5-Fluorouracil (5-FU) is a cornerstone chemotherapeutic agent that is extensively utilized in the management of malignancies; however, its clinical utility is constrained by its narrow therapeutic index and dose-limiting toxicities. The study aimed to study the hepato-nephroprotective effects of epigallocatechin gallate (EGCG) and EGCG mediated selenium nanoparticles and their effect in mitigating the toxicity induced by 5-FU. EGCG-functionalized selenium nanoparticles (EGCG-SeNPs) were produced by mixing sodium selenite, with EGCG acting as both the reducing and stabilizing agent. Nanoparticles were characterized using UV-vis spectroscopy, FT-IR, dynamic light scattering, zeta potential analysis, and transmission electron microscopy. 35 adult rats were randomly assigned to control, 5-FU, 5-FU + Na₂SeO₃, 5-FU + EGCG, and 5-FU + EGCG-SeNPs groups. Hepatorenal toxicity was induced by intraperitoneal 5-FU administration during the final five days of the experiment. Serum biochemical markers, tissue oxidative stress, antioxidant enzyme, inflammatory cytokine levels, and apoptosis-related gene expression were evaluated. Immunohistochemical analysis of Nrf2 and Keap1 and histopathological examination of tissues were performed. 5-FU induced severe hepatorenal toxicity, evidenced by marked elevations in liver and kidney function biomarkers, excessive oxidative stress, inflammatory cytokine overproduction, NF-κB activation, and apoptotic signaling. Treatment with EGCG-SeNPs markedly ameliorated 5-FU-induced hepatic and renal dysfunction, restoring liver enzyme and kidney biomarker levels to near-normal levels more effectively than EGCG or sodium selenite alone. EGCG-SeNPs significantly suppressed lipid peroxidation, NGAL, and inflammatory mediators while robustly enhancing antioxidant defenses and activating the Nrf2/HO-1 pathway with concomitant Keap-1 downregulation, strongly inhibited NF-κB signaling, normalized cytokine balance, reduced poly (ADP-ribose) (PAR) activation, and attenuated apoptosis. EGCG–SeNPs confer superior protection against 5-FU–induced hepatorenal toxicity compared to EGCG or inorganic selenium alone. The potent protective effects of EGCG–SeNPs are mediated through coordinated antioxidant, anti-inflammatory, and anti-apoptotic mechanisms, primarily via activation of the Nrf2/HO-1 axis and suppression of NF-κB signaling.

The present study was to investigate the effective role of renewable sources of Ca⁺² from eggshell (ES) with different doses to restrict obesity disorders. Rats were classified as follows, G₁: normal diet for 26 weeks; G₂: high‐fat diet (HFD) for 26 weeks; G₃, G₄, and G₅ were supplemented with HFD for 16 weeks and treated with 7.2 g Ca⁺² ES/Kg rat chow, 18 g Ca⁺² ES/Kg rat chow, and 2% diet containing fat (DCF), respectively, for the remaining 10 weeks. Results revealed a significant effect of the low dose of Ca⁺² supplement in form of ES than high dose and 2% DCF; on basis of anthropometric parameters, lipid, leptin, adiponectin, thyroid hormones, Ca⁺², 25‐hydroxyl vitamin‐D, and oxidative and inflammatory parameters were regulated. Results were confirmed with the histopathological study. Therefore, it was concluded that Ca⁺² supplementation can be used as a beneficial source for obesity management with anticholesterol actions. Practical applications Obesity represented public health hazards. The eggshell is one of the waste products that contain a high percentage of Ca⁺². The current data exposed using a low dose of ES as a new source of Ca⁺² supplement for treatment of HFD rats leads to significant enhancement of lipid profiles, liver enzymes, kidney functions, leptin, adiponectin, Ca⁺², 25(OH)‐D, TSH, fT_4, and PTH levels. Also, there was a reduction in weight gain, Bwt, BMI, BG, insulin, and HOMA‐IR. Moreover, the oxidant‐pro‐oxidant system was improved in both hepatic and adipose tissues where NO and TBARS concentrations were diminished, and SOD specific activity was elevated. Additionally, TNF‐α and ADAM17 expression were downregulated. Hence, it was concluded that there was good evidence that diets supplemented with ES were associated with the reduction of obesity complications especially regulating fat processing and storage in the body.

Impaired lung epithelial cell regeneration following injury may contribute to the development of pulmonary fibrosis. Epithelial-mesenchymal transition (EMT) is a critical event in embryonic development, wound healing following injury, and even cancer progression. Previous studies have shown that the combination of transforming growth factor beta-1 (TGFβ1) and fibroblast growth factor 2 (FGF2) induces EMT during cancer metastasis. However, this synergy remains to be elucidated in inducing EMT associated with wound healing after injury. We set out this study to determine the effect of fibroblast growth factor 2 (FGF2) on TGFβ1-induced EMT in the human lung epithelium. BEAS-2B and A549 cells were treated with TGFβ1, FGF2, or both. EMT phenotype was investigated morphologically and by measuring mRNA expression levels; using quantitative real-time PCR. E-cadherin expression was assayed by western blot and immunofluorescence staining. Cell migration was confirmed using a wound-healing assay. TGFβ1 induced a morphological change and a significant increase in cell migration of BEAS-2B cells. TGFβ1 significantly reduced E-cadherin (CDH1) mRNA expression and markedly induced expression of N-cadherin (CDH2), tenascin C (TNC), fibronectin (FN), actin alpha 2 (ACTA2), and collagen I (COL1A1). While FGF2 alone did not significantly alter EMT gene expression, it enhanced TGFβ1-induced suppression of CDH1 and upregulation of ACTA2, but not TNC, FN, and CDH2. FGF2 significantly inhibited TGFβ1-induced COL1A1 expression. Furthermore, FGF2 maintained TGFβ1-induced morphologic changes and increased the migration of TGFβ1-treated cells. This study suggests a synergistic effect between TGFβ1 and FGF2 in inducing EMT in lung epithelial cells, which may play an important role in wound healing and tissue repair after injury.

A new ligand, benzylidene–phenol–thiazole (HBHTP), and its M(ii) complexes (M = Co, Ni, Cu, or Zn) were synthesized using a hybrid pharmacophore approach.