Mitochondrial dysfunction and decreased mitochondrial content are hallmarks of aging that leads to decreased physical endurance. Our aim was to explore the anti-aging effect of resveratrol (RSVT) supplementation, a polyphenol, and/or exercise training, started at an older age, on improving physical activity, therefore, help in frailty avoidance and promotion of healthy aging in elderly. Eighteen-month-old aged mice received RSVT (15 mg/kg/day) and/or exercise trained for 4 weeks showed significant longer time to exhaustion with decreased blood lactate and free fatty acids levels associated with improved oxidative stress evidenced by decreased gastrocnemius muscle lipid peroxidation and increased antioxidant enzymes activities, catalase and superoxide dismutase, when compared to aged mice control group. These changes were accompanied by over-expression of skeletal muscle peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) mRNA, the master regulator of mitochondrial biogenesis, and increased muscle citrate synthase activity, a marker for mitochondrial function. These findings may provide evidence for improved physical endurance by RSVT supplementation or exercise training with better results of their combination, even at an older age, through increasing mitochondrial biogenesis and function. Increased muscle PGC-1α mRNA expression and citrate synthase enzyme activity in addition to improved aging-associated oxidative damage were among the mechanisms involved in this protection.

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Background & Aim Dyslipidaemia is highly prevalent among postmenopausal women and its management represents a keystone in the prevention of the worldwide increase in cardiovascular morbidity and mortality. Therapy choices for menopause-associated dyslipidaemia are limited and a matter of debate. So, it becomes prudent to search for natural safe alternatives. Vitamin D (VD) has been acknowledged as an essential factor in cardiovascular health. Thus, we aimed to illustrate the impact of different VD status on dyslipidaemia and atherogenic indices. Method 5 groups of rats were conducted; SHAM group fed control diet, ovariectomized rats fed control diet (OVX), ovariectomized rats fed VD-sufficient-high fat diet (HFD) (1 000 IU/ kg diet), ovariectomized rats fed VD-deficient-HFD (25 IU/ kg diet), and ovariectomized rats fed VD-replete-HFD (10 000 IU/ kg diet) for 16 weeks. Results Dyslipidaemia with an increased atherogenic index of plasma, atherosclerosis coefficient, cardiac risk ratio, and aortic total cholesterol accumulation in addition to reduced serum 25-hydroxy-VD levels was observed in the OVX and VD-sufficient HFD versus SHAM. These findings were aggravated by VD-deficient-HFD while reversed by VD-replete-HFD. The VD-mediated abundance of aortic ATP-binding cassette transporter A1 (ABCA1) expression, reduced activity of the inflammatory Jun N-terminal kinases (JNK), and downregulation of aortic cluster of differentiation-36 (CD36) receptors expression together with increased serum total antioxidant capacity and reduced serum malondialdehyde were among the supposed mechanisms. Conclusions Our study sheds light on alarming levels of VD deficiency among ovariectomized rats. VD repletion improved the menopause-associated dyslipidaemia and atherogenic indices through hypolipidemic, antioxidant, and anti-inflammatory effects.

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Background: Reactive Oxygen Species (ROS) production has been established as an essential contributor in the development cardiotoxicity. The increase of ROS production simultaneously leads to the inhibition of anti-oxidant systems. Forkhead transcription factor O1 (FOXO1) plays an important role in regulating metabolism and oxidant stress. Clozapine was used to induce cardiotoxicity. Forskolin the well-known anti-oxidant and anti-inflammatory agent was used to modulate the effect on both FOXO1 gene and its target gene catalase and to what extent it may protect against clozapine-induced cardiotoxicity. Methods:The animals were classified into: control group, forskolin group; forskolin was administered for 8 weeks; clozapine group, and forskolin + clozapine group; forskolin was pre-administered for 5 weeks then continued along with clozapine for the last 3 weeks. RT-qPCR and gel electrophoresis were done. We analyzed the relation between FoxO1 gene and oxidative stress.Results: These effects are achieved by the ability of Forskolin to modulate the expression of Foxo-1 and catalase, the levels of CKMB, troponin I, GST, MDA, and TNF-α, Caspase-3 were decreased, histopathological changes were improved. Forskolin reduce cardiomyocytes damage, and improve cardiac function by decreasing oxidative stress. Conclusion:Forkolin with its biological activities and anti-oxidative effects control cardiotoxicity induced by ROS in addition to its anti-inflammatory activity. This may be considered as therapy in cardiac problems management.