Artificial Cells, Nanomedicine, and Biotechnology最新文献

Helicobacter pylori (H. pylori) is recognized as a pathogen associated with several gastrointestinal diseases. The current treatments exhibit numerous drawbacks, including antibiotic resistance. H. pylori can adhere to and colonize the gastric mucosa through H. pylori adhesin A (HpaA), and antibodies against HpaA may be an effective therapeutic approach. The variable domain of immunoglobulin new antigen receptor (VNAR) is a novel type of single-domain antibody with a small size, good stability, and easy manufacturability. This study isolated VNARs against HpaA from an immune shark VNAR phage display library. The VNARs can bind both recombinant and native HpaA proteins. The VNARs, 2A2 and 3D6, showed high binding affinities to HpaA with different epitopes. Furthermore, homodimeric bivalent VNARs, biNb-2A2 and biNb-3D6, were constructed to enhance the binding affinity. The biNb-2A2 and biNb-3D6 had excellent stability at gastrointestinal pH conditions. Finally, a sandwich ELISA assay was developed to quantify the HpaA protein using BiNb-2A2 as the capture antibody and BiNb-3D6 as the detection antibody. This study provides a potential foundation for novel alternative approaches to treatment or diagnostics applications of H. pylori infection.

Abstract

Carbon quantum dots (CQDs) were synthesized from blue honeysuckle (Lonicera caerulea) berry fruit extracts using a well-known, cost-effective, and environmental friendly hydrothermal process. The material was characterized using UV-vis spectroscopy, photoluminescence (PL), XPS, and TEM studies. The as-synthesized carbon dots exhibit excellent PL properties, with a quantum yield of ∼35.92%. CQDs vary in size from ∼2 nm to 9 nm. This study established the neuroprotective effects of CQDs against lipopolysaccharide (LPS)-induced human microglial cell model. LPS was found to induce cytotoxicity, reactive oxygen species, and pro-inflammatory cytokines interleukin (IL)-1β, IL-6, and tumour necrosis factor-α) and downregulated enzymatic antioxidants such as nuclear factor-erythroid factor 2-related factor 2 (Nrf2), superoxide dismutase, catalase, haem oxygenase (HO)-1, HO-2, and glutathione peroxidase, while CQDs treatment reversed LPS induced cytotoxicity, induced anti-inflammatory cytokines (IL-4, IL-10, and transforming growth factor β) and induce enzymatic antioxidants both at transcriptional and translational levels. The study suggested the potential role of CQDs prepared from Lonicera caerulea, as anti-inflammatory and antioxidative agents in neuroinflammatory and neurodegenerative diseases. In addition, CQDs could be exploited in various biomedical applications such as biosensing, drug delivery and tissue engineering.

Carbon monoxide (CO) is a toxic gas that causes neuropathy. However, CO is endogenously produced in small amounts showing various beneficial effects. We hypothesized that CO-bound haemoglobin-vesicle (HbV) administration would reduce cerebral ischaemia-reperfusion injury without causing neuropathy. Three experiments were conducted. First, rats were exposed to CO inhalation to create a CO-poisoning group, and they were sacrificed on 0, 7, 14, and 21 days after CO exposure. Histopathologically, hippocampal damage was prominent at 14 days. Second, the rats were administered with CO-HbV equivalent to 50 or 25% of circulating blood volume (CO-HbV50 or CO-HbV25 group). Rats were sacrificed 14 days after administration. Third, rats put into haemorrhagic shock by 50% of circulating blood withdrawal were resuscitated using saline, autologous blood, and CO-HbV. They were sacrificed 14 days after resuscitation. Hippocampal damage assessment clarified that almost no necrotic cells were observed in the CO-HbV50 group. Necrotic cells in the CO-HbV25 group were comparable to those found for the control group. In rats resuscitated from haemorrhagic shock, the hippocampal damage in the group using CO-HbV was the mildest. Administration of CO-HbV did not lead to marked hippocampal damage. Furthermore, CO-HbV was effective at preventing cerebral ischaemia-reperfusion injury after haemorrhagic shock.