Life sciences · 2026
Pirfenidone ameliorates dexamethasone-induced steatohepatitis and vascular resistance in rats.
СтатьяНазвание и аннотация: Перевод в очереди
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Alsaedi Abdullah Q, Nader Manar A, El-Kashef Dalia H, Abdelmageed Marwa E
Аннотация
UNLABELLED: In clinics, glucocorticoids (GC) are frequently recommended as immunosuppressive and anti-inflammatory medications. The side effects of GC are the main concerns, which mostly include insulin resistance (IR), vascular changes, and fatty liver. Knowing the mechanism underlying GC-induced hepatic steatosis and vascular alterations helps identify a target to prevent these side effects.
AIM: The target of this investigation was to assess the beneficial influences of pirfenidone (PFD) versus dexamethasone (DEX)-induced steatohepatitis and vascular resistance.
MAIN METHODS: Rats were classified haphazardly into five categories: control group, PFD control group, DEX group and two groups received PFD for 14 days (50 and 100 mg/kg) by oral route and injected with DEX (1 mg/kg) over the second week of the study.
KEY FINDINGS: PFD reverted morphological alterations, mitigate oxidative dysfunctions, elevated lipid profile and normalize liver transaminases. PFD also attenuated inflammatory markers, PFD also downregulated aortic NF-κB, JNK, ET-1, VCAM and VEGF that were dysregulated by DEX. Moreover, hepatic and aortic IRS1, AKT, P-AKT (ser473) level, aortic eNOS and CD34 levels were elevated upon PFD treatment. Furthermore, PFD pretreatment decreased hepatic and aortic levels of autophagy biomarkers.
CONCLUSION: PFD may provide hepato- and vasculo-protective effects via its insulin-sensitization, hypoglycemic, hypolipidemic, antioxidant and anti-inflammatory activities.
AIM: The target of this investigation was to assess the beneficial influences of pirfenidone (PFD) versus dexamethasone (DEX)-induced steatohepatitis and vascular resistance.
MAIN METHODS: Rats were classified haphazardly into five categories: control group, PFD control group, DEX group and two groups received PFD for 14 days (50 and 100 mg/kg) by oral route and injected with DEX (1 mg/kg) over the second week of the study.
KEY FINDINGS: PFD reverted morphological alterations, mitigate oxidative dysfunctions, elevated lipid profile and normalize liver transaminases. PFD also attenuated inflammatory markers, PFD also downregulated aortic NF-κB, JNK, ET-1, VCAM and VEGF that were dysregulated by DEX. Moreover, hepatic and aortic IRS1, AKT, P-AKT (ser473) level, aortic eNOS and CD34 levels were elevated upon PFD treatment. Furthermore, PFD pretreatment decreased hepatic and aortic levels of autophagy biomarkers.
CONCLUSION: PFD may provide hepato- and vasculo-protective effects via its insulin-sensitization, hypoglycemic, hypolipidemic, antioxidant and anti-inflammatory activities.