Scarless Healing of Injured Vocal Folds Using an Injectable Hyaluronic Acid-Waterborne Polyurethane Hybrid Hydrogel to Tune Inflammation and Collagen Deposition.

Vocal fold (VF) scarring results from injury to the unique layered structure and is one of the main reasons for long-lasting dysphonia. A minimally invasive procedure with injectable hydrogels is a promising method for therapy. However, current surgical techniques or standard injectable fillers do not yield satisfactory outcomes. In this work, an injectable hybrid hydrogel consisting of oxide hyaluronic acid and hydrazide-modified waterborne polyurethane emulsion was injected precisely into the injury site and cross-linked in situ by a dynamic hydrazone bond. The prepared hydrogel displays excellent injectability and self-healing ability, showing favorable biocompatibility and biodegradability to facilitate endogenous newborn cell migration and growth for tissue regeneration. With the aim of evaluating the antifibrosis and regeneration capacity of the hybrid hydrogel in the VF scarring model, the morphology and vibration characteristics of VFs, inflammatory response, and healing status were collected. The hybrid hydrogel can decrease the inflammation and increase the ratio of collagen III/collagen I to heal damaged scar-free tissue. Fascinatingly, the mucosal wave oscillations of healing VF by injecting the hybrid hydrogel were vibrated like the normal VF, achieving functional restoration. This work highlights the utility of hybrid hydrogels consisting of synthetic biodegradable waterborne polyurethane emulsions and natural hyaluronic acid as promising biomaterials for scarless healing of damaged VFs.

Luteolin promotes long-term potentiation and improves cognitive functions in chronic cerebral hypoperfused rats.

Processes of synaptic plasticity, such as long-term potentiation (LTP), has been considered a cellular correlate of learning and memory and many neurological disorders accompanied by cognitive deficits exhibit abnormal synaptic function. This emerging concept is exemplified by Alzheimer's disease. Mounting evidence suggests that Alzheimer's disease begins with subtle alterations of hippocampal synaptic efficacy prior to frank neuronal degeneration, which make it critical to identify LTP enhancers to slow down or stop the progression of Alzheimer's disease. In this study, we found flavonoid luteolin could enhance basal synaptic transmission and facilitate the induction of LTP by high frequency stimulation in the dental gyrus of rat hippocampus. Furthermore, we investigated the effects of luteolin on chronic cerebral hypoperfusion-induced spatial learning dysfunction and LTP impairment in rat. The results showed chronic cerebral hypoperfusion produced by 2-vessel occlusion significantly impaired spatial learning and memory, and luteolin reversed the learning and memory deficit. 2-vessel occlusion resulted in dramatic inhibition of LTP formation in the hippocampus and luteolin significantly rescued the LTP impairment. These results demonstrate that luteolin not only directly modulates LTP formation, but also protects synapses from the detrimental effects of chronic cerebral hypoperfusion on LTP formation, which may contribute to the protective effects of luteolin on learning and memory. By immunoblotting, we found the effects of luteolin on LTP and memory may due to the activation of cAMP response element-binding protein (CREB). Therefore, flavonoid luteolin shows great potential as a novel treatment agent for protecting synaptic function and enhancing memory in neurodegenerative disorders.