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In a recent study, we used chemical analysis to show that the Caesalpinia mimosoides aqueous extract, which contains a high concentration of simple phenolics, has strong anti-influenza activity. We determined through molecular docking methods that its potential target inhibitor is the neuraminidase. Therefore, our study objectives were to evaluate whether the aqueous-ethanol extract (30% v/v) of this plant species exhibits greater antiviral activity than the aqueous plant extract. The C. mimosoides hydroethanolic extract exhibited potent antioxidant activity in the DPPH assay, with an IC 50 value of 15.01 µg/mL, comparable to authentic quercetin (IC 50  = 12.72 µg/mL) and approximately 4.91 times greater than standard gallic acid (IC 50  = 3.06 µg/mL). Through untargeted metabolomic analyses (UPLC-ESI(±)-QTOF-MS/MS) and subsequent stepwise computational metabolomics analyses, we identified the extract as primarily containing simple phenolics (e.g., gallic acid, ellagic acid, shikimic acid, and chlorogenic acid), flavonoid derivatives (e.g., quercetin, taxifolin, myricitrin, and afzelin), and other bioactive components, including dicarboxylic acids and germacrone. The polyphenol-rich extract showed strong anti-influenza activity, with an IC 50 of 2.33 µg/mL against the influenza A/PR/8/34 virus and no cytotoxic effects, as indicated by a CC 50 greater than 50 µg/mL. This represents an approximately 3.35-fold increase in effectiveness compared to its corresponding aqueous extract (IC 50  = 7.81 µg/mL). Furthermore, the extract demonstrated no hemolytic activity, even at a maximum concentration of 2,000 µg/mL, suggesting its potential as a safe antiviral agent. Molecular docking analyses revealed that the identified phytochemicals can simultaneously interact with the "drug-target binding sites" of neuraminidase (NA) and PB2 subunit of influenza RNA polymerase, indicating their potential polypharmacological effects. The antiviral activity of the ethanolic-aqueous extract against other strains is being explored due to the versatile biological effects of phenolic substances., Competing Interests: Declarations. Competing interests: The authors declare no competing interests., (© 2025. The Author(s).)

Lactoferrin (LCF), a potent naturally occurring antioxidant, is a crucial component in preventing potassium dichromate (PDC) toxicity. The goal of the current work was to study the potential efficacy of LCF in preventing PDC(CrVI)-induced testicular toxicity and oxidative injury in rats. Six groups of male rats of Wistar stain were randomly categorized into: group 1, which served as the control; group 2 and 3 received LCF (200 and 300 mg/kg orally, respectively); group 4 received PDC (2 mg/kg i.p.); group 5 and 6 pretreated with LCF, followed by PDC as in group 4 with 90 min apart for 28 days. PDC-intoxicated rats showed a significantly altered spermogram with abnormal sperm morphology. PDC significantly upregulated serum FSH and downregulated testosterone levels. Additionally, PDC decreased the levels of testicular key antioxidant biomarkers (catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH)) with elevated lipid peroxidation marker (TBARS) and testicular chromium content. Moreover, it upregulated testicular proinflammatory cytokines, IL-1, IL-6, IL-10, and TNF-α, induced histopathological changes in testes with significant immunohistochemical expression of FasL and moderate expression of Nrf2. Pretreatment with LCF significantly mitigated PDC-induced testicular toxicity by enhancing spermogram, improving hormonal levels, restoring testicular oxidant/antioxidant balance, and decreasing testicular IL-1, IL6, IL-10, and TNFα levels, and amending both FasL and Nrf2 immunohistochemical-expression. Additionally, LCF improved testicular histopathological picture and spermatogenesis. Our results highlight the importance of LCF as a superior protective modulator of PDC-induced testicular injury., (© 2023. The Author(s).)

Fibrosis is a common outcome of nearly all chronic diseases of liver that results in changes of its functions which requires medical attention. The current research aims to investigate the potential anti-fibrotic efficacy of Carvacrol against thioacetamide (TAA)-induced liver fibrosis in male rats using Ursodeoxycholic acid (UDCA) as a reference anti-fibrotic product. Carvacrol (25 and 50 mg/kg) markedly declined TAA-increased serum liver enzymes; alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT) as well as total bilirubin (TB) and direct bilirubin (DB) levels as well as increased levels of total protein (TP) and albumin. Carvacrol significantly reduced glutathione depletion (GSH), Nitric oxide (NO X ) and malondialdehyde (MDA) accumulation in liver tissue. Additionally, its anti-oxidant effect brightened up via affecting markers of stress found in the cell as nuclear factor erythroid 2-related factor 2 (Nrf-2) where it still had high content and decreased Thioredoxin (Trx) level. The anti-inflammatory effect of Carvacrol was confirmed by decreasing nuclear factor kappa B (NF-κB), interleukin-1beta (IL-1β) and inducible nitric oxide synthase (iNOS) contents. Carvacrol showed anti-fibrotic effect clarified by turning down fibrosis-related markers; TGF-β1, matrix metalloproteinase-3 and 9 (MMP-3 and 9) and Autotaxin (ATX) contents. Furthermore, it decreased alpha smooth muscle actin (α-SMA) and caspase-3 immune-expression. The overall outcome of aforementioned markers results showed that Carvacrol suppresses the progression of liver fibrosis via its anti-oxidant, anti-inflammatory, anti-apoptotic effect and its ability in lowering Thioredoxin and Autotaxin; hence it can be categorized as a hepatoprotective natural substance.