This multinational cross-sectional study examined the satisfaction of academic medical staff with integrated medical curricula across governmental and private medical schools. Using an online survey of 525 faculty members, the study found that overall satisfaction was low (44.2%), with dissatisfaction strongly associated with nationality (Jordanian and Egyptian), male gender, longer teaching experience, and employment in governmental institutions. Key sources of dissatisfaction included poor integration of basic and clinical sciences, assessment methods, and curriculum implementation schedules. The findings highlight the need for improved faculty support, resource allocation, and reconsideration of curriculum design, with the potential value of adopting a hybrid model that balances integrated and conventional curriculum approaches

This experimental study investigated the potential of R51211 (itraconazole) to enhance the therapeutic efficacy of sorafenib in hepatocellular carcinoma by targeting the hedgehog signaling pathway. Using in vitro liver cancer cell models and an in vivo diethylnitrosamine-induced rat model, the study demonstrated a synergistic interaction between R51211 and sorafenib, leading to enhanced apoptosis, activation of autophagy, suppression of hedgehog pathway components (Shh, SMO, GLI1/2), and significant improvement in liver histopathology and tumor-related biomarkers. These findings support the repurposing of R51211 as a promising adjuvant strategy to overcome sorafenib resistance in liver cancer therapy

This experimental study evaluated a novel combination therapy targeting the sonic hedgehog (Hh) signaling pathway through dual inhibition of HMG-CoA reductase and HSP90 in a rat model of non-alcoholic steatohepatitis (NASH). Using lovastatin and the HSP90 inhibitor PU-H71, the study demonstrated significant synergistic effects in vitro and in vivo, including improved survival, restoration of liver function, attenuation of oxidative stress, and marked reductions in inflammation and fibrosis. These effects were associated with suppression of key Hh pathway components (Shh, SMO, GLI1, GLI2), reduced hepatic stellate cell activation, and downregulation of profibrotic mediators. The findings support dual targeting of cholesterol metabolism and protein chaperone pathways as a promising therapeutic strategy for NASH and related fibrotic liver disorders

This study investigated the therapeutic potential of β-hydroxybutyrate and a ketone monoester (BD-AcAc₂) in a dextran sodium sulfate–induced rat model of ulcerative colitis. The ketone monoester demonstrated superior efficacy in reducing disease activity, improving survival, restoring intestinal barrier integrity, and attenuating inflammation, oxidative stress, apoptosis, and pyroptosis. These effects were mediated through inhibition of the NF-κB/NLRP3 inflammasome pathway, modulation of pro- and anti-inflammatory cytokines, and enhancement of autophagy markers. The findings highlight ketone monoester therapy as a promising metabolic and anti-inflammatory strategy for ulcerative colitis

This experimental study investigated the hepatoprotective and anti-neoplastic potential of linagliptin, a DPP-4 inhibitor, in a diethylnitrosamine-induced rat model of liver injury and early carcinogenesis. The study demonstrated that linagliptin markedly attenuated liver inflammation, oxidative stress, and histopathological damage while suppressing early neoplastic markers. Mechanistically, linagliptin activated the AMPK/FOXO3a signaling axis, enhanced nuclear FOXO3a localization, induced apoptosis and autophagy, and inhibited NF-κB–mediated inflammatory pathways. These findings provide novel mechanistic insights supporting the repurposing of linagliptin as a potential therapeutic strategy for preventing chronic liver damage and early hepatocellular carcinoma development

This experimental study evaluated a novel antifibrotic strategy targeting the TGF-β signaling pathway in bleomycin-induced pulmonary fibrosis. Using an HSP90 inhibitor (alvespimycin) combined with the proteasome activator oleuropein, the study demonstrated synergistic protection against lung fibrosis, evidenced by improved lung histopathology, reduced collagen deposition, suppression of fibroblast activation markers, and attenuation of inflammation and oxidative stress. Mechanistically, the combination therapy promoted proteasomal degradation of TGF-β receptors, inhibited SMAD2/3 signaling, and downregulated key profibrotic mediators, highlighting a promising dual-target approach for the treatment of pulmonary fibrosis

This experimental study evaluated STA9090, a next-generation HSP90 inhibitor, as a potential antifibrotic therapy in thioacetamide-induced liver fibrosis using integrated in vitro and in vivo models. STA9090 significantly improved hepatocyte survival, reduced oxidative stress and inflammation, restored liver function, and markedly attenuated collagen deposition and fibrosis. Mechanistically, STA9090 enhanced 20S proteasomal activity, leading to proteasome-mediated degradation of the fibrogenic TGF-β receptor II (TβRII), suppression of TGF-β/SMAD signaling, inhibition of NF-κB–driven inflammation, and destabilization of HIF-1α with downstream reduction of VEGF. These findings highlight STA9090 as a promising multi-target antifibrotic agent acting through modulation of the HSP90/TβRII/proteasome axis

This preclinical study evaluated the therapeutic efficacy of the ketone ester (R,R)-BD-AcAc₂ in a dextran sodium sulfate–induced rat model of chronic ulcerative colitis. The ketone ester significantly reduced disease activity, improved survival, restored intestinal barrier integrity, and ameliorated histopathological damage. Mechanistically, (R,R)-BD-AcAc₂ suppressed NF-κB/NLRP3 inflammasome activation, inhibited caspase-1–mediated pyroptosis and apoptosis, reduced oxidative stress, and robustly enhanced macroautophagy, as evidenced by increased Beclin-1 and reduced p62 expression. In addition, treatment normalized pro-inflammatory cytokine profiles and improved gut tight-junction protein expression, highlighting a multi-pronged, metabolism-based therapeutic strategy with strong translational potential for ulcerative colitis

This experimental study evaluated the protective effect of ferulic acid against doxorubicin-induced multi-organ toxicity in a rat model, with particular focus on the NF-κB signaling pathway. Ferulic acid significantly attenuated cardiac, hepatic, and renal injury, as evidenced by improved biochemical markers, reduced oxidative stress, and marked histopathological recovery. Mechanistically, treatment reduced lipid peroxidation, restored antioxidant defenses (GSH, SOD, catalase), and significantly suppressed NF-κB expression and nuclear translocation in affected tissues. These findings support ferulic acid as a promising natural adjuvant therapy for mitigating doxorubicin-associated toxicity through antioxidant and anti-inflammatory mechanisms

This comprehensive review article summarizes the current understanding of the pathogenesis and pharmacological management of hepatic ischemia–reperfusion (I/R) injury, a major complication of liver surgery and transplantation. The review details the cellular and molecular mechanisms underlying hepatic I/R injury, including mitochondrial dysfunction, oxidative stress, calcium overload, Kupffer cell and neutrophil activation, inflammatory cytokine cascades, NF-κB signaling, and microcirculatory disturbances. It also critically discusses experimental and emerging therapeutic strategies—such as antioxidants, ischemic preconditioning, calcium channel blockers, cytokine modulation, NF-κB inhibition, and renin–angiotensin system targeting—highlighting their translational potential and current limitations. The article provides an integrated framework to guide future research and improve pharmacological control of hepatic I/R injury.

This experimental study investigated the hepatoprotective effects of captopril and valsartan against hepatic ischemia–reperfusion (I/R) injury in a rat model, with emphasis on NF-κB–mediated inflammation and oxidative stress. Pretreatment with either drug significantly attenuated liver injury, as evidenced by reduced serum transaminases (ALT, AST), decreased pro-inflammatory cytokines (TNF-α, IL-1β), suppression of lipid peroxidation (MDA), and restoration of antioxidant defenses (SOD). Both agents markedly inhibited hepatic NF-κB activation and improved histopathological outcomes, with valsartan showing relatively greater efficacy. These findings highlight modulation of the renin–angiotensin system as a promising pharmacological strategy for preventing hepatic I/R injury