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Medicines for CHD
Published in Mark C Houston, The Truth About Heart Disease, 2023
Statins (also called HMG-CoA reductase inhibitors) block an enzyme called HMG-CoA reductase (3-hydroxy-3-methylglutaryl coenzyme A reductase) that is involved in the synthesis of mevalonate, a naturally occurring substance that is then used by the body to make sterols, including cholesterol.
Non-Congenital Acquired Myopathies
Published in Maher Kurdi, Neuromuscular Pathology Made Easy, 2021
Statins are inhibitors for HMG-CoA reductase, an enzyme that catalyzes the conversion of HMG-CoA to mevalonic acid, the precursor of cholesterol. They lower the cholesterol and LDL levels in the blood. They could interrupt cholesterol metabolism causing damage to the muscle sarcolemma and mitochondria, allowing the influx of calcium to the cells resulting in myonecrosis.
Chemopreventive Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
The statins are a class of lipid-lowering medications known as 3-hydroxy-3-methyl-glutaryl(HMG)-CoA reductase inhibitors, which reduce mortality in individuals with a high risk of cardiovascular disease by lowering cholesterol levels. It has been recently discovered that some HMG-CoA reductase inhibitors such as simvastatin (Figure 12.55) can reduce the proliferation, growth, and metastasis of tumor cells growing in vitro. The mechanism of this activity is presently unclear, but simvastatin appears to promote apoptosis in cancer cells growing in vitro (Figure 12.46). Structure of simvastatin.
Ezetimibe attenuates experimental diabetes and renal pathologies via targeting the advanced glycation, oxidative stress and AGE-RAGE signalling in rats
Published in Archives of Physiology and Biochemistry, 2023
Rabia Nabi, Sahir Sultan Alvi, Arunim Shah, Chandra P. Chaturvedi, Mohammad Faisal, Abdulrahman A. Alatar, Saheem Ahmad, M. Salman Khan
HMG-CoA reductase (HMG-R) is the key enzyme in the cholesterol biosynthetic pathway which catalyses the conversion of HMG-CoA to mevalonate and CoA (Alvi et al.2015, 2016). The activity of HMG-R was estimated by following the standard protocols (Alvi et al.2017a, 2017b). In brief, fresh 10% tissue homogenate was mixed with 9 ml of 0.1% saline arsenate and then 10 ml of 5% perchloric acid was added. This mixture was incubated at RT for 5 min and centrifuged at 2,000 rpm for 10 min. After centrifugation, 1 ml of the supernatant from each tube was taken out and mixed either with 0.5 ml of 1 M aqueous hydroxylamine hydrochloride or alkaline hydroxylamine hydrochloride for the determination of mevalonate and HMG-CoA, respectively. Thus obtained mixture was mixed with 1.5 ml of 0.616 M FeCl3 reagent (containing 5.2% TCA, prepared in 0.65 N HCl), incubated at RT for 10 min and the absorbance was read at 540 nm against a reagent blank in Eppendorf Bio-spectrophotometer.
Effects of Bushen Yiyuan recipe on testosterone synthesis in Leydig cells of rats with exercise-induced low serum testosterone levels
Published in Pharmaceutical Biology, 2022
Yirong Wang, Xiyang Peng, Zhihong Zhou, Changfa Tang, Wenfeng Liu
HMG-CoA, LDL-R, SR-BI, STAR and CYP11A1 are key enzymes in the synthesis process of testosterone in testicular Leydig cells (Liu et al. 2013). HMG-CoA reductase is a rate-limiting enzyme in the endogenous synthesis of cholesterol (Yu et al. 2015; Osaki et al. 2015; Yeganehjoo et al. 2017). HIE training causes the down-regulated expression of HMG-CoA reductase, which may be attributed to the decrease of serum testosterone levels caused by exercise (Cai et al. 2015). While serum testosterone was significantly increased in EFE, low-dose BYR and high-dose BYR groups, the expression of LDL-R mRNA was slightly reduced, suggesting that the biosynthesis of cholesterol in rats testicular Leydig cells that regulated by HMG-CoA reductase may be increased after drug dosing, which would inhibit the pathway of LDL-R transcription to intake exogenous cholesterol. In addition, compared with the normal group, SR-BI mRNA expression of the model, EFE, low-dose BYR and high-dose BYR groups were decreased, but there was no significant difference. However, the high-dose BYR group was closer to the normal group than the EFE and low-dose BYR group. Meanwhile, there was no significant change in total serum cholesterol, LDL-C, and HDL-C. Our study showed that SR-BI-mediated reverse uptake of exogenous cholesterol pathway was obstructed. Moreover, the changes in serum cholesterol may be related to the time, intensity, and the mode of exercise training.
Repurposing of atorvastatin emulsomes as a topical antifungal agent
Published in Drug Delivery, 2022
Alaa S. Eita, Amna M. A. Makky, Asem Anter, Islam A. Khalil
Statins are a recognized group of drugs that are primarily used as plasma cholesterol-lowering agents upon inhibiting the hydroxy-methyl-glutaryl-CoA (HMG-CoA) reductase enzyme (Sirtori, 2014). New studies on statins realized new therapeutic fields such as cancer therapy (Jiang et al., 2021), antibacterial (Ko et al., 2018), and antifungal treatment. Tavakkoli et al. showed the antifungal effects of statins against wide pathogenic species and reported that the HMG-CoA reductase enzyme was also revealed as a fungal enzyme; so, it will expose to inhibition by statins, which leads to fungal growth suppression due to ergosterol level decline (Tavakkoli et al., 2020). Atorvastatin (ATO) was reported as one of the statin categories effectively involved in antifungal therapeutic studies as it was investigated previously against Candida albicans (Nasr Esfahani et al., 2019). ATO-loaded solid lipid nanoparticles were reported to promote drug permeation through skin layers for anti-inflammatory activity (Shahraeini et al., 2020).