Introduction This study aimed to determine the relationship between Systemic Immune-Inflammation Index (SII) and muscle strength in patients with CKD.Methods This cross-sectional study examined adults with CKD using data from the National Health and Nutrition Examination Survey (2011-2014). The SII was calculated as: platelet count & times; neutrophil count/lymphocyte count. Muscle strength was determined from measurements of handgrip strength. Multivariate logistic regression and additional methods were used to assess the relationship between SII and muscle strength.Results We examined 1620 patients with CKD (mean age: 61.4 years; 47% male). The overall prevalence of low muscle strength was 12.04%, and curve fitting indicated a positive, linear relationship between SII and low muscle strength. However, multivariate logistic regression analysis indicated that this relationship was not significant after adjustment for multiple confounders (odds ratio: 1.01, 95% CI: 0.99-1.02). These results were robust, and subgroup analyses showed no interactions.Discussion Inflammation, malnutrition, and chronic comorbidities can affect muscle metabolism in CKD patients. The relationship between SII and low muscle strength is complex and variable. Although SII reflects systemic immune activation, it is less capable than markers, such as IL-6 and CRP, in directly capturing tissue-level inflammation that leads to muscle atrophy.Conclusion There was no significant association between SII and low muscle strength in patients with CKD, even after adjustment for nutritional status, comorbidities, and renal function. Although previous studies showed that CKD patients had increased inflammatory responses and decreased muscle strength, our results suggest underlying complexities may confound this relationship.
Introduction Diabetes mellitus can be complicated by a variety of ocular diseases, among which the postoperative complications of diabetic cataract (DC) are significantly higher than those of non-DC patients. Therefore, finding drugs with natural active ingredients is an urgent challenge in the prevention and treatment of DC. Discovering the potential molecular mechanism of celosiae semen (CS) for the treatment of DC and providing new ideas and programs for the treatment and prevention of DC.Methods In this study, network pharmacology, molecular docking, and molecular dynamics simulations were utilized to predict the binding and functional enrichment of the main active ingredients of CS with DC-related targets, and to explore the potential pathways and mechanisms of CS for the treatment of DC.Results Through database searching and screening, a total of 45 potential targets of CS for the treatment of DC were identified, functionally enriched, and a protein-protein interaction network was constructed, and the key target, SRC, was finally found. The results of molecular docking and molecular dynamics simulation showed that the main active ingredient of CS, stigmasterol, could bind stably to the key target SRC protein.Discussion This study not only elucidates the phyto-pharmacological basis of CS in DC management but also provides a framework for developing natural product-derived targeted therapies against diabetic ocular complications. The integration of modern genomics and computational chemistry to deconstruct the therapeutic effects of traditional Chinese herbal medicines has great clinical significance in expanding the scope of traditional Chinese medicines for the treatment of DC and promoting precision targeting. However, this requires verification through basic experiments.Conclusion These computational findings suggest that CS may exert its anti-cataract effects through the multi-target modulation of diabetic metabolic pathways and SRC-mediated signaling cascades.
Introduction: This study employed combined transcriptomics and metabolomics analyses as well as experimental verification methods to comprehensively elucidate the molecular mechanism of ginsenoside Rb1 in preventing and treating dyslipidemia. Methods: First, a hyperlipidemia model was established using SPF-grade male SD rats, followed by an integrated analysis of metabolomics and transcriptomics. Subsequently, the target genes and metabolites identified through the multi-omics analysis were validated using experiments such as lipid assays, hematoxylin-eosin (HE) staining, Oil Red O staining, enzyme-linked immunosorbent assay (ELISA), quantitative real-time polymerase chain reaction (qRT-PCR), and Western blot analysis. Results: Metabolomic analysis revealed that 14 metabolites in the Rb1 group underwent alterations, involving pathways such as glycosylphosphatidylinositol (GPI) anchor biosynthesis, sphingolipid metabolism, and arachidonic acid metabolism. By integrating transcriptomic and metabolomic data, we identified 55 genes, including glucokinase (GCK) and phosphoglycerate mutase 1 (PGAM1), which are involved in glycolysis-related metabolic pathways and the regulation of glycolytic processes. Experimental results demonstrated that, compared with the model group, Rb1 administration significantly reduced the levels of glycolytic pathway enzymes, including GCK, PGAM1, GPI, PFKL, PGK, and LDHD, as well as associated metabolites. Simultaneously, the level of pyruvate carboxylase (ACC), a key enzyme in fatty acid synthesis, was also markedly decreased. Discussion: This study provides significant insights into research on dyslipidemia and offers new strategies and approaches for its clinical prevention and management. Conclusion: This suggests that Rb1 may affect fatty acid synthesis through the glycolytic pathway, thereby influencing dyslipidemia.
Introduction: Oxidative stress-induced osteoblast dysfunction is an important event in osteoporosis (OP). Jiawei Duhuo Jisheng Mixture (JDJM) is clinically used for bone-related disorders, but its molecular basis in OP remains unclear. This study explored OP-related candidate targets of JDJM and evaluated its cytoprotective effects in a hydrogen peroxide (H2O2)-induced primary osteoblast injury model. Methods: Candidate JDJM targets were predicted from its identified constituents and intersected with OP-related genes. The study integrated network-based and enrichment analyses with single-cell mapping, followed by molecular docking and molecular dynamics simulation. An H2O2-induced primary osteoblast injury model was used for experimental validation. Results: A total of 210 shared targets were identified. Network pharmacology and enrichment analyses implicated JDJM in the regulation of oxidative stress, inflammatory responses, extracellular matrix remodelling, osteogenesis and apoptosis, primarily through the MAPK, JAK–STAT and PI3K–Akt signalling pathways. Single-cell transcriptomic analysis further localized these candidate targets to osteogenic, stromal, vascular, and inflammatory cell populations. Molecular docking and dynamics simulations predicted stable interactions between representative JDJM-derived compounds and selected protein targets. In H2O2-injured primary osteoblasts, JDJM significantly reduced mean DCF fluorescence intensity, increased the alkaline phosphatase (ALP)-positive area and Alizarin Red S absorbance, and partially restored osteocalcin/bone Gla protein (OCN/BGP) protein and Bglap mRNA expression.JDJM was also associated with decreased total JAK1, STAT3, MAPK3, MMP9, and Bad expression and partial restoration of ESR1 expression. Discussion: JDJM attenuated H2O2-induced oxidative injury and osteogenic dysfunction in primary osteoblasts, accompanied by changes in JAK1, STAT3, MAPK3, MMP9, ESR1, and Bad expression. These results support a multi-target cytoprotective effect of JDJM under oxidative-stress conditions, although direct regulation of the corresponding signaling pathways remains to be confirmed. Conclusion: JDJM attenuated H2O2-induced oxidative injury and partially restored osteogenic function in primary osteoblasts, accompanied by coordinated expression changes in JAK1, STAT3, MAPK3, MMP9, ESR1, and Bad. These findings support a multi-target protective effect of JDJM against oxidative stress-related osteoblast dysfunction.
Background/Objective: Krüppel-Like Factor 14 (KLF14) polymorphism has been investigated as a potential genetic risk factor for type 2 diabetes mellitus (T2DM). This study aimed to evaluate the association between KLF14 rs4731702 (C/T) polymorphism and T2DM susceptibility in Egyptians. Methods: A case–control study was conducted on 100 patients with T2DM and 100 healthy controls. Genotyping of KLF14 rs4731702 (C/T) was performed using restriction fragment length polymorphism polymerase chain reaction (RFLP-PCR). Clinical and biochemical parameters were compared among different genotypes. Results: The CT and TT genotypes were significantly more frequent in diabetic patients (40% and 30%, respectively) than in controls (15% and 20%, respectively) (p<0.001). Subjects carrying CT and TT genotypes showed significantly higher fasting blood glucose, HbA1c, total cholesterol, and triglyceride levels than those carrying the CC genotype. Discussion: These findings suggest a possible association between the T allele and metabolic abnormalities associated with T2DM. Conclusion: KLF14 rs4731702 (C/T) polymorphism is significantly associated with susceptibility to T2DM in the Egyptian population. The increased prevalence of CT and TT genotypes, along with their association with hyperglycemia and dyslipidemia, suggests that the T allele may contribute to metabolic disturbances and disease development. Further large-scale studies are needed to confirm these findings and clarify the underlying mechanisms.
