Ulcerative Colitis (UC) is a chronic disease, in the progression of which an immune overreaction may play an important role. IL-22 is a member of the IL-10 superfamily of cytokines and is pleiotropic in immune regulation and inflammatory responses. IL-22 can produce protective effects, promote wound healing and tissue regeneration, while it can also induce inflammatory reactions when it is chronically overexpressed. Extensive literatures reported that IL-22 played an essential role in the pathogenic development of UC. IL-22 participates in the whole disease process of UC involving signaling pathways, gene expression regulation, and intestinal flora imbalance, making IL-22 a possible candidate for the treatment of UC. In this paper, the latest knowledge to further elucidate the role of IL-22 in UC was summarized and analyzed.

The intestinal barrier is a complex configuration that defends against external assaults and maintains intestinal health. Disruption of barrier function can lead to intestinal inflammation and various diseases. Mucins are the primary structural components of the intestinal barrier, and their extensive glycosylation is critical for their protective function. Mucin glycans enhance the physicochemical integrity of the mucus barrier, protect against enzymatic degradation, modulate host immune responses, and shape the gut microbiota by providing adhesion sites and selective nutrient sources. While proper glycosylation maintains barrier integrity, supports a balanced microbial ecosystem, and limits unnecessary immune activation, its disruption leads to compromised barrier function, microbial dysbiosis, increased intestinal permeability, and ultimately contributes to the development of chronic colitis and colorectal cancer. Therefore, mucin glycosylation plays a crucial role in preserving intestinal barrier integrity and preventing colonic diseases. This review summarizes the classifications and structural features of intestinal mucin glycosylation, elucidates their roles in maintaining barrier function and their pathological alterations in intestinal disorders, and highlights the implications of mucin glycosylation for precision diagnosis and targeted therapy of intestinal diseases.

Introduction: Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by cognitive decline; recent studies suggest that neuronal ferroptosis plays a key role in its pathogenesis. Danggui Shaoyao San (DSS), a traditional Chinese medicine formula, has shown demonstrated neuroprotective effects, but its precise mechanisms in AD treatment remain unclear. This study aims to investigate the mechanism of DSS in treating AD by inhibiting neuronal ferroptosis, explore whether DSS alleviates AD by suppressing neuronal ferroptosis via the AMPK/Sp1/ACSL4 pathway.Methods: Chemical composition of DSS was identified by LC-MS/MS, followed by network pharmacology to predict targets and pathways. Molecular docking assessed binding affinities between DSS compounds and key proteins (AMPK, Sp1, ACSL4). In vivo experiments on APP/PS1 mice evaluated DSS effects on cognitive function, oxidative stress markers, lipid peroxidation, and ferroptosis-related proteins.Results: Network pharmacology analysis suggested that DSS regulates lipid metabolism and inhibits neuronal ferroptosis via the AMPK pathway. Molecular docking revealed strong binding affinities between DSS compounds and AMPK downstream proteins, Sp1 and ACSL4. In vivo experiments showed that DSS improved cognitive function, enhanced antioxidant capacity, reduced lipid peroxide accumulation, and decreased Fe²⁺ content in brain tissue. Furthermore, DSS increased the expression of FTH, p-AMPK, and GPX4 while decreasing Sp1 and ACSL4 levels, thereby inhibiting ferroptosis.Conclusion: DSS alleviates AD symptoms by suppressing neuronal ferroptosis via the AMPK/Sp1/ACSL4 axis, representing a novel lipid metabolism-targeted therapeutic strategy.

Acute pancreatitis (AP) is a common critical disease in clinical practice, characterized by acute onset, rapid progression, aggressive conditions, and high lethality. Pancreatic acinar cell death is a central event in the pathological process of AP and a key factor in determining the extent of local or systemic inflammatory injury and overall prognosis. Programmed cell death (PCD) is a form of active cell death regulated by multiple genes, including apoptosis, autophagy, ferroptosis, pyroptosis, and necroptosis. PCD plays a critical role in eliminating unwanted organisms and damaged cells, which is of great significance. Numerous studies have demonstrated a strong association between various forms of PCD and AP, and targeted interventions in PCD signaling pathways and key targets can influence the progression of AP. Furthermore, existing research indicates that natural products sourced from plants, fruits, and vegetables exhibit considerable potential in targeting and regulating PCD for the treatment of AP. Therefore, this paper focuses on summarizing the common types of PCD in AP and discusses the specific signaling pathways and key targets reported in the treatment of AP using natural products. This review aims to provide a reference for natural products in guiding AP treatment and to lay the foundation for developing new drugs to effectively prevent and manage AP.

Pulmonary fibrosis (PF) is a disease characterised by diffuse nonspecific alveolar inflammation with interstitial fibrosis, which clinically manifests as dyspnoea and a significant decline in lung function. Many studies have shown that the epithelial–mesenchymal transition (EMT) plays a pivotal role in the pathogenesis of pulmonary fibrosis. Based on our previous findings, hypericin (Hyp) can effectively inhibit the process of the EMT to attenuate lung fibrosis. Therefore, a series of hyperoside derivatives were synthesised via modifying the structure of hyperoside, and subsequently evaluated for A549 cytotoxicity. Among these, the pre-screening of eight derivatives inhibits the EMT. In this study, we evaluated the efficacy of Z6, the most promising hyperoside derivative, in reversing TGF-β1-induced EMTs and inhibiting the EMT-associated migration of A549 cells. After the treatment of A549 cells with Z6 for 48 h, RT-qPCR and Western blot results showed that Z6 inhibited TGF-β1-induced EMTs in epithelial cells by supressing morphological changes in A549 cells, up-regulating E-cadherin (p < 0.01, p < 0.001), and down-regulating Vimentin (p < 0.01, p < 0.001). This treatment significantly reduced the mobility of transforming growth factor β1 (TGF-β1)-stimulated cells (p < 0.001) as assessed by wound closure, while increasing the adhesion rate of A549 cells (p < 0.001). In conclusion, our results suggest that hyperoside derivatives, especially compound Z6, are promising as potential lead compounds for treating pulmonary fibrosis, and therefore deserve further investigation.