Journal of basic and clinical physiology and pharmacology · 2026
Ferulic acid and not ascorbic acid reversed cardiac energy metabolism disruption in acute aluminum chloride exposed mice via PPARα/AMPK pathway.
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Oluranti Olufemi I, Adedayo Lawrence D, Ojo-Ayangoke Esther O, Adio Kolawole O, Aluko Olamide F, Orefuwa Michelle D, Oladejo Ifeoluwa D, Toye Praise O, Ayantoyinbo Omobolanle E, Alabi Babatunde A
Аннотация
OBJECTIVES: Proper cardiac function depends on adequate supply and metabolism of energy substrates. Aluminum chloride exposure has been linked to adverse cardiac events. This study investigated the ameliorative effect of ferulic acid and ascorbic acid in dysregulated cardiac energy metabolism in aluminum chloride-exposed mice.
METHODS: Thirty mice were randomized into five groups (n=6): control (0.1 % distilled water), aluminum chloride (AlCl3, 100 mg/kg, p.o), aluminum chloride and ferulic acid (AlCl3, 100 mg/kg; FA20, 10 mg/kg, p.o), aluminum chloride and ferulic acid (AlCl3, 100 mg/kg; FA10, 10 mg/kg, p.o), aluminum chloride and ascorbic acid (AlCl3, 100 mg/kg; Vit. C, 100 mg/kg), daily for 7 days. Cardiac metabolic enzymes activities were analyzed spectrophotometrically; substrate transporters and regulators of energy metabolism were analyzed using immunohistochemistry.
RESULTS: AlCl3 increased hexokinase activity and reduced pyruvate-dehydrogenase activity compared with the control. AlCl3 significantly reduced the expression of glucose transporter-4 (GLUT 4), carnitine palmitoyl-transferase 1β (CPT1β), peroxisome proliferator-activated receptor-alpha (PPARα) and AMP-activated protein kinase (AMPK) compared with the control. However, FA reversed the effect of AlCl3 by significantly increasing hexokinase and pyruvate dehydrogenase activities, increasing the expression of GLUT4, CPT1β, PPARα and AMPK.
CONCLUSIONS: FA mitigate against cardiac metabolic disruption caused by acute exposure to AlCl3 through PPARα and AMPK modulation.
METHODS: Thirty mice were randomized into five groups (n=6): control (0.1 % distilled water), aluminum chloride (AlCl3, 100 mg/kg, p.o), aluminum chloride and ferulic acid (AlCl3, 100 mg/kg; FA20, 10 mg/kg, p.o), aluminum chloride and ferulic acid (AlCl3, 100 mg/kg; FA10, 10 mg/kg, p.o), aluminum chloride and ascorbic acid (AlCl3, 100 mg/kg; Vit. C, 100 mg/kg), daily for 7 days. Cardiac metabolic enzymes activities were analyzed spectrophotometrically; substrate transporters and regulators of energy metabolism were analyzed using immunohistochemistry.
RESULTS: AlCl3 increased hexokinase activity and reduced pyruvate-dehydrogenase activity compared with the control. AlCl3 significantly reduced the expression of glucose transporter-4 (GLUT 4), carnitine palmitoyl-transferase 1β (CPT1β), peroxisome proliferator-activated receptor-alpha (PPARα) and AMP-activated protein kinase (AMPK) compared with the control. However, FA reversed the effect of AlCl3 by significantly increasing hexokinase and pyruvate dehydrogenase activities, increasing the expression of GLUT4, CPT1β, PPARα and AMPK.
CONCLUSIONS: FA mitigate against cardiac metabolic disruption caused by acute exposure to AlCl3 through PPARα and AMPK modulation.