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KIOM-79 可预防糖尿病肥胖 Zucker 大鼠晶状体上皮细胞凋亡和白内障形成。

KIOM-79 Prevents Lens Epithelial Cell Apoptosis and Lens Opacification in Zucker Diabetic Fatty Rats.

机构信息

Diabetic Complications Research Center, Division of Traditional Korean Medicine (TKM) Integrated Research, Korea Institute of Oriental Medicine (KIOM), 483 Exporo, Yuseong-gu, Daejeon 305-811, Republic of Korea.

出版信息

Evid Based Complement Alternat Med. 2011;2011. doi: 10.1155/2011/717921. Epub 2010 Sep 7.

Abstract

Damage of lens epithelial cells (LECs) has been implicated in cataract formation. The aim of this study was to investigate the protective effect of KIOM-79, a combination of four plant extracts, on LECs. We examined the levels of advanced glycation end products (AGEs), nuclear factor-kappaB (NF-κB) activation and inducible nitric oxide synthase (iNOS) expression in LECs during cataract development using the Zucker diabetic fatty (ZDF) rat, an animal model of type 2 diabetes. KIOM-79 was orally administered by gavage to ZDF rats once a day for 13 weeks. Apoptosis was detected by TUNEL assay, and NF-κB activation and iNOS expression were studied by southwestern histochemistry and immunohistochemistry, respectively. In diabetic cataractous lenses, TUNEL-positive LECs were markedly increased 20-fold, and AGEs were highly accumulated (2.7-fold) in LECs. In addition, both NF-κB activation, and iNOS expression were significantly enhanced 3- to 5-fold, respectively, compared to levels found in normal ZL rats. However, the administration of KIOM-79 delayed the development of diabetic cataracts and prevented LEC apoptosis (70%) through the inhibition of AGEs, NF-κB-activation and iNOS expression. These observations suggest that KIOM-79 is useful in inhibiting diabetic cataractogenesis and acts through an antiapoptotic mechanism to protect LECs from injury.

摘要

晶状体上皮细胞 (LEC) 的损伤与白内障的形成有关。本研究旨在探讨 KIOM-79(四种植物提取物的组合)对 LEC 的保护作用。我们使用 2 型糖尿病动物模型 Zucker 糖尿病肥胖 (ZDF) 大鼠,研究了白内障形成过程中 LEC 中晚期糖基化终产物 (AGEs)、核因子-κB (NF-κB) 激活和诱导型一氧化氮合酶 (iNOS) 的表达水平。KIOM-79 通过灌胃每天一次给予 ZDF 大鼠,共 13 周。通过 TUNEL 测定法检测细胞凋亡,通过西南印迹组织化学和免疫组织化学分别研究 NF-κB 激活和 iNOS 表达。在糖尿病性白内障晶状体中,TUNEL 阳性 LEC 显著增加 20 倍,LEC 中 AGEs 高度累积(2.7 倍)。此外,与正常 ZL 大鼠相比,NF-κB 激活和 iNOS 表达分别显著增强了 3 至 5 倍。然而,KIOM-79 的给药延缓了糖尿病性白内障的发展,并通过抑制 AGEs、NF-κB 激活和 iNOS 表达来防止 LEC 凋亡(70%)。这些观察结果表明,KIOM-79 可有效抑制糖尿病性白内障的发生,并通过抗凋亡机制保护 LEC 免受损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4a50/2952320/2b8053403aba/ECAM2011-717921.001.jpg

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