首页> 外文期刊>Food and Chemical Toxicology: An International Journal Published for the British Industrial Biological Research >Octaphlorethol A, a novel phenolic compound isolated from Ishige foliacea, protects against streptozotocin-induced pancreatic β cell damage by reducing oxidative stress and apoptosis
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Octaphlorethol A, a novel phenolic compound isolated from Ishige foliacea, protects against streptozotocin-induced pancreatic β cell damage by reducing oxidative stress and apoptosis

机译:Octaphlorethol A,一种从叶茂石提取的新型酚类化合物,可通过减少氧化应激和凋亡来预防链脲佐菌素诱导的胰腺β细胞损伤

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摘要

Pancreatic β cells are extremely sensitive to oxidative stress, which probably has an important role in β cell damage in diabetes. The protective effect of octaphlorethol A (OPA), a novel phenolic compound isolated from Ishige foliacea, against streptozotocin (STZ)-induced pancreatic β cell damage was investigated using a rat insulinoma cell line (RINm5F pancreatic β cells). Pretreatment with OPA decreased the death of STZ-treated pancreatic β cells at concentrations of 12.5. μg/ml or 50. μg/ml, and reduced the generation of thiobarbituric acid reactive substances and intracellular reactive oxygen species in a dose-dependent manner in STZ-treated pancreatic β cells. In addition, the OPA pretreatment increased the activities of antioxidant enzymes such as catalase, superoxide dismutase, and glutathione peroxidase in STZ-treated pancreatic β cells. Moreover, OPA treatment elevated the level of insulin, which was reduced by STZ treatment, and protected pancreatic β cells against damage under STZ-treated conditions. These effects were mediated by suppressing apoptosis and were associated with increased anti-apoptotic Bcl-xL expression and reduced pro-apoptotic Bax and cleaved caspase-3 expression. These findings indicate that OPA may be useful as a potential pharmaceutical agent to protect against pancreatic β cell damage caused by oxidative stress associated with diabetes.
机译:胰腺β细胞对氧化应激极为敏感,这可能在糖尿病β细胞损伤中起重要作用。使用大鼠胰岛素瘤细胞系(RINm5F胰腺β细胞),研究了从叶芝叶中分离出的一种新型酚类化合物八辛醇A(OPA)对链脲佐菌素(STZ)诱导的胰腺β细胞损伤的保护作用。用OPA预处理可降低浓度为12.5的STZ处理的胰腺β细胞的死亡。 μg/ ml或50.μg/ ml,并在STZ处理的胰腺β细胞中以剂量依赖性方式减少了硫代巴比妥酸反应性物质和细胞内活性氧的产生。此外,OPA预处理可提高STZ处理的胰腺β细胞中抗氧化酶(如过氧化氢酶,超氧化物歧化酶和谷胱甘肽过氧化物酶)的活性。此外,OPA处理可提高胰岛素水平,而STZ处理可降低胰岛素水平,并在STZ处理的条件下保护胰腺β细胞免受损伤。这些作用是通过抑制细胞凋亡来介导的,并与增加的抗凋亡Bcl-xL表达和减少的促凋亡Bax和Caspase-3表达减少有关。这些发现表明,OPA可以用作潜在的药物,以预防由与糖尿病相关的氧化应激引起的胰岛β细胞损伤。

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