Lili Dai,Yi Geng,Xiaofeng Ding,Zhikun Zhang,Chenhuan Lai,Daihui Zhang,Changlei Xia,Yongxian Lai
Hydrogels are widely recognized for their excellent flexibility and biocompatibility, making them promising materials for skin regeneration and wound care. However, the practical application of traditional hydrogels is limited by their inadequate mechanical strength and poor adhesive properties, hindering their effectiveness in wound healing. In this study, we designed a cellulose-based composite hydrogel, which overcomes these limitations by combining cellulose dialdehyde (DAC), carboxymethyl chitosan (CMCS) and polymerizable acrylamide (AM). The hydrogel features a double network structure: a dynamic chemical bonding network via a Schiff base reaction and a covalent bonding network formed through free radical polymerization. The resulting hydrogel exhibited remarkable mechanical properties, including tensile strength (>400 kPa), stretchability (>1400 %), toughness (>2900 kJ m −3 ), and good self-adhesion to skin (2.7 kPa). Additionally, it demonstrated excellent biocompatibility and significantly accelerated wound healing in a mouse model of full-thickness skin defects. The synthesized hydrogel represents a promising advancement in the development of wound care materials. Its enhanced mechanical strength, self-adhesion, and biocompatibility make it a strong candidate for clinical applications in skin regeneration and wound therapy, addressing critical gaps in the current hydrogel-based wound care technologies.
Bo Zou,Yue Fu,Chaofan Cao,Dianzhu Pan,Wei Wang,Lingfei Kong
Allergic asthma is a common airway inflammatory disorder with increasing morbidity and mortality worldwide. Gentiopicroside (GPS) is a secoiridoid glycoside compound that exhibits anti-inflammatory property. However, the effect of GPS on allergic asthma has not been reported yet. In this study, we investigated the role of GPS in a mouse model of ovalbumin (OVA)-induced allergic asthma and explored its potential mechanism. Mice were sensitized with OVA and gavaged with 20, 40, or 80 mg/kg GPS. Administration of GPS decreased lung wet-to-dry weight ratio. Histological analysis of H&E and PAS staining showed that GPS treatment alleviated inflammatory cell infiltration and goblet cell hyperplasia in lung tissue of OVA-sensitized mice. Moreover, GPS inhibited the recruitment of inflammatory cells including total cells, macrophages, eosinophils , lymphocytes and neutrophils and the secretion of T helper type 2 (Th2) cytokines (interleukin (IL)-4, IL-5 and IL-13) in bronchoalveolar lavage fluid (BALF) of OVA-sensitized mice in a dose dependent manner. The levels of OVA-specific immunoglobulin E (IgE) and pro-inflammatory tumor necrosis factor (TNF)-α were also attenuated by GPS treatment. Interestingly, GPS upregulated the expression of silent information regulator 1 (SIRT1) while downregulated the expression of acetyl-nuclear factor kappa B (NF-κB) p65 in lung tissue of OVA-sensitized mice. Furthermore, treatment with an SIRT1 inhibitor (EX-527) partially abolished the inhibitory effect of GPS on OVA-induced airway inflammation, suggesting that the anti-inflammation of GPS might be achieved through regulating SIRT1/NF-κB p65 signaling pathway . These findings indicate that GPS might be a novel drug candidate in the treatment of allergic asthma.
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