Blood is a treasure trove whose constituents have attracted increasing attention for use in understanding and controlling disease. However, the functions of blood, especially with regard to its composition at the nanoscale, remain largely unknown. Inspired by exosomes and lipoproteins, the present work isolated and characterized biotic nanodiscs from human blood (BNHBs) using multiple techniques. The isolated BNHBs had diameters of 10–30 nm and a thicknesses of approximately 2.9 nm. The BNHB concentration in blood peaked at 34.5 ± 5.19 mg/mL (20-fold higher than that of high-density lipoproteins and exosomes). BNHBs had high biocompatibility, facile cell internalization and strong biological control of pulmonary fibrosis. The BNHBs were hybrids of many metalloproteins and metabolites and contained a few functional proteins similar to lipoproteins or exosomal proteins. BNHBs inhibited transforming growth factor-beta 1 (TGF-β1)-induced fibrosis damage in human embryonic lung fibroblasts (HELFs) by inhibiting the expression of α-smooth muscle actin and collagen-1 protein. BNHBs also intensively bound TGF-β1 to inhibit TGF-β1 activity in fibrogenesis. BNHBs successfully reduced pulmonary inflammation and collagen deposition in a mouse model, preventing pulmonary fibrosis. Applying the protective properties of nanodiscs may be a novel therapeutic approach for pulmonary and other diseases.

血液是一个宝库，其成分已被越来越多的注意力用于理解和控制疾病。然而，血液的功能，特别是关于其在纳米级的组成方面的功能，在很大程度上仍是未知的。受外泌体和脂蛋白的启发，本研究使用多种技术从人血（BNHB）中分离并鉴定了生物纳米光盘。分离出的BNHB的直径为10–30 nm，厚度约为2.9 nm。血液中的BNHB浓度达到34.5±5.19 mg / mL的峰值（比高密度脂蛋白和外泌体的浓度高20倍）。BNHBs具有高度的生物相容性，细胞内在化的便利性以及对肺纤维化的强大生物控制能力。BNHB是许多金属蛋白和代谢产物的杂种，并包含一些类似于脂蛋白或外泌体蛋白的功能蛋白。BNHB通过抑制α平滑肌肌动蛋白和1型胶原蛋白的表达，抑制转化生长因子β1（TGF-β1）诱导的人胚肺成纤维细胞（HELFs）的纤维化损伤。BNHBs还强烈结合TGF-β1，以抑制TGF-β1在纤维发生中的活性。BNHB在小鼠模型中成功减少了肺部炎症和胶原蛋白沉积，从而预防了肺纤维化。应用纳米光盘的保护特性可能是一种针对肺部疾病和其他疾病的新颖治疗方法。BNHB通过抑制α平滑肌肌动蛋白和1型胶原蛋白的表达，抑制转化生长因子β1（TGF-β1）诱导的人胚肺成纤维细胞（HELFs）的纤维化损伤。BNHBs还强烈结合TGF-β1，以抑制TGF-β1在纤维发生中的活性。BNHB在小鼠模型中成功减少了肺部炎症和胶原蛋白沉积，从而预防了肺纤维化。应用纳米光盘的保护特性可能是一种针对肺部疾病和其他疾病的新颖治疗方法。BNHB通过抑制α平滑肌肌动蛋白和1型胶原蛋白的表达，抑制转化生长因子β1（TGF-β1）诱导的人胚肺成纤维细胞（HELFs）的纤维化损伤。BNHBs还强烈结合TGF-β1，以抑制TGF-β1在纤维发生中的活性。BNHB在小鼠模型中成功减少了肺部炎症和胶原蛋白沉积，从而预防了肺纤维化。应用纳米光盘的保护特性可能是一种针对肺部疾病和其他疾病的新颖治疗方法。