AIMS: To investigate the effect of atorvastatin on cardiac aging in rats. MATERIALS: Ninety 20-month-old Wistar rats were administered oral atorvastatin (AVT; 10 or 1 mg·kg(-1)·day(-1)) or saline for 4 months. At the end of the experiment, age-related changes in hearts were measured. RESULTS: Compared with young rats, obvious increases were found in the aging rats in left ventricle thickness, diameter of cardiocytes, collagen deposition, the ratio of type I/type III collagen, β-galactosidase and malondialdehyde (MDA), and obvious decreases were found in superoxide dismutase (SOD), catalase (CAT) and nitric oxide synthase (NOS). The treatment with AVT led to significant decreases in the thickness of the left ventricle, diameter of cardiocytes, collagen deposition, I/III collagen ratio, MDA, β-galactosidase and increases in the activity of SOD, CAT and NOS. Some aging-related inflammatory cytokines like interleukin (IL)-1β, tumour necrosis factor (TNF)-α and matrix metalloproteinase (MMP)-9 were found to be overexpressed in the aging rats. AVT treatment could inhibit the expression of IL-1β, TNF-α and MMP-9 on both the mRNA and protein levels, and increase the expression of peroxisome proliferator-activated receptors (PPAR-α/β/δ/γ). Pretreatment with PPAR inhibitors attenuated the inhibitory effect of AVT on the expression of inflammatory cytokines. CONCLUSION: AVT may retard the cardiac aging process by upregulating PPARs.
AIMS: To investigate the effect of atorvastatin on cardiac aging in rats. MATERIALS: Ninety 20-month-old Wistar rats were administered oral atorvastatin (AVT; 10 or 1 mg·kg(-1)·day(-1)) or saline for 4 months. At the end of the experiment, age-related changes in hearts were measured. RESULTS: Compared with young rats, obvious increases were found in the aging rats in left ventricle thickness, diameter of cardiocytes, collagen deposition, the ratio of type I/type III collagen, β-galactosidase and malondialdehyde (MDA), and obvious decreases were found in superoxide dismutase (SOD), catalase (CAT) and nitric oxide synthase (NOS). The treatment with AVT led to significant decreases in the thickness of the left ventricle, diameter of cardiocytes, collagen deposition, I/III collagen ratio, MDA, β-galactosidase and increases in the activity of SOD, CAT and NOS. Some aging-related inflammatory cytokines like interleukin (IL)-1β, tumour necrosis factor (TNF)-α and matrix metalloproteinase (MMP)-9 were found to be overexpressed in the aging rats. AVT treatment could inhibit the expression of IL-1β, TNF-α and MMP-9 on both the mRNA and protein levels, and increase the expression of peroxisome proliferator-activated receptors (PPAR-α/β/δ/γ). Pretreatment with PPAR inhibitors attenuated the inhibitory effect of AVT on the expression of inflammatory cytokines. CONCLUSION:AVT may retard the cardiac aging process by upregulating PPARs.
Authors: Yonggang Ma; Ying Ann Chiao; Ryan Clark; Elizabeth R Flynn; Andriy Yabluchanskiy; Omid Ghasemi; Fouad Zouein; Merry L Lindsey; Yu-Fang Jin Journal: Cardiovasc Res Date: 2015-04-15 Impact factor: 10.787
Authors: Irene Alfaras; Clara Di Germanio; Michel Bernier; Anna Csiszar; Zoltan Ungvari; Edward G Lakatta; Rafael de Cabo Journal: Circ Res Date: 2016-05-13 Impact factor: 17.367
Authors: Cesar A Meschiari; Lucas C Pinheiro; Danielle A Guimaraes; Raquel F Gerlach; Jose E Tanus-Santos Journal: Naunyn Schmiedebergs Arch Pharmacol Date: 2015-11-28 Impact factor: 3.000