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Fluorescent Nanoparticles for Observing Primo Vascular System Along Sciatic Nerve
Zhao-Feng Jia,Ki-Hoon Eom,Jin-Myung Cha,Jin-Kyu Lee,Zhen-Dong Su,Wen-Hui Yu,Pan Dong Ryu,소광섭,Byung-Cheon Lee 사단법인약침학회 2010 Journal of Acupuncture & Meridian Studies Vol.3 No.3
The primo vascular system was found in the epineurium along the rat sciatic nerve following subcutaneous injection of fluorescent nanoparticles at the Zusanli acupoint (ST-36). Nanoparticles were injected into the primo-vessel near ST-36 and flowed along the sciatic nerve. Fluorescence revealed a structure in the epineurium that was hardly detectable. Images of the isolated sample stained with 4’,6-diamidino-2-phenylindole were captured using confocal microscopy. These images showed the distinctive nuclei distribution and multi-lumen structure of primo-vessels that differentiate them from lymphatic vessels, blood capillaries and nerves. This study demonstrates a new use for nanoparticles in fluorescence reflectance imaging techniques during in vivo imaging of primo-vessels.
Ze-Qin Dai,Hang Su,Min Luo,Yu Ou,Xiao-Zhong Fu,Yong-Xi Dong,Yu-Feng Cha,Shun Zhang,Yong Huang,Yong-Lin Wang 대한화학회 2015 Bulletin of the Korean Chemical Society Vol.36 No.8
A series of 4′-N-substituted (aminomethyl)benzoate derivatives of scutellarein were designed and synthesized. Evaluation of their physiochemical properties showed that the designed target compounds 5a–e exhibit higher chemical stability and aqueous solubility than scutellarin and scutellarein. The permeability (Papp AP to BL ) of 5c–e in Caco-2 cells were 2.8, 8.1, and 12.6 times higher than that of scutellarin and 1.3, 4.1, and 6.0 times higher than that of scutellarein; especially, 5e had the highest P app AP to BL value (7.19 ± 0.31 × 10−6 cm/s) and the lowest ER (P app BL to AP /P app AP to BL ) value of 0.17. In vitro antioxidative evaluation results revealed that 5e could protect against H2O2 -induced PC12 cells’ oxidative damage by attenuating mitochondrial membrane potential loss and decreasing H2O2 -induced reactive oxygen species (ROS) production.
Yang Hui-Hui,Jiang Hui-Ling,Tao Jia-Hao,Zhang Chen-Yu,Xiong Jian-Bing,Yang Jin-Tong,Liu Yu-Biao,Zhong Wen-Jing,Guan Xin-Xin,Duan Jia-Xi,Zhang Yan-Feng,Liu Shao-Kun,Jiang Jian-Xin,Zhou Yong,Guan Cha-Xi 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Necroptosis is the major cause of death in alveolar epithelial cells (AECs) during acute lung injury (ALI). Here, we report a previously unrecognized mechanism for necroptosis. We found an accumulation of mitochondrial citrate (citratemt) in lipopolysaccharide (LPS)-treated AECs because of the downregulation of Idh3α and citrate carrier (CIC, also known as Slc25a1). shRNA- or inhibitor–mediated inhibition of Idh3α and Slc25a1 induced citratemt accumulation and necroptosis in vitro. Mice with AEC-specific Idh3α and Slc25a1 deficiency exhibited exacerbated lung injury and AEC necroptosis. Interestingly, the overexpression of Idh3α and Slc25a1 decreased citratemt levels and rescued AECs from necroptosis. Mechanistically, citratemt accumulation induced mitochondrial fission and excessive mitophagy in AECs. Furthermore, citratemt directly interacted with FUN14 domain-containing protein 1 (FUNDC1) and promoted the interaction of FUNDC1 with dynamin-related protein 1 (DRP1), leading to excessive mitophagy-mediated necroptosis and thereby initiating and promoting ALI. Importantly, necroptosis induced by citratemt accumulation was inhibited in FUNDC1-knockout AECs. We show that citratemt accumulation is a novel target for protection against ALI involving necroptosis.