, Zahra Salimi, Fatemeh Zarei, Farshad Moradpour, Mohammad Rasool Khazaei, Mozafar Khazaei, Maryam Pourjalili Alzheimer disease (AD) is a common neurodegenerative disorder, characterized by memory impairment, dementia, and diminished cognitive function. This disease affects more than 20 million people worldwide. Amyloid beta (Aβ) plaques and neurofibrillary tangles (NFTs) are important pathological markers of AD. Multiple studies have indicated a potential association between elevated cholesterol levels and increased risk of AD, suggesting that lowering the cholesterol level could be a viable strategy for AD treatment or prevention. Statins, potent inhibitors of cholesterol synthesis, are widely used in clinical practice to decrease the plasma levels of LDL cholesterol in patients with hyperlipidemia. Statins are known to play a neuroprotective role in limiting Aβ pathology through cholesterol-lowering therapies. In addition to Aβ plaques and neurofibrillary tangles, the brains of AD patients exhibit signs of oxidative stress, neuroinflammatory responses, and synaptic disruption. Consequently, compounds with antioxidant, anti-inflammatory, and/or neuroprotective properties could be beneficial components of AD treatment strategies. In addition to lowering LDL cholesterol, statins have demonstrated therapeutic efficacy in various forms, including antioxidant, anti-inflammatory, and neuroprotective effects. These properties of statins are potential mechanisms underlying their beneficial effects in treating neurodegenerative diseases. Therefore, this review was conducted to provide an overview of the protective effects of statins against AD.
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, Kwan Chang Kim, Young Mi Hong Simvastatin has been reported to attenuate the development of pulmonary hypertension through increased apoptosis as well as reduced proliferation of smooth muscle cells in obstructive vascular lesions. Microarray experiment can accomplish many genetic tests in parallel. The purpose of this study is to evaluate altered expressions of gene in rat hearts with monocrotaline (MCT)-induced pulmonary arterial hypertension after simvastatin treatment.
Six-week-old male rats were grouped as follows: control group (C group, saline injection), M group (MCT 60 mg/kg), and S group (MCT 60 mg/kg plus 10 mg/kg/day simvastatin by gavage during 28 days). Body weight, right ventricular pressure and right ventricular/left ventricle+septum ratio in each group were measured. The rats were sacrificed after 28 days. Total RNA was extracted from the rat heart tissue and microarray analysis was performed.
Administration of simvastatin significantly inhibited the progression of right ventricular hypertrophy at day 28 in the S group than in the M group. Compared with the C group, MCT was associated with a significant difference in expression of genes related to biosynthesis and with the regulation of heart contraction rate. Simvastatin treatment resulted in a significantly changed expression of genes about the regulation of progression through cell cycle and system development compared to the M group. The expressions of nitric oxide synthase and brain natriuretic peptide were significantly decreased after simvastatin treatment.
Administration of simvastatin exerted inhibitory effects on right ventricular hypertrophy during the development of MCT-induced pulmonary arterial hypertension in rats. Simvastatin changes the expression of genes associated with various functions.
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