All-in-one hydrogel patches with sprayed bFGF-loaded GelMA microspheres for infected wound healing studies.

The current wound healing process faces numerous challenges such as bacterial infection, inflammation and oxidative stress. However, wound dressings used to promote wound healing, are not well suited to meet the clinical needs. Hyaluronic acid (HA) not only has excellent water absorption and good biocompatibility but facilitates cell function and tissue regeneration. Dopamine, on the other hand, increases the overall viscosity of the hydrogel and possesses antioxidant property. Furthermore, chitosan exhibits outstanding performance in antimicrobial, anti-inflammatory and antioxidant activities. Basic fibroblast growth factor (bFGF) is conducive to cell proliferation and migration, vascular regeneration and wound healing. Hence, we designed an all-in-one hydrogel patch containing dopamine and chitosan framed by hyaluronic acid (HDC) with sprayed gelatin methacryloyl (GelMA) microspheres loaded with bFGF (HDC-bFGF). The hydrogel patch exhibits excellent adhesive, anti-inflammatory, antioxidant and antibacterial properties. In vitro experiments, the HDC-bFGF hydrogel patch not only showed significant inhibitory effect on RAW cell inflammation and Staphylococcus aureus (S. aureus) growth but also effectively scavenged free radicals, in addition to promoting the migration of 3 T3 cells. In the mice acute infected wound model, the HDC-bFGF hydrogel patch adhered to the wound surface greatly accelerated the healing process via its anti-inflammatory and antioxidant activities, bacterial inhibition and pro-vascularization effects. Therefore, the multifunctional HDC-bFGF hydrogel patch holds great promise for clinical application.

Ultrasmall polyvinylpyrrolidone-modified iridium nanoparticles with antioxidant and anti-inflammatory activity for acute pancreatitis alleviation.

Acute pancreatitis (AP) is a common and serious acute inflammatory disease with high severity rate and mortality. Inflammation and oxidative stress play an extremely important role in the development of AP disease. Polyvinylpyrrolidone-modified iridium nanoparticles (IrNP-PVP) have multienzyme mimetic activity, and the aim of this article is to discuss the therapeutic alleviative effects of the ultrasmall nanozymes IrNP-PVP on AP through their antioxidant and anti-inflammatory effects. IrNP-PVP were proved to inhibit inflammation and scavenge reactive oxygen species (ROS) at the cellular level. The synthetic IrNP-PVP exhibit remarkable antioxidant and anti-inflammatory activities in the prevention and treatment of AP mice by establishing murine AP model, which can reduce the oxidative stress and inflammatory response. The results of this article indicated that the ultrasmall nanozymes IrNP-PVP effectively alleviate AP via scavenging ROS as well as suppressing inflammation both in vivo and in vitro, which might provide enormous promise for the AP management.

Piperine alleviates acute pancreatitis: A possible role for FAM134B and CCPG1 dependent ER-phagy.

BACKGROUND: Acute pancreatitis was a common acute abdominal disease characterized by pancreatic acinar cell death and inflammation. Endoplasmic reticulum autophagy (ER-phagy) coud maintain cell homeostasis by degrading redundant and disordered endoplasmic reticulum and FAM134B and CCPG1 was main ER-phagy receptors. As a natural alkaloid, piperin is found in black pepper and has anti-inflammatory properties, whose effect on ER-phagy in pancreatitis has not been studied. PURPOSE: The objective of this study was to demonstrate the pivotal role of FAM134B and CCPG1 dependent ER-phagy for alleviating acute pancreatitis and explore the molecular mechanism of piperine in alleviating acute pancreatitis. METHOD: In this study we investigated the role of ER-phagy in acute pancreatitis and whether piperine could alleviate pancreatitis through ER-phagy regulation. We first detected endoplasmic reticulum stress (ER-stress) and ER-phagy in different degrees of acute pancreatitis. Then we used ER-stress and autophagy regulators to explore the relationship between ER-stress and ER-phagy in acute pancreatitis and their regulation of cell death. Through using FAM134B-/- and CCPG1-/-, we investigated the mechanism of piperine in the treatment of acute pancreatitis. RESULTS: In this study, we confirmed that with the progression of acute pancreatitis, the pancreatic endoplasmic reticulum stress increased continuously, but the ER-phagy increased first and then was inhibited. Meanwhile, in acute pancreatitis, ER-stress and ER-phagy interacted: endoplasmic reticulum stress can induce ER-phagy, but serious ER-stress would inhibit ER-phagy; and ER-phagy could alleviate ER-stress. Next, we found that piperine reduced ER-stress by enhancing FAM134B and CCPG1 dependent ER-phagy, thereby alleviating pancreatic injury. CONCLUSION: Impaired ER-phagy was both a cause and a consequence of ER-stress in AP mice, which contributed to the transition from AP to SAP. Piperine targeting ER-phagy provided a new insight into the pharmacological mechanism of piperine in treating AP.