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JLB:传统中药治疗代谢性疾病和肥胖症

  1. 代谢性疾病
  2. 甘草
  3. 肥胖症

来源:生物谷 2014-12-03 11:35

2014年12月3日讯 /生物谷BIOON/ --发表于Journal of Leukocyte Biology杂志的一项新研究表明:在植物甘草的一种成分可以通过停止NLRP3的活化,抑制代谢紊乱的发展。NLRP3是参与该疾病过程的蛋白质。具体而言,研究人

2014年12月3日讯 /生物谷BIOON/ --发表于Journal of Leukocyte Biology杂志的一项新研究表明:在植物甘草的一种成分可以通过停止NLRP3的活化,抑制代谢紊乱的发展。

NLRP3是参与该疾病过程的蛋白质。具体而言,研究人员发现异甘草素能抑制小鼠高脂肪饮食引起的肥胖,2型糖尿病和脂肪肝。

科学家们在异甘草素存在情况下,用不同的炎性因子激活刺激小鼠巨噬细胞。然后,通过测量培养物上清液中IL-1β的生成评价NLRP3炎性体的活化程度。

结果表明与已知的NLRP3炎性抑制剂如白菊和磺酰脲类药物格列本脲相比,相对低浓度的异甘草素可非常有效抑制IL-1β的生成。

在动物研究中使用了三组小鼠。第一组小鼠饲喂正常饮食,第二组小鼠饲喂高脂肪的饮食,第三组小鼠高脂肪饮食中添加0.5%的异甘草素。

高脂肪饮食喂养20周会诱发肥胖,2型糖尿病和小鼠肝细胞脂肪变性,但添加异甘草素能显著改善这些疾病。最后,异甘草素会抑制高脂肪饮食诱导脂肪组织中IL-1β的生成。(生物谷Bioon.com)

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Isoliquiritigenin is a potent inhibitor of NLRP3 inflammasome activation and diet-induced adipose tissue inflammation.

H. Honda, Y. Nagai, T. Matsunaga, N. Okamoto, Y. Watanabe, K. Tsuneyama, H. Hayashi, I. Fujii, M. Ikutani, Y. Hirai, A. Muraguchi, K. Takatsu.

Inflammasome activation initiates the development of many inflammatory diseases, including obesity and type 2 diabetes. Therefore, agents that target discrete activation steps could represent very important drugs. We reported previously that ILG, a chalcone from Glycyrrhiza uralensis, inhibits LPS-induced NF-κB activation. Here, we show that ILG potently inhibits the activation of NLRP3 inflammasome, and the effect is independent of its inhibitory potency on TLR4. The inhibitory effect of ILG was stronger than that of parthenolide, a known inhibitor of the NLRP3 inflammasome. GL, a triterpenoid from G. uralensis, had similar inhibitory effects on NLRP3 activity, but high concentrations of GL were required. In contrast, activation of the AIM2 inflammasome was inhibited by GL but not by ILG. Moreover, GL inhibited NLRP3- and AIM2-activated ASC oligomerization, whereas ILG inhibited NLRP3-activated ASC oligomerization. Low concentrations of ILG were highly effective in IAPP-induced IL-1β production compared with the sulfonylurea drug glyburide. In vivo analyses revealed that ILG potently attenuated HFD-induced obesity, hypercholesterolemia, and insulin resistance. Furthermore, ILG treatment improved HFD-induced macrovesicular steatosis in the liver. Finally, ILG markedly inhibited diet-induced adipose tissue inflammation and IL-1β and caspase-1 production in white adipose tissue in ex vivo culture. These results suggest that ILG is a potential drug target for treatment of NLRP3 inflammasome-associated inflammatory diseases.

 

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