N-tert-Butyl-α-phenylnitrone 是一种基于硝酮的自由基清除剂,可形成一氧化氮自旋加合物。N-tert-Butyl-α-phenylnitrone 抑制 COX2 的催化活性。N-tert-Butyl-α-phenylnitrone 具有有效的 ROS 清除,抗炎,神经保护,抗衰老和抗糖尿病的作用,并且可以穿透血脑屏障。
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N-tert-Butyl-α-phenylnitrone is a nitrone-based free radical scavenger that forms nitroxide spin adducts. N-tert-Butyl-α-phenylnitrone inhibits COX2 catalytic activity. N-tert-Butyl-α-phenylnitrone has potent ROS scavenging, anti-inflammatory, neuroprotective, anti-aging and anti-diabetic activities, and can penetrate the blood-brain barrier[1][2][3][4].
In Vitro:N-tert-Butyl-α-phenylnitrone (PBN) (25-100 μM) 处理可显著降低 2,2'-偶氮二 (2-脒基丙烷) 二盐酸盐 (AAPH) 诱导的细胞内 ROS 积累。N-tert-Butyl-α-phenylnitrone 还可减弱 AAPH 诱导的细胞毒性、基质降解和细胞凋亡。N-tert-Butyl-α-phenylnitrone 抑制 AAPH 诱导的 ERK/MAPK 通路激活。N-tert-Butyl-α-phenylnitrone 具有用于椎间盘退变 (IDD) 研究的潜力[1]。
In Vivo:N-tert-Butyl-α-phenylnitrone (PBN;100 mg/kg;腹腔注射;每天两次;C57Bl/6 小鼠) 处理不仅消除了 LPS 诱导的脂质过氧化、硝基酪氨酸残留水平和 GSH 消耗,而且减少外部畸形的发生率[2]。
参考文献:
[1]. Zhenggang Zhou, et al. PBN Protects NP Cells From AAPH-induced Degenerative Changes by Inhibiting the ERK1/2 Pathway. Connect Tissue Res. 2020 Mar 30;1-10.
[2]. Lei Zhao, et al. Reactive Oxygen Species Contribute to Lipopolysaccharide-Induced Teratogenesis in Mice. Toxicol Sci. 2008 May;103(1):149-57.
[3]. Y Kotake, et al. Inhibition of NF-kappaB, iNOS mRNA, COX2 mRNA, and COX Catalytic Activity by phenyl-N-tert-butylnitrone (PBN). Biochim Biophys Acta. 1998 Nov 19;1448(1):77-84.
[4]. R A Floyd. Antioxidants, Oxidative Stress, and Degenerative Neurological Disorders. Proc Soc Exp Biol Med. 1999 Dec;222(3):236-45.