Polysaccharides, also known as glycans, are biological macromolecules consisting of many monosaccharide units. Alongside proteins, nucleic acids, and lipids, they constitute the four fundamental substances crucial for life activities and essential for the growth and development of living organisms. As natural products with inherent biological activity, polysaccharides are widely available, nontoxic, and possess numerous functional properties, holding immense potential for advancement in food, medicine, and cosmetics. Furthermore, the exploration of polysaccharide‐based drugs, as an alternative to conventional therapies, emerges as a promising avenue for addressing future disease challenges. This article comprehensively reviews the sources, structural characteristics, synthesis, degradation, functions, and applications of polysaccharides. The potential of polysaccharides for pharmacological applications, in antitumor, antiaging, antioxidant, hypoglycemic, anti‐inflammatory, antiviral, and anticoagulant properties, is summarized. Additionally, the role of polysaccharides in environmental protection is discussed. It is anticipated that this review will offer innovative strategic insights, serving as a theoretical foundation and inspiration for the subsequent research on polysaccharides in healthcare.

Recent studies suggested that radiation exposure causes local and systemic inflammatory responses and induces cell and tissue damage. We have reported that IL-18 plays an important role in radiation-induced injury. Here, we demonstrate that IL-18 binding protein (IL-18BP), a natural antagonist of IL-18, was significantly increased (1.7–63 fold) in mouse serum on day 1 after 0.5–10 Gy TBI. However, this high level of IL-18BP was not sufficient to neutralize the active IL-18 in irradiated mice, resulting in a radiation dose-dependent free IL-18 increase in these mice’s serum which led to pathological alterations to the irradiated cells and tissues and finally caused animal death. Administration of recombinant human (rh) IL-18BP (1.5 mg/kg) with single (24, 48 or 72 h post-TBI) or double doses (48 h and 5 days post-TBI) subcutaneous (SC) injection increased 30-day survival of CD2F1 mice after 9 Gy TBI 12.5–25% compared with the vehicle control treated group, respectively. Furthermore, the mitigative effects of rhIL-18BP included balancing the ratio of IL-18/IL-18BP and decreasing the free IL-18 levels in irradiated mouse serum and significantly increasing blood cell counts, BM hematopoietic cellularity and stem and progenitor cell clonogenicity in mouse BM. Furthermore, IL-18BP treatment inhibited the IL-18 downstream target interferon (IFN)-γ expression in mouse BM, decreased reactive oxygen species (ROS) level in the irradiated mouse heart tissues, attenuated the stress responsive factor GDF-15 (growth differentiation factor-15) and increased the intestine protector citrulline level in total body irradiated mouse serum, implicating that IL-18BP may protect multiple organs from radiation-induced inflammation and oxidative stress. Our data suggest that IL-18 plays a key role in radiation-induced cell and tissue damage and dysfunction; and for the first time demonstrated that IL-18BP counters IL-18 activation and therefore may mitigate/treat radiation-induced multiple organ injuries and increase animal survival with a wider therapeutic window from 24 h and beyond after lethal doses of radiation exposure.

Leukemia stem cells (LSCs) are recognized as the root cause of leukemia initiation, relapse, and drug resistance. Lipid species are highly abundant and essential component of human cells, which often changed in tumor microenvironment. LSCs remodel lipid metabolism to sustain the stemness. However, there is no useful lipid related biomarker has been approved for clinical practice in AML prediction and treatment. Here, we constructed and verified fatty acid metabolism-related risk score (LFMRS) model based on TCGA database via a series of bioinformatics analysis, univariate COX regression analysis, and multivariate COX regression analysis, and found that the LFMRS model could be an independent risk factor and predict the survival time of AML patients combined with age. Moreover, we revealed that Galectin-1 (LGALS1, the key gene of LFMRS) was highly expressed in LSCs and associated with poor prognosis of AML patients, and LGALS1 repression inhibited AML cell and LSC proliferation, enhanced cell apoptosis, and decreased lipid accumulation in vitro. LGALS1 repression curbed AML progression, lipid accumulation, and CD8⁺ T and NK cell counts in vivo. Our study sheds light on the roles of LFMRS (especially LGALS1) model in AML, and provides information that may help clinicians improve patient prognosis and develop personalized treatment regimens for AML.

Replication‐competent adenovirus (RCAd) has been used extensively in cancer gene therapy, and tumor‐selection is critical for the use of replication‐competent adenovirus. Here we investigated the anti‐tumor characterization of oncolytic virus, whose E1A gene is under the control of a renal cell carcinoma specific promoter – the G250 promoter. The constructed oncolytic virus G250‐Ki67 is armed with transgene of Ki67‐siRNA, and G250‐ZD55‐Ki67 also with E1B‐55 KD deleted. The tumor‐specific expression of E1A and Ki67 was demonstrated by Western blot and immunohistochemistry staining, and the tumor‐specific cytotoxicity was assessed by crystal violet staining and cell viability assays. The G250‐Ki67 and G250‐ZD55‐Ki67 adenoviruses could express E1A protein in 786‐O and OSRC cell lines but not in ACHN and HK‐2 cell lines. The expression of Ki67 gene in 786‐O and OSRC cell lines were suppressed by these adenoviruses. The cytotoxic effects induced by G250‐ZD55‐Ki67 and G250‐Ki67 were more obvious on the 786‐O cell lines than on the OSRC cell lines. Each group of adenoviruses could inhibit the proliferation of the 786‐O cells and OSRC cells. However, the effects induced by G250‐ZD55‐Ki67 and G250‐Ki67 on 786‐O cells were stronger than on OSRC cells. Moreover, G250‐ZD55‐Ki67 had enhanced antitumor activities in these renal cancer cells compared with G250‐Ki67. G250 promoter‐derived CRAds carrying Ki67‐siRNA could highly amplify and express Ki67‐siRNA in renal cancer cells with expression of G250 antigen, inhibit renal cancer cells proliferation and induce apoptosis. These results demonstrated that the G250‐specific oncolytic adenovirus expressing Ki67‐siRNA is applicable for human renal clear cell cancer therapy.