Background Rheumatoid Arthritis (RA) is a long-term, autoimmune, and inflammatory disorder that results in progressive joint destruction and functional disability of joint tissue as well as potential systemic side effects. Because of this, the limitations of current treatments, including the side effects of disease-modifying antirheumatic drugs (DMARDs) and biologic agents, highlight the need to explore complementary therapies for treatment beyond the effects of these currently available agents. Ginger (Zingiber officinale) contains bioactive phenolic compounds, such as gingerol and shogaols, that contribute to a reduction in inflammation and oxidative stress, and may be effective in the management of RA. Objective A review of the published literature evaluating the effects of ginger and its active compounds on the clinical symptoms of RA, gut microbiota, and related outcomes within the framework of the gut–joint axis. Results Active compounds of ginger, especially 6-gingerol and 6-shogaol, can reduce inflammatory cytokines (Tumor Necrosis Factor-α (TNF-α), Interleukin-1 beta (IL-1β), Interleukin-6 (IL-6)) and improve inflammation and joint destruction in animal models, and this effect has been achieved through inhibition of the Nuclear Factor Kappa-Light-Chain-Enhancer of Activated B Cells (NF-κB) and Cyclooxygenase-2 (COX-2) pathways and activation of Nuclear factor erythroid 2-related factor 2 (NRF2). Studies have shown that ginger helps regulate the gut–joint axis by modulating the gut microbiota and increasing the production of short-chain fatty acids (SCFAs). However, low bioavailability and the heterogeneity of ginger’s constituents are among its clinical limitations. Conclusion Ginger, with its multiple anti-inflammatory and antioxidant mechanisms, shows potential as a complementary option for RA. Based on the promising preclinical evidence, it is crucial to carry out randomized clinical trials (RCTs). These studies will help confirm the safety and effectiveness of the treatment, as well as establish a standard dosage. Considering ginger’s safety and affordability, it may represent an affordable complementary dietary option for managing RA.
Polycystic ovary syndrome (PCOS) is a common endocrine and metabolic disorder associated with insulin resistance, dyslipidemia, hyperandrogenism, and impaired ovarian function. Interest in plant-derived products has increased because of their potential to address multifactorial metabolic disorders. In the present study, a polyherbal formulation (PHF) prepared from Linum usitatissimum, Coriandrum sativum, and Foeniculum vulgare was evaluated in a letrozole-induced rat model of PCOS. Thirty female rats were divided into normal control, PCOS, and treatment groups. PCOS was induced using letrozole® (1 mg/kg) combined with a high-fat diet for 21 days. Treated animals received low-dose PHF (100 mg/kg), high-dose PHF (400 mg/kg), or metformin for 20 days. PHF administration improved several metabolic and reproductive alterations associated with PCOS. PHF treatment significantly reduced serum testosterone and fasting insulin and improved HOMA-IR compared with the PCOS group (P < 0.0001). The formulation also improved the serum lipid profile, with greater effects observed at 400 mg/kg. PHF treatment increased GLUT4 expression compared with the PCOS group (P < 0.0001), indicating improved glucose utilization. Ultrasonographic examination showed apparent improvement in ovarian morphology, including fewer visible cystic structures following PHF treatment, which was further supported by histopathological findings showing mature follicles and corpus lutea. The high-dose formulation produced more pronounced effects than the low-dose treatment. These findings support the potential of PHF as a plant-derived candidate for further investigation of metabolic and reproductive disturbances associated with PCOS. Further preclinical and clinical studies are required to establish its efficacy, safety, and clinical applicability.
Psoriasis and atopic dermatitis are among the chronic inflammatory skin diseases with long-term therapeutic needs. Current treatments are effective, but their continuous use can be limited by tolerability and safety concerns. Plant-derived bioactive compounds offer immunomodulatory potential; however, their clinical use is restricted by poor solubility and instability, as well as insufficient delivery into diseased skin. Nanoformulation can address these delivery limitations by improving phytochemical stability, cutaneous deposition, retention, and penetration where appropriate. This improvement becomes more meaningful when the carrier, the active compound, the disease-specific barrier structure, and the dominant immunological targets are aligned. The review focuses on topically applied phytochemical-loaded nanodelivery systems, while conventional phytochemical studies are considered only to contextualize their underlying pharmacology and immunomodulatory mechanisms. In psoriasis, the thick and compact barrier of hyperkeratotic plaques creates a need for penetration-enhancing systems. Curcumin- and indigo-naturalis-derived preparations have relatively developed evidence in psoriasis, although evidence specifically supporting their nanoformulated forms remains predominantly preclinical. Altered barrier integrity in atopic dermatitis may vary the optimal delivery strategy due to anatomical site, disease severity, therapeutic target, and the skin compartment requiring drug exposure. Therefore, it is important to consider controlled drug deposition and skin compatibility alongside penetration enhancement. Across both diseases, NF-κB and STAT signaling pathways deliver overlapping therapeutic targets, although their involvement was often inferred from downstream cytokine changes rather than measured directly. However, the prime immune responses like Th17/IL-23 and type 2/Th2 immune axes are particularly prominent for psoriasis and atopic dermatitis, respectively. The translational gap is clearer in atopic dermatitis, where the reviewed systems have not yet been evaluated in randomized controlled trials with validated endpoints. For psoriasis, some phytochemical interventions have reached clinical evaluation, but clinical evidence specifically for nanoformulated phytochemicals remains limited. Further progress requires endotype-informed trial design, biomarker-stratified patient selection, and mechanistic endpoints beyond cytokine suppression.
Introduction Acute kidney injury (AKI) is a life-threatening condition associated with oxidative stress, inflammation, apoptosis, and disruption of renal cellular homeostasis. Glycitein is a bioactive isoflavone that has various biological activity, but little is known about its possible protective effects and underlying molecular processes in AKI caused by cisplatin (CP). Thus, combining network pharmacology, molecular docking, and experimental validation, study examined the possible protective function of glycitein against CP-induced kidney injury. Materials and methods The databases SwissTargetPrediction, SuperPred, and Traditional Chinese Medicine Systems Pharmacology (TCMSP) were used to find targets linked to glycitein, while DisGeNET and GeneCards provided targets related to AKI. A Venn diagram was used to find overlapping targets, which were then examined using Cytoscape and STRING's compound-target and protein-protein interaction (PPI) networks. The CytoHubba plugin and the maximal clique centrality algorithm were used to identify hub genes. DAVID was used for Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment studies. Molecular docking was used to assess interaction between glycitein and hub proteins. NRK-52E renal tubular epithelial cells treated with CP were used for experimental validation. CP (30 μM) was administered to the cells alone or with glycitein (10, 20, and 30 μM), with apigenin (30 μM) as the positive control. We used MTT, GSH/SOD, and MDA assays, ELISA, qRT-PCR, western blotting, immunofluorescence, TUNEL, and H2DCFDA-based fluorescence analysis to measure cell viability, oxidative stress, lipid peroxidation, inflammatory biomarkers, apoptosis, gene expression, protein expression, and intracellular ROS levels respectively. Result Glycitein and AKI were found to have overlapped potential targets by network pharmacology, and PPI analysis indicated several major hub genes, such as PIK3R1, HIF1A, ESR1, EGFR, NFKB1, BCL2, NFE2L2, and MAPK1. According to GO and KEGG enrichment studies, these targets were connected to signalling pathways and biological processes related to oxidative stress, inflammation, apoptosis, fibrosis and cellular responses. The result of molecular docking showed that glycitein and the chosen hub proteins interacted favourably, with binding energies falling within the predetermined range of ≤ −5 kcal/mol. Glycitein administration was further assessed for its impact on oxidative stress, inflammatory mediators, apoptotic responses, and kidney injury-associated markers, such as KIM-1, IL-18, Nrf2, and NF-κB, in the CP-treated NRK-52E cells line. Conclusion The findings indicate that glycitein may protect against CP-induced renal injury via a multi-target mechanism involving the regulation of oxidative stress, inflammatory signalling, and apoptosis. The integrated approach of network pharmacology, molecular docking, and in vitro experiments offers insights into glycitein's role in CP treated-AKI and suggests the need for further in vivo studies.
Background Carbon tetrachloride (CCl₄)–induced hepatotoxicity is associated with profound immune dysregulation that contributes to the progression of liver injury. Medicinal plants with immunomodulatory potential may influence disease outcomes by reshaping immune responses during toxic insult. This study investigated the immunomodulatory effects of an ethanol leaf extract of Rauwolfia vomitoria in a rat model of Carbon tetrachloride (CCl₄)-induced liver injury. Methods Forty-two male Wistar rats were randomly assigned to six groups: negative control, Carbon tetrachloride (CCl₄)-treated control, silymarin-treated control (25 mg/kg), and three extract-treated groups receiving Rauwolfia vomitoria ethanol leaf extract (100, 200, or 400 mg/kg) for 28 days. A single intraperitoneal dose of Carbon tetrachloride (CCl₄) induced hepatotoxicity. Peripheral leukocyte profiles were assessed using differential white blood cell counts, while CD4⁺ T cell percentages were quantified by flow cytometry. The phytochemical composition of the extract was characterized using gas chromatography–mass spectrometry (GC–MS). Results Gas Chromatography–Mass Spectrometry (GC–MS) analysis identified thirty-nine phytochemical constituents in Rauwolfia vomitoria ethanol leaf extract, including phytol, phytol acetate, squalene, vitamin E, and fatty acid derivatives. Extract treatment reduced Malondialdehyde (MDA), Alanine Aminotransferase (ALT), and Aspartate Aminotransferase (AST) activities and improved catalase and Superoxide dismutase (SOD) activities in Carbon tetrachloride (CCl₄)-exposed rats. Immunologically, the extract produced dose-related increases in neutrophil and monocyte percentages and reductions in lymphocyte, eosinophil, total WBC, and estimated CD4⁺ T-cell indices. These findings indicate alterations in circulating immune-cell profiles during Carbon tetrachloride (CCl₄)-induced liver injury. Conclusion Rauwolfia vomitoria ethanol leaf extract demonstrated immunomodulatory effects in Carbon tetrachloride (CCl₄)-induced liver injury by altering peripheral leukocyte distribution and estimated CD4⁺ T-cell indices. The observed pattern suggests selective immune redistribution, with increased innate immune-cell representation and moderation of adaptive immune components, rather than generalized immunostimulation. These preliminary findings support further mechanistic studies to clarify the extract’s role in immune regulation during toxic liver injury.
