No abstract

HCHO could reduce Ag+ to Ag on the surface of AuNRs to form Au core–Ag shell nanorods (Au@Ag↓NRs) in AuNRs–Ag+–HCHO system, which caused LPAB of AuNRs to redshift. Thus, a responsive AuNRs colorimetric sensor for the detection HCHO has been developed.

It has been known that SARS-CoV-2 which is considered similar to SARS-CoV invades human respiratory epithelial cells through interaction with the human angiotensin converting enzyme II (ACE2). In this work, SARS-CoV-2S-RBD and its cell receptor ACE2 were used to investigate the blocking effect and mechanism of β-chitosan to the binding of them. Besides, inhibitory effect of β-chitosan on inflammation induced by SARS-CoV-2S-RBD was also studied. Firstly, Native-PAGE results showed that β-chitosan could bind with ACE2 or SARS-CoV-2S-RBD and the conjugate of β-chitosan and ACE2 could no longer bind with SARS-CoV-2S-RBD. HPLC analyses suggested that was found the conjugate of β-chitosan and SARS-CoV-2S-RBD displayed high binding affinity under the condition of high pressure (40 MPa) compared with that of ACE2 and SARS-CoV-2S-RBD. Furthermore, immunofluorescence detections on Vero E6 cells and hACE2 mice showed that β-chitosan had a significant prevention and treatment effect on SARS-CoV-2S-RBD binding. Meanwhile, SARS-CoV-2S-RBD binding could activate the inflammation signaling pathways of cells and mice, however, β-chitosan could dramatically suppress the inflammations activated by SARS-CoV-2S-RBD. Subsequently, Western blot analyses revealed that the expression levels of ACE2 in experimental groups treated with β-chitosan significantly reduced. However, after the intervention of ADAM17 inhibitor (TAPI), the decreased ACE2 expressions affected by β-chitosan up-regulated correspondingly. The results indicated that β-chitosan has a similar antibody function, which can neutralize SARS-CoV-2S-RBD and effectively block the binding of SARS-CoV-2S-RBD with ACE2. ADAM17 activated by β-chitosan can enhance the cleavage of ACE2 extracellular domain with a catalytic activity of Ang II degradation, and then the extracellular region was released into the extracellular environment. So, β-chitosan could prevent the binding, internalization and degradation of ACE2 with SARS-CoV-2S-RBD and inhibit the activation of inflammatory signaling pathways at the same time. This work provides a valuable reference for the prevention and control of SARS-CoV-2 by β-chitosan.

Glucosamine hydrochloride (GAH), one of the most basic and important derivatives of chitin, is obtained by hydrolysis of chitin in concentrated hydrochloric acid. At present, little is known about how GAH functions in skeletal development. In this report, we demonstrate that GAH, extracted from the cell wall of Agaricus bisporus, acts in a dose-dependent manner to promote not only cartilage and bone development in larvae but also caudal fin regeneration in adult fish. Furthermore, GAH treatment causes a significant increase in expression of bone-related marker genes, indicating its important role in promoting skeletal development. We show that in both larval and adult osteoporosis models induced by high iron osteogenic defects are significantly ameliorated after treatment with GAH, which regulates expression of a series of bone-related genes. Finally, we demonstrate that GAH promotes skeletal development and injury repair through bone morphogenetic protein (Bmp) signaling, and it works at the downstream of the receptor level. Taken together, our findings not only provide a strong research foundation and strategy for the screening of natural osteoporosis drugs and product development using a zebrafish model but also establish the potential for the development of Agaricus bisporus-derived GAH as a new drug for osteoporosis treatment.