Deciphering the role of ferulic acid against streptozotocin-induced cellular stress in the cardiac tissue of diabetic rats.
The cardiomyocytes are one of the major sources of hyperglycemia induced ROS generation. The present study focuses on the ameliorative role of ferulic acid in combating cardiac complications in diabetic rats. Induction of diabetes by STZ in male Wistar rats (at a dose of 50 mg kg-1body wt, i.p.) reduced body weight and plasma insulin level, enhanced blood glucose, disturbed the intra-cellular antioxidant machineries and disintegrated the normal radiation pattern of cardiac muscle fibers. Induction of ER stress (up-regulation in the levels of CHOP, GRP78, eIF2α signaling, increased calpain-1 expression), caspase-3 activation, PARP cleavage and DNA fragmentation were evidenced from immunoblot analyses and DNA fragmentation assay. However, ferulic acid administration, (at a dose of 50 mg kg-1body wt, orally for eight weeks) in post-hyperglycemia could reverse such adverse effects. Also, the molecule increased GLUT-4 translocation to the cardiac membrane by enhanced phosphorylation of PI3Kinase, AKT and inactivation of GSK-3β thereby altering the hyperglycemic condition in the cardiac tissue of diabetic rats. Therefore, as a potential therapeutic, ferulic acid, exhibiting antioxidant and hypoglycemic effects, may hold promise in circumventing stress mediated diabetic cardiomyopathy in rats.
Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata, West Bengal, 700054, India.
Sayantani
S
Chowdhury
Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata, West Bengal, 700054, India.
Sumit
S
Ghosh
Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata, West Bengal, 700054, India.
Kahkashan
K
Rashid
Division of Molecular Medicine, Bose Institute, P-1/12, CIT Scheme VII M, Kolkata, West Bengal, 700054, India. Electronic address: parames@jcbose.ac.in.
Parames C
PC
Sil
D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D000975:Antioxidants / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects; D001786:Blood Glucose / Q000032:analysis; D003373:Coumaric Acids / Q000494:pharmacology*; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D000091342:Endoplasmic Reticulum Chaperone BiP; D006321:Heart / Q000187:drug effects / Q000503:physiopathology*; D006801:Humans; D006943:Hyperglycemia / Q000503:physiopathology*; D015151:Immunoblotting; D007328:Insulin / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000187:drug effects
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; D001786:Blood Glucose; D003373:Coumaric Acids; D000091342:Endoplasmic Reticulum Chaperone BiP; C000717247:HSPA5 protein, human; D007328:Insulin; C004999:ferulic acid
Apoptosis; Cardiac dysfunction; Ferulic acid; Hyperglycemia; Oxidative and ER stress; STZ-induced diabetes