration of CD8(+) T cells. This activity delayed the incidence of virus-induced diabetes and improved survival rates.
CONCLUSION: Tunicamycin may offer therapeutic opportunities for T cell-mediated autoimmune diseases such as diabetes.
Предметные рубрики MeSH
AnimalsApoptosisAutoimmune DiseasesBlood GlucoseCD8-Positive T-LymphocytesCell ProliferationCytokinesDiabetes Mellitus, ExperimentalEndoplasmic Reticulum StressFlow CytometryGlycoproteinsHypoglycemic AgentsImmunosuppressive AgentsLymphocyte ActivationLymphocytic choriomeningitis virusMiceMice, Inbred C57BLMice, KnockoutPancreasPromoter Regions, GeneticRatsReverse Transcriptase Polymerase Chain ReactionTranscription Factor CHOPTunicamycin