Dexpanthenol Attenuates High-Fructose Corn Syrup-Induced Hepatic Injury in Young Adult Rats by Modulating Oxidative Stress, Apoptosis, and Inflammasome-Associated Pyroptotic Signaling

Histopathology and NF-κB/Caspase-3 Expression in High Fructose Corn Syrup–Induced Lung Injury: Protective Effect of Dexpanthenol

Aim: High-fructose corn syrup (HFCS) has been associated with metabolic and inflammatory disturbances, including pulmonary inflammatory injury. Due to its known anti-inflammatory and tissue-protective properties, this study aimed to investigate the protective effects of dexpanthenol (DEXP) against HFCS-induced structural and molecular lung damage in rat lungs.Material and Methods: Thirty-two male Wistar rats were allocated at random into four groups (Control, HFCS, HFCS+DEXP, DEXP). HFCS (30%) was provided in drinking water for 8 weeks. DEXP was administered intraperitoneally at a dose of 500 mg/kg/day for the last 2 weeks. Lung tissues were processed for hematoxylin–eosin and Picro Sirius Red staining. Hyperemia, edema, epithelial loss, inflammatory cell infiltration, and fibrosis were evaluated semi-quantitatively. The immunohistochemical expression of NF-κB and Caspase-3 was assessed as markers of inflammatory and apoptotic activities.Results: Exposure to HFCS produced alterations such as thickened alveolar walls, interstitial edema, vascular hyperemia, degeneration and loss of epithelial cells, accumulation of inflammatory cells, and early deposition of collagen compared with the control group. Histopathological scores for inflammation, edema, hyperemia, epithelial loss, and fibrosis were significantly increased in the HFCS group (p=0.001, p=0.001, p=0.001, p=0.006, and p=0.011, respectively). In addition, NF-κB and Caspase-3 expression levels were significantly elevated in the HFCS group compared with the control group (p=0.001). DEXP treatment significantly reduced histopathological scores (p=0.001), as well as NF-κB and Caspase-3 expression levels compared with the HFCS group (p=0.001 and p=0.0018, respectively). In the DEXP-only group, lung morphology was preserved.Conclusion: Chronic ingestion of HFCS elicits prominent inflammatory, apoptotic, and fibrotic responses in rat lung tissue. DEXP exerts strong histoprotective and immunomodulatory actions, suggesting potential therapeutic value against HFCS-induced pulmonary injury.

Juglone Attenuates CCl₄‐Induced Hepatic Injury in Mice With Associated Modulation of Oxidative Stress and Inflammasome‐Related mRNA Expression

Results are best interpreted as gene‐level associations compatible with modulation of oxidative stress, inflammasome‐ and pyroptosis‐related mRNA expression, ER stress responses, apoptosis‐linked transcripts, and remodeling‐associated transcripts, rather than as confirmed pathway inhibition or established antifibrotic activity.

Kefir Mitigates Testicular Histopathological and Immunohistochemical Alterations Induced by High-fructose Corn Syrup in Juvenile Wistar Rats

Chrysin attenuates pentadecafluorooctanoic acid-induced hepatotoxicity in male Wistar rats via modulation of oxidative stress, inflammation, and metabolic dysfunction

Overall, chrysin demonstrates potent protective potential against PFOA-induced liver injury and may serve as a promising therapeutic candidate for environmental toxin-associated hepatotoxicity.

Hepatoprotective potential of cardionogen-1, a Wnt/β-catenin signaling inhibitor against alcohol-induced chronic liver injury in C57BL/6J mice.

Alcoholic liver disease (ALD) develops following chronic alcohol consumption and is characterized by steatosis, inflammation, fibrosis, and cirrhosis. Increasing evidence suggests that dysregulated Wnt/β-catenin signaling contributes to the progression of ALD. Therefore, the present study investigated the hepatoprotective effect of cardionogen-1 (CDNG-1), a Wnt/β-catenin signaling modulator, against alcohol-induced chronic liver injury in C57BL/6 J mice. Mice were administered ethanol for 14 weeks to induce chronic liver injury, followed by treatment with CDNG-1 (50 and 100 μM/100 g, i.p.) or silymarin (100 mg/kg, p.o.) for 4 weeks. Chronic ethanol exposure elevated serum liver marker enzymes, increased oxidative stress, altered lipid metabolism-associated gene expression, and promoted inflammatory and fibrotic responses in liver tissue. CDNG-1 treatment significantly reduced serum transaminases, improved antioxidant status, and favorably regulated the expression of genes associated with alcohol metabolism, lipid dysregulation, inflammation, fibrosis, and Wnt/β-catenin signaling. Histopathological analysis also demonstrated reduced alcohol-induced hepatocellular ballooning and inflammatory infiltration following CDNG-1 treatment. The findings of the present study suggest that CDNG-1 attenuates alcohol-induced chronic liver injury and may represent a potential therapeutic candidate for ALD.

Isoferulic acid alleviates LPS/D-galactosamine-induced acute liver injury in mice by inhibiting ERK/NF-κB signaling and modulating the NLRP3 inflammasome.