Stem Cell Research & Therapy•2024•DOI: 10.1186/s13287-024-03856-4
Mesenchymal stem cells (MSCs) therapy is a highly researched treatment that has the potential to promote immunomodulation and anti-inflammatory, anti-apoptotic, and antimicrobial activities. It is thought that it can enhance internal organ function, reverse tissue remodeling, and achieve significant organ repair and regeneration. However, the limited infusion, survival, and engraftment of transplanted MSCs diminish the effectiveness of MSCs-based therapy. Consequently, various preconditioning methods have emerged as strategies for enhancing the therapeutic effects of MSCs and achieving better clinical outcomes. In particular, the use of natural small molecule compounds (NSMs) as a pretreatment strategy is discussed in this narrative review, with a focus on their roles in regulating MSCs for injury repair in vital internal organs. Additionally, the discussion focuses on the future directions and challenges of transforming mesenchymal stem cell research into clinical applications.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025070
Schisandrin A (SchA), a bioactive lignan that was isolated from the dried fruit of Schisandra chinensis, has attracted much attention because of its diverse spectrum of pharmacological effects. The aim of this study is to clarify the function of SchA in diabetes-related fear memory impairment and its molecular mechanisms. Rats are randomly assigned to 4 groups: the control group (Con group), the DM group, the DM + SchA group, and the Con + SchA group. The results demonstrate that SchA treatment improves insulin sensitivity, reduces blood glucose, and significantly reduces memory impairment. SchA treatment also prevents histological damage, enhances synaptic protein production, and significantly decreases Aβ42 formation in the diabetic prefrontal cortex. Further research reveals that SchA therapy decreases microglial activation and the expression levels of variables linked to inflammation while increasing the phosphorylation of proteins implicated in the insulin resistance signaling pathway. Furthermore, in the prefrontal cortex of diabetic rats, SchA decreases ferroptosis by increasing the protein expressions of GPX4, SLC7A11, Nrf2, HO-1, and SIRT1. Overall, our findings suggest that SchA may lessen diabetes-associated fear memory impairment symptoms by, most likely, lowering ferroptosis and inflammatory responses in the prefrontal brain of diabetic rats. SchA may be a useful therapy for diabetes, including memory impairment.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025075
Chondrocytes store lipids in the form of lipid droplets (LDs) and maintain cartilage lipid metabolic homeostasis by consuming or regenerating LDs. This modulation is largely mediated by a series of biochemical factors. Fibroblast growth factor 8 (FGF8) is one of the most important factors involved in the proliferation, differentiation, and migration of chondrocytes and has attracted increasing attention in the physiology and pathology of cartilage. However, the effect of FGF8 on LD accumulation in chondrocytes remains unclear. This study aims to elucidate the role of FGF8 in LDs and explore the underlying biomechanism involved. The results reveal that FGF8 promotes LD accumulation in chondrocytes by upregulating perilipin1 (Plin1) expression. FGF8 activates the cytoplasmic p-p38 signaling pathway via fibroblast growth factor receptor 1 (FGFR1) to increase LD accumulation in chondrocytes. Subsequent experiments with siRNAs and specific inhibitors further confirm the importance of the FGFR1/p38 axis for LD accumulation in chondrocytes exposed to FGF8. The results increase our understanding of the role of FGF8 in the lipid metabolic homeostasis of chondrocytes and provide insights into the physiology and pathology of cartilage.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025070
Diabetes mellitus (DM) is a metabolic and endocrine disorder with a projected global prevalence of 783 million by 2045. Individuals with type 2 diabetes face a 20–60% elevated risk of cognitive dysfunction, yet therapeutic options remain limited. This study investigates the efficacy of Schisandrin A (SchA), a bioactive lignan from Schisandra chinensis, in a streptozotocin-induced diabetic rat model. Rats were randomized into control, DM, DM+SchA, and Con+SchA groups. SchA treatment improved insulin sensitivity, reduced blood glucose, and significantly attenuated fear memory impairment. Histological analysis revealed decreased prefrontal cortex damage, enhanced synaptic protein expression, and reduced Aβ42 formation. Mechanistically, SchA suppressed microglial activation and inflammatory markers while increasing phosphorylation of insulin resistance pathway proteins. Furthermore, SchA mitigated ferroptosis by upregulating GPX4, SLC7A11, Nrf2, HO-1, and SIRT1 in the diabetic prefrontal cortex. These findings suggest that SchA alleviates diabetes-associated memory impairment by concurrently reducing neuroinflammation and ferroptosis, positioning SchA as a potential therapeutic agent for diabetes-related cognitive decline.