Search Results (5,415)

Objectives: In localized upper-tract urothelial carcinoma (UTUC), radical nephroureterectomy (RNU) represents the surgical gold standard, but kidney-sparing surgery (KSS) offers an alternative. The surgical perspective, including complications, remains understudied in this context. This study aimed to compare KSS and RNU, assess kidney function and survival, and identify the surgical risk factors. Methods: This retrospective analysis included UTUC patients undergoing KSS (n = 46) or RNU (n = 46) at a single center from 2016 to April 2024, matched by propensity scores. The primary endpoint was Clavien–Dindo complications. Other endpoints included Days Alive and Out of the Hospital within 30 days (DAOH30), changes in the eGFR, cancer-specific survival (CSS), and disease-free survival (DFS). A UTUC Surgery Risk Score was developed to identify the surgical risk factors for severe complications. Results: KSS was significantly associated with higher rates of Clavien–Dindo grades ≥ 3 (KSS: 14; RNU: 3). DAOH30 was significantly longer following RNU. The UTUC Surgery Risk Score, based on a non-endoscopic KSS approach, an ASA score ≥ 3, and preoperative creatinine > 0.9 mg/dL, was significantly associated with overall and severe complications and DAOH30 (both p < 0.001). KSS showed significantly better early postoperative eGFR preservation (+0.55 mL/min vs. −4.3 mL/min for RNU, p = 0.015). No significant differences were observed in the median CSS or DFS between the groups. Conclusions: KSS is associated with a higher rate of certain postoperative complications, but offers superior kidney function preservation, with comparable oncological outcomes to RNU. The novel UTUC Surgery Risk Score can aid in patient counseling and personalized decision-making prior to surgery. Full article

Background: Chronic kidney disease (CKD) is largely driven by inflammation. Mesenchymal stem cells (MSCs) show therapeutic potential; however, their efficacy across CKD etiologies remains unclear. Methods: Comprehensive searches were conducted in PubMed, Cochrane, ScienceDirect, Scopus and Google Scholar. Effect sizes for inflammation and renal function outcomes were meta-analyzed. Results: Of 2514 studies screened, 52 met inclusion criteria (49 animal studies, 3 randomized controlled trials). In animal models, MSCs significantly reduced interleukin-6 (mean difference [MD] = −155.80; 95% CI: −249.10, −62.51; p = 0.001) and tumor necrosis factor-α (TNF-α) (MD = −35.53; 95% CI: −52.75, −18.30; p < 0.0001). In patients, TNF-α reduction was not significant (MD = −0.74; 95% CI: −2.20, 0.73; p = 0.32). Serum creatinine decreased in animals (MD = −0.38; 95% CI: −0.46, −0.29; p < 0.00001), but not in patients (MD = −0.59; 95% CI: −1.92, 0.74; p = 0.39). Blood urea nitrogen decreased in animals (MD = −19.27; 95% CI: −23.50, −15.04; p < 0.00001), and glomerular filtration rate improved (standardized MD = 1.83; 95% CI: 0.51, 3.15; p = 0.007), with no change in patients. Conclusion: MSCs improve inflammation and renal function in CKD animal models; however, evidence in patients remains inconclusive. Full article

Background: Acute kidney injury (AKI) in critically ill neonates is usually of pre-renal origin and, often, pharmacological treatment is not sufficient for resolution, requiring kidney replacement therapy (KRT). Due to the small body size and the unavailability of adequate devices for these patients, peritoneal dialysis (PD) appears to be the most easily achievable procedure. However, guidelines for PD management are lacking in this population. Objective: We aimed to report a single-center experience with preterm infants who underwent PD, describing the technical issues and the outcomes, and to review the existing literature. Methods: This retrospective study included preterm infants undergoing PD because of AKI unresponsive to pharmacological treatment. Data were compared to those available in the current literature. Results: Neonatal outcomes of twelve preterm infants were reported. PD was started before the onset of anuria in two oliguric patients, while it was started within 60 h of anuria in four patients, and between 72 and 144 h of anuria in the remaining six patients. One oliguric patient and one who started PD after 60 h of anuria had a complete recovery of kidney function with normalization of diuresis and renal function parameters. The other infants did not achieve complete resolution of AKI. The mortality rate was 91.7%, and even one of the two infants who had recovered kidney function later died due to an infectious complication. Conclusions: Our experience with a limited sample size did not allow us to obtain definitive conclusions. Our data and the current literature suggested that the prognosis is still negative, with a high mortality rate. Further research is needed to develop guidelines to optimize the management of preterm infants with AKI. Full article

Introduction: Tertiary hyperparathyroidism following kidney transplantation is a well-recognized complication in patients with pre-existing mineral imbalances due to chronic renal failure. Parathyroidectomy remains the only definitively curative option for tertiary hyperparathyroidism. The optimal timing of parathyroidectomy, before or after transplantation, is debated in the literature. This study aims to assess whether parathyroidectomy timing affects the successful resolution of tertiary hyperparathyroidism in patients with a functional kidney transplant. Methods: We conducted a systematic review and meta-analysis of the available literature collating the effect of pre- versus post-transplantation parathyroidectomy on the resolution of tertiary hyperparathyroidism. We compared the follow-up parathyroid hormone and calcium levels of patients subjected to either of these two approaches. Results: Three studies were identified, encompassing a total of 223 patients. The meta-analysis of available data yielded no statistically significant difference between pre- and post-kidney transplantation parathyroidectomy in terms of serum parathyroid hormone (SMD −0.19, 95% CI −0.92 to 0.55, p = 0.62) and calcium levels (SMD −0.75, 95% CI −2.30 to 0.80, p = 0.35). Conclusions: We demonstrated no significant difference between pre- and post-transplantation parathyroidectomy when it comes to the treatment of tertiary hyperparathyroidism. This meta-analysis is limited by the small number of studies included, reducing its statistical power. Therefore, additional studies are required to identify the optimal timing of intervention for the effective management of tertiary hyperparathyroidism in kidney transplant recipients. Full article

Background: Multi-organ failure (MOF) is a common complication of advanced heart failure (HF), significantly influencing patient prognosis. This study aimed to assess and compare the impact of orthotopic heart transplantation (HTx) and left ventricular assist device (LVAD) implantation on the severity of MOF, as measured by the model for end-stage liver disease excluding INR (MELD-XI) score. Methods: Data from 1 month before to 1 year after HTx or LVAD implantation were analysed. The MELD-XI score was calculated using average bilirubin and creatinine values. Comparative assessments of MELD-XI scores were performed within the HTx and LVAD groups at various time points pre- and post-procedure. Results: The analysis included 107 HTx patients and 30 LVAD patients. The median MELD-XI score 1 month pre-procedure was 11.7 (9.4–16.7) in all patients. There were no significant differences in MELD-XI scores between the groups at 3-, 6-, and 12-month follow-ups. However, a significant difference was observed 1 month post-procedure [HTx: 14.8 (9.4–17.7) vs. LVAD: 11.2 (7.3–14.9), p = 0.02]. In the LVAD group, a significant decrease in MELD-XI score was noted for 3 months post-procedure compared to 1 month pre-procedure (p < 0.001), whereas at 6- and 12-month follow-ups the score did not differ from pre-procedural scores. In the HTx group, significant decreases in MELD-XI scores were observed from 3 months, 6 months, and 1 year post-procedure compared to 1 month pre-procedure (p < 0.002). Conclusions: The MELD-XI scale reveals different MOF trajectories between HTx and LVAD recipients. Both interventions lead to early improvements in liver and kidney function, with sustained benefits in HTx patients, highlighting the distinct impacts on organ function. Full article

Nuclear factors of activated T cells (NFATs) are pivotal regulatory factors of immune responses, primarily by modulating T cell activity and regulating inflammatory cytokine gene transcription. The grass carp reovirus (GCRV) triggers a serious hemorrhagic condition, posing a significant threat to sustainable grass carp (Ctenopharyngodon idella) aquaculture. However, the precise function of NFAT in the host’s defense against GCRV infection is mostly undefined. This study comprehensively identified and characterized the NFAT genetic family in grass carp, cloned grass carp NFAT1 (CiNFAT1), and investigated its expression and function during GCRV infection. Eight NFAT genes encoding seventeen isoforms have been detected within the grass carp’s genomic sequence, distributed across six different chromosomes. Comparative analysis revealed homology with zebrafish NFATs. CiNFAT1 possesses a 2697 bp open reading frame, encoding 898 amino acids, and contains conserved Rel homology domain (RHD) and NFAT-homology (IPT) domains. Quantitative PCR (qPCR) revealed ubiquitous CiNFAT1 expression in healthy grass carp tissues, with the highest expression in gills and skin and the lowest in liver. Following GCRV challenge in vivo, CiNFAT1 expression in immune tissues (liver, spleen, kidney, gill, intestine) showed dynamic changes over time. In vitro experiments in CIK cells demonstrated that CiNFAT1 expression peaked at 12 h post-GCRV infection. Further functional studies revealed that overexpression of CiNFAT1 significantly reduced GCRV replication at 36 h post-infection. This reduction was accompanied by elevated expression of type I interferon (IFN-I) and interferon regulatory factor 7 (IRF7) at 24 and 36 h, respectively, as well as modulated IL-2, IL-8, and IL-10. Conversely, RNA interference-mediated knockdown of CiNFAT1 enhanced GCRV VP5 and VP7 mRNA levels and suppressed IL-2 and IL-8 expression. These results suggest that CiNFAT1 contributes to anti-GCRV immunity by promoting antiviral and inflammatory cytokine responses, thereby inhibiting viral replication. This study provides a foundational understanding of the NFAT genetic family in grass carp and highlights an important role of CiNFAT1 in mediating the body’s inherent defense mechanism against GCRV infection, offering insights for disease control strategies in aquaculture. Full article

The accumulation of blood toxins, including urea, uric acid, creatinine, bilirubin, p-cresyl sulfate, and indoxyl sulfate, poses severe health risks for patients with renal failure. Effective removal strategies are essential to mitigate complications associated with chronic kidney disease (CKD) and improve patient outcomes. Functional carbon-based materials, such as activated carbon (activated charcoal) and graphene oxide, have emerged as promising adsorbents due to their large surface area, adjustable porosity, and biocompatibility. This review comprehensively explores the latest advancements in carbon-based materials for blood purification across three key therapeutic modalities: (1) Hemoperfusion, where activated and modified carbonaceous materials enhance the adsorption of small-molecule and protein-bound toxins; (2) Hemodialysis, where functionalized carbon materials improve clearance rates and reduce treatment duration; and (3) Oral Therapeutics, where orally administered carbon adsorbents show potential in lowering systemic toxin levels in CKD patients. Furthermore, we present a comparative analysis of these approaches, highlighting their advantages, limitations, and future research directions for optimizing carbon-based detoxification strategies. The findings discussed in this review emphasize the significance of material engineering in advancing blood purification technologies. By enhancing the efficiency of toxin removal, carbon-based materials have the potential to revolutionize renal failure treatment, offering improved clinical outcomes and enhanced patient quality of life. Full article

Renocardiac syndrome type 4 (RCS4) is a common comorbid pathology, but the mechanisms of kidney dysfunction-induced cardiac remodeling and the involvement of cardiac progenitor cells (CPCs) in this process remain unclear. The aim of this study was to investigate the structural and functional changes in the cardiac muscle in RCS4 induced by unilateral ureteral obstruction (UUO) and the role of nestin⁺ CPCs in these. Heart function and localization of nestin⁺ cells in the myocardium were assessed using nestin-GFP transgenic mice subjected to UUO for 14 and 28 days. UUO resulted in cardiac hypertrophy, accompanied by an elongation of the QRS wave on the ECG, decreased expression of Cxcl1, Cxcl9, and Il1b, reduced the number of CD11b⁺ cells, and increased in titin isoform parameters, such as T1/MHC and TT/MHC ratios, without changes in fibrosis markers. The number of nestin⁺ cells increased in the myocardium with increased duration of UUO and displayed an SCA-1⁺TBX5⁺ phenotype, consistent with CPCs. Thus, cardiac pathology in RCS4 was manifested by cardiomyocyte hypertrophy with changes in the electrophysiological phenotype of the heart, not accompanied by fibrosis or inflammation. Nestin⁺ cardiac cells retained the CPC phenotype during UUO, and their number increased, which suggests their participation in regenerative processes in the heart. Full article

Sarcopenia is a prevalent and disabling complication of chronic kidney disease (CKD), associated with frailty, diminished quality of life, and increased morbidity and mortality. Despite its clinical significance, no pharmacological treatments are currently approved to address muscle wasting in this population. Glucagon-like peptide-1 receptor agonists (GLP-1RAs), widely used in the management of type 2 diabetes and obesity, have shown potential to support muscle mass and function through pleiotropic mechanisms. These include anti-inflammatory and antioxidant actions, improvements in insulin sensitivity and energy metabolism, and mitochondrial support. Given the high burden of sarcopenia in CKD and the frequent overlap with metabolic and cardiovascular comorbidities, GLP-1RAs may offer a novel therapeutic approach. This review examines the biological plausibility and emerging evidence supporting the role of GLP-1RAs in preserving muscle health in CKD, highlighting the need for targeted clinical trials and mechanistic investigations to establish their efficacy in this high-risk group. Full article

Acute kidney injury (AKI) is characterized by a sudden rise in serum creatinine levels, a reduction in urine output, or both. Despite its frequent occurrence in clinical settings, AKI remains poorly understood from a pathophysiological standpoint. As a result, management primarily relies on supportive care rather than targeted treatments. Emerging evidence underscores the pivotal role of oxidative stress in both the initiation and progression of AKI, thereby identifying it as a potential therapeutic target. This review aims to comprehensively examine the pharmacological effects and underlying mechanisms of apocynin (APO) in the context of AKI, with a particular focus on ischemia–reperfusion injury (IRI) and nephrotoxic-induced AKI. Experimental preclinical studies have consistently demonstrated that APO offers protective effects primarily through its inhibition of NADPH oxidase-mediated oxidative stress. In renal IRI and drug-induced nephrotoxicity models, APO has been shown to attenuate oxidative damage, reduce inflammatory responses, and preserve renal structure and function. These results suggest that it may serve as an effective treatment for reducing kidney damage caused by acute ischemia or exposure to nephrotoxic agents. Although the results are encouraging, further investigation is required to establish the optimal dosing strategy and treatment protocol, as well as to confirm the translational relevance of these findings in human clinical settings. Full article

Food allergy represents a prevalent immunological disorder, with current clinical management primarily emphasizing allergen avoidance and emergency pharmacological intervention. Eucommia ulmoides polysaccharides, the principal bioactive constituents of the traditional Chinese medicinal plant Eucommia ulmoides, have demonstrated anti-inflammatory and antioxidant properties; however, their specific effects on food allergies remain inadequately characterized. A total of thirty-six female BALB/c mice were randomly allocated into three groups (n = 12 per group): the control group (CON group, receiving saline treatment), the allergic model group (OVA group, subjected to ovalbumin sensitization), and the intervention group (OVA+PS group, undergoing OVA sensitization followed by Eucommia ulmoides polysaccharides administration via gavage). The anti-allergic efficacy of Eucommia ulmoides polysaccharides was comprehensively evaluated through clinical allergy symptom scoring, histological and pathological tissue analysis, real-time fluorescence quantitative PCR (qRT-PCR) for the assessment of key gene expression, and 16S rDNA sequencing. The findings indicated the following: (1) The allergy scores in the OVA+PS group were significantly lower than those in the OVA group (p < 0.01). Following OVA stimulation, the rectal temperature of mice in the OVA group decreased sharply, whereas the temperature decline in the OVA+PS group was more gradual compared to the model group. (2) The liver, kidney, spleen, and intestinal tissues of mice in the OVA+PS group exhibited normal morphology, consistent with the CON group, which suggests that Eucommia ulmoides polysaccharides effectively mitigates the local inflammatory response induced by food allergy. (3) The expression of NICD in the spleen of mice in the OVA+PS group was significantly higher than in the OVA group (p < 0.05), while the expression of the Hes1 gene was significantly elevated in the OVA group compared to both the CON and OVA+PS groups (p < 0.05). In the OVA group, the expression level of Gata-3 was significantly elevated compared to both the CON group and the OVA+PS group (p < 0.05). Similarly, the expression of STAT5 in the OVA group was markedly higher than in the other groups (p < 0.05). (4) Eucommia ulmoides polysaccharides were found to modulate the intestinal microbiota composition in allergic mice, notably increasing the expression abundance of Enterobacter, Oscillibacter, and Butyricicoccus, while decreasing the expression abundance of Clostridium sensu stricto 1 and Turicibacter. (5) There was a correlation between alterations in the intestinal microbiota of mice and the expression of key genes. Specifically, the relative abundance of Blautia was negatively correlated with the expression of NICD and Gata-3 genes (p < 0.05), and the relative abundance of the Lachnospiraceae_FCS020_group was negatively correlated with the expression of the Hes1 gene (p < 0.05). In conclusion, Eucommia ulmoides polysaccharides demonstrate potential in alleviating allergic symptoms, providing a scientific foundation for the development of novel natural anti-allergic functional foods. Full article

Mannan oligosaccharide (MOS), a prebiotic derived from yeast cell walls, has been shown to enhance growth performance and health status in various aquatic species. As an exogenous antigen adjuvant, MOS modulates T-cell-mediated immune responses, thereby improving immune function and suppressing excessive inflammatory reactions. This study aimed to evaluate the effects of dietary MOS supplementation on growth performance, serum biochemical parameters, muscle composition, digestive enzyme activity, antioxidant and immune status, and the mTOR signaling pathway in juvenile GIFT tilapia (Oreochromis niloticus). Juveniles (initial body weight: 16.17 ± 1.32 g) were randomly assigned to six treatment groups (three replicate tanks per group) and fed diets supplemented with MOS at 0, 0.2%, 0.4%, 0.6%, 0.8%, and 1% (equivalent to 0, 2, 4, 6, 8, and 10 g/kg of diet, respectively) for 60 days. Compared with the control group, fish fed MOS-supplemented diets exhibited significantly higher (p < 0.05) weight gain rates, specific growth rates, and protein efficiency ratios, along with a significantly lower (p < 0.05) feed conversion ratio. Serum albumin, high-density lipoprotein, and lysozyme levels were significantly increased (p < 0.05), whereas triglycerides, low-density lipoprotein, aspartate aminotransferase, and alanine aminotransferase levels were significantly decreased (p < 0.05). In the liver, head kidney, and spleen, the expression of pro-inflammatory genes (tumor necrosis factor α, interleukin 1β, interleukin 6, interleukin 8, and interferon γ) was significantly downregulated (p < 0.05), while the expression of antioxidant and protective genes (superoxide dismutase, catalase, glutathione peroxidase, glutathione S-transferase, nuclear factor erythroid 2-related factor 2, lysozyme, alkaline phosphatase, interleukin-10, transforming growth factor β, and heat shock protein 70) as well as mTOR signaling pathway-related genes (mammalian target of rapamycin, akt protein kinase B, phosphatidylinositol 3 kinase, and ribosomal protein S6 kinase polypeptide 1) was significantly upregulated (p < 0.05). Overall, MOS positively affects tilapia’s growth, health, and immunity, with 0.60% identified as the optimal dietary level based on growth performance. Full article

Background: Post-Intensive Care Syndrome (PICS), which includes Intensive Care Unit-Acquired Weakness (ICU-AW), can lead to lasting functional impairments even after patients are discharged from the hospital. Early mobilization is a key strategy for preventing ICU-AW, a major contributor to PICS. The primary objective of this study is to assess the impact of early mobilization on ICU-AW in critically ill sepsis patients, while also evaluating the feasibility of a larger, multicenter study through comparison with previous data. Methods: This multicenter observational study, conducted in four hospitals in Nagano Prefecture, Japan, from April 2020 to March 2023, included sepsis patients admitted to the ICU or emergency departments. Patients were classified into ICU-AW and non-ICU-AW groups based on admission data. Background factors and discharge outcomes (complications, ADL, physical function) were assessed. Logistic regression analysis was performed to evaluate the relationship between early mobilization and ICU-AW incidence, with a subgroup analysis on the impact of a dedicated team or physiotherapist. Results: A total of 154 sepsis patients were enrolled, with 76 (49.4%) diagnosed with ICU-AW at discharge. The most common infection source in ICU-AW patients was the urinary tract (31%). Early mobilization (≥3 days) significantly reduced ICU-AW incidence, with adjusted odds ratios of 3.73 (95% CI = 1.79–7.77) for treatment details and 2.93 (95% CI = 1.22–7.08) for patient factors. However, the presence of a dedicated team or physiotherapist did not significantly affect ICU-AW incidence, with adjusted odds ratios of 0.50 (95% CI = 0.24–10.6) and 0.99 (95% CI = 0.40–2.47), respectively. Conclusions: Early mobilization effectively reduced ICU-AW incidence in sepsis patients, though a dedicated team or physiotherapist had no significant impact. Urinary tract infections were the most common infection source in ICU-AW patients. Early mobilization during dialysis for acute kidney injury shows promising potential and warrants further promotion. Full article

Type 2 diabetes (T2D) is a complex metabolic disease characterized by chronic hyperglycemia due to insulin resistance and inadequate insulin secretion. Beyond the classically implicated organs, emerging evidence highlights the gut as a central player in T2D pathophysiology through its interactions with metabolic organs. The gut hosts trillions of microbes and enteroendocrine cells that influence inflammation, energy homeostasis, and hormone regulation. Disruptions in gut homeostasis (dysbiosis and increased permeability) have been linked to obesity, insulin resistance, and β-cell dysfunction, suggesting multifaceted “Gut-X axes” contribute to T2D development. We aimed to comprehensively review the evidence for gut-mediated crosstalk with the pancreas, endocrine system, liver, and kidneys in T2D. Key molecular mechanisms (incretins, bile acids, short-chain fatty acids, endotoxins, etc.) were examined to construct an integrated model of how gut-derived signals modulate metabolic and inflammatory pathways across organs. We also discuss clinical implications of targeting Gut-X axes and identify knowledge gaps and future research directions. A literature search (2015–2025) was conducted in PubMed, Scopus, and Web of Science, following PRISMA guidelines (Preferred Reporting Items for Systematic Reviews). Over 150 high-impact publications (original research and review articles from Nature, Cell, Gut, Diabetologia, Lancet Diabetes & Endocrinology, etc.) were screened. Data on gut microbiota, enteroendocrine hormones, inflammatory mediators, and organ-specific outcomes in T2D were extracted. The GRADE framework was used informally to prioritize high-quality evidence (e.g., human trials and meta-analyses) in formulating conclusions. T2D involves perturbations in multiple Gut-X axes. This review first outlines gut homeostasis and T2D pathogenesis, then dissects each axis: (1) Gut–Pancreas Axis: how incretin hormones (GLP-1 and GIP) and microbial metabolites affect insulin/glucagon secretion and β-cell health; (2) Gut–Endocrine Axis: enteroendocrine signals (e.g., PYY and ghrelin) and neural pathways that link the gut with appetite regulation, adipose tissue, and systemic metabolism; (3) Gut–Liver Axis: the role of microbiota-modified bile acids (FXR/TGR5 pathways) and bacterial endotoxins in non-alcoholic fatty liver disease (NAFLD) and hepatic insulin resistance; (4) Gut–Kidney Axis: how gut-derived toxins and nutrient handling intersect with diabetic kidney disease and how incretin-based and SGLT2 inhibitor therapies leverage gut–kidney communication. Shared mechanisms (microbial SCFAs improving insulin sensitivity, LPS driving inflammation via TLR4, and aryl hydrocarbon receptor ligands modulating immunity) are synthesized into a unified model. An integrated understanding of Gut-X axes reveals new opportunities for treating and preventing T2D. Modulating the gut microbiome and its metabolites (through diet, pharmaceuticals, or microbiota therapies) can improve glycemic control and ameliorate complications by simultaneously influencing pancreatic islet function, hepatic metabolism, and systemic inflammation. However, translating these insights into clinical practice requires addressing gaps with robust human studies. This review provides a state-of-the-art synthesis for researchers and clinicians, underlining the gut as a nexus for multi-organ metabolic regulation in T2D and a fertile target for next-generation therapies. Full article

Identifying effective adjuvants to prevent and alleviate the adverse effects of chemotherapy remains a critical challenge in cancer therapy. This study investigated the protective effects of longan polysaccharide (LP) against cyclophosphamide-induced immunosuppression and oxidative stress in mice. Our findings revealed that LP administration significantly improved systemic immune function, as evidenced by marked increases in serum immunoglobulin levels (IgG2a: 1.82-fold, IgG2b: 1.46-fold, IgM: 1.26-fold, and IgG1: 1.22-fold) and key cytokines (IL-10: 1.53-fold, IL-12: 1.22-fold, and IFN-γ: 1.20-fold), accompanied by substantial reductions in pro-inflammatory mediators (TGF-β1: 28.72% decrease and IL-21: 36.28% decrease). Concurrently, LP restored oxidative balance by increasing SOD, GSH, and NO levels in multiple organs (liver, kidneys, and small intestine) and serum. Mechanistic studies using an in vitro Caco-2/RAW264.7 coculture system revealed that four purified LP fractions (LPIa-LPIVa) effectively suppressed NF-κB pathway activation through downregulation of TLR4 expression, reduction of the p-IκB-α/IκB-α ratio, and inhibition of nuclear NF-κB translocation. These molecular effects correlated with decreased production of inflammatory mediators (TNF-α, IL-6, IL-8, iNOS, and NO). Collectively, these findings provide compelling evidence that LP possesses dual immunomodulatory and antioxidant capabilities, highlighting its potential as a natural adjuvant for alleviating chemotherapy-induced side effects. Full article