1.Simvastatin (Simvastatin, ZOCOR, Simcor, Simcor, Kybixin)
It is an inhibitor of hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase, which can reduce the concentration of normal and elevated low-density lipoprotein cholesterol (LDL-C). The mechanisms include, among others, reduction of VLDL cholesterol concentrations, induction of LDL receptors, leading to a decrease in LDL cholesterol and an increase in LDL-C catabolism. Apolipoprotein B (apo B) levels were also significantly reduced during simvastatin treatment. Since each LDL particle contains one molecule of apo B and apo B is rarely found in other lipoproteins, this also suggests that simvastatin not only causes loss of cholesterol from LDL but also reduces the concentration of circulating LDL particles. In addition, simvastatin elevates high-density lipoprotein sterol (HDL C) concentrations and lowers plasma triglycerides (TG). All of these can lead to a decrease in total cholesterol/HDL-C and LDL-C/HDL-C. Yu Mengyue, Department of Cardiovascular Medicine, Fu Wai Hospital, Beijing, China
2.Lovastatin (Lovastatin, Xinlu, Elotin)
It competitively inhibits hydroxymethylglutaryl coenzyme A reductase, the rate-limiting enzyme in the process of cholesterol synthesis in vivo, which reduces the synthesis of cholesterol and increases the synthesis of LDL receptors, with the main site of action being in the liver, resulting in lower blood cholesterol and LDL cholesterol levels, thus having an effect on the prevention and treatment of atherosclerosis and coronary heart disease. This product also reduces serum triglyceride level and increases blood HDL level.
3.Fluvastatin (Lescol)
It is a fully synthetic cholesterol-lowering drug, which is an inhibitor of antelope methylglutaryl coenzyme A (HMG a CoA) reductase, and can convert HMG a CoA into 3 methyl a 3,5 a dihydroxypentanoic acid. This product works in the liver, inhibiting endogenous cholesterol synthesis and reducing the cholesterol content in hepatocytes. It stimulates the synthesis of LDL receptors and improves the uptake of LDL particles to reduce the concentration of total plasma cholesterol.
4.Pravastatin (Pravastatin Mevalotin, Mevalotin, Pravachol)
It is a competitive inhibitor of 3-hydroxy 3-methylglutaryl coenzyme A reductase (HMG-CoA reductase), which is the rate-limiting enzyme in the initial stage of cholesterol biosynthesis, and this drug reversibly inhibits HMG-CoA reductase, thereby inhibiting cholesterol biosynthesis. This drug exerts its hypolipidemic effect in two ways: firstly, by reversibly inhibiting the activity of HMG-CoA reductase, the amount of intracellular cholesterol is reduced to a certain extent, leading to an increase in the number of low-density lipoprotein (LDL) receptors on the cell surface, thus enhancing the receptor-mediated catabolism of LDL-C and the clearance of LDL-C from the blood; secondly, by inhibiting the LDL-C precursor-very low density lipoprotein (VLDL-C) synthesis in the liver, thus inhibiting the production of LDL-C.
5. Atorvastatin (Atorvastatin Lipitor, Lipitor, Arle)
It is a selective and competitive inhibitor of HMG-CoA reductase, a rate-limiting enzyme that converts 3-hydroxy-3-methyl-glutaryl coenzyme A into mevalonate (a precursor of sterols including cholesterol). . Triglycerides and cholesterol are combined in the liver to form very low density lipoprotein cholesterol (VLDL) and released into the plasma for further transport to surrounding tissues. LDL is formed from VLDL and is metabolized primarily by the high-affinity LDL receptor.
6.Risuvastatin (Rosuvastatin)
Rosuvastatin is a selective and competitive antagonist of HMG-CoA reductase, the rate-limiting enzyme that converts hydroxymethylglutaric acid monoacyl coenzyme A into formaldehyde valeric acid, a precursor of cholesterol. In vivo studies in animals and in vitro studies in cultured animal and human cells have shown that reseruvastatin acts highly selectively in the liver – the target organ for cholesterol lowering. In both in vivo and in vitro studies, Rosuvastatin exerts its lipid-modulating effects in two ways: 1. by increasing the number of LDL receptors on the cell surface of the liver, thereby increasing LDL uptake and catabolism; 2. by inhibiting hepatic synthesis of VLDL and reducing the total number of VLDL and LDL particles.
7.Blood Lipid Kang (Xue Zhi Kang)
The main ingredient is red yeast, which is a proprietary Chinese medicine. It can lower blood cholesterol, triglyceride, LDL cholesterol and raise HDL cholesterol; inhibit the formation of atherosclerotic plaque and protect vascular endothelial cells; inhibit lipid deposition in the liver.
8.Clofibrate (Clofibrate)
It is a lipid regulator of clofibrate derivatives, which can lower lipids by lowering very low density lipoproteins. However, the mechanism of its lipid-lowering effect is not fully understood, which may involve inhibiting the release of hepatic lipoproteins (especially very low density lipoproteins) and cholesterol synthesis, changing hepatic triglyceride synthesis, strengthening the role of lipoprotein esterase, increasing steroid secretion and excretion from feces, and increasing circulating triglyceride (very low density lipoprotein) clearance.
9.Fenofibrate (Fenofibrate 力平之，诺之妥)
Clofibrate derivatives are lipid regulating drugs, which reduce LDL, cholesterol and triglyceride by inhibiting the production of very low density lipoprotein and triglyceride and increasing their catabolism at the same time; they also increase the production of Apo A1 and A11, thus increasing HDL. This product also has the effect of lowering blood uric acid in normal people and patients with hyperuricemia. Animal experiments have shown that fenofibrate has teratogenicity and carcinogenicity.
10.Benzafibrate (Bezafibrate Staphylococcus, Abeta, Yizit)
Clofibrate derivatives are lipid regulating drugs. First, it increases the activity of lipoprotein lipase and hepatic lipase to promote the catabolism of very low-density lipoprotein and reduce the level of blood triglycerides. Secondly, it decreases the secretion of very low density lipoprotein. This product lowers blood LDL and cholesterol, probably by enhancing the clearance of receptor-bound LDL. It has a stronger effect on triglycerides than on cholesterol, and also increases HDL. In addition, it may lower fibrinogen. The study has not found that this product has carcinogenic and mutagenic effects.
11.Colestyramine
Combine with bile acid in the small intestine, forming insoluble compounds to prevent its reabsorption, and excreted in the feces. The combination of this product with bile acids in the small intestine leads to an increase in the synthesis of bile acids in the liver. Since the synthesis of bile acids is based on cholesterol as a substrate, it leads to a decrease in intrahepatic cholesterol, which leads to an increase in the activity of hepatic LDL receptors and the removal of LDL from plasma. It increases the synthesis of hepatic very low density lipoproteins, thereby increasing the concentration of plasma triglycerides, especially in people with hypertriglyceridemia. It decreases bile acids in serum and relieves itching due to excessive deposition of bile acids in the skin. This product increases the incidence of small intestinal tumors in rats taking strong carcinogens.
12.Ezetimibe (Ezetimibe益适纯, Ezetrol)
It is an oral, potent lipid-lowering drug with a mechanism of action different from other lipid-lowering drugs (e.g., statins, bile acid chelators (resins), phenoxyacid derivatives and plant-based sterol esters). The product adheres to the brush border of the small intestinal villi and inhibits the absorption of cholesterol, thereby reducing the transport of cholesterol from the small intestine to the liver, resulting in a decrease in hepatic cholesterol storage and thus increasing the clearance of cholesterol from the blood. It does not increase bile secretion (e.g., bile acid chelators) or inhibit cholesterol synthesis in the liver (e.g., statins). It inhibits cholesterol absorption from the small intestine by 54% compared to placebo. Statins reduce the synthesis of cholesterol in the liver. The combination of the two drugs can further reduce cholesterol levels and is superior to the two drugs alone.
13.Nicotinic acid (Nicotinic Acid, Niaspan, Benjoy)
Nicotinic acid is converted into nicotinamide in the body, and then formed with ribose adenine and other nicotinamide adenine dinucleotide (coenzyme I) and nicotinamide adenine dinucleotide phosphate (coenzyme II), which is necessary for the metabolism of lipid amino acids, proteins, purines, oxidation of tissue whistle and glycogen decomposition. Niacin decreases the utilization of coenzyme A; it affects the transport of cholesterol in the blood by inhibiting the synthesis of very low density lipoprotein (VLDL) and lowers serum cholesterol and triglyceride concentrations at high doses. Niacin has peripheral vasodilator effect.
14.Acipimox (Acipimox Lezyme, Olbetam, Yiping)
The pharmacological effect of this product is mainly to reduce triglycerides, but also has a certain effect on cholesterol reduction.
15.Inositol Nicotinate (Inositol Nicotinate)
This product is a mild peripheral vasodilator, gradually hydrolyzed into niacin and inositol in the body, so it has the pharmacological effects of both niacin and inositol, including lipid-lowering effects. Its vasodilator effect is milder and longer lasting than that of niacin, and there are no adverse effects such as flushing and stomach discomfort after taking niacin. It can selectively dilate blood vessels at lesion sites and sensitive sites stimulated by cold, while the dilating effect on normal blood vessels is weaker. In addition, it also has weak thrombus dissolution, anticoagulation, anti-fatty liver, reduce capillary fragility and other effects.
16.Probucol (Probucol Changtai)
It is a lipid regulator and has anti-atherosclerotic effect. Its lipid-lowering effect is to reduce blood cholesterol and LDL by reducing cholesterol synthesis and promoting cholesterol decomposition, and also change the nature and function of HDL subtypes, so that blood HDL cholesterol is reduced. The clinical significance of its HDL cholesterol-lowering effect is unknown. The effect of this product on blood triglycerides (triacylglycerols) is small. It has significant antioxidant effect, can inhibit the formation of foam cells, delay the formation of atherosclerotic plaque, and subside the formed atherosclerotic plaque.
Selection principle: Statin lipid-lowering drugs should be preferred for hypercholesterolemia. Niacin reduces TC, LDL-C and TG, but the side effects limit their application. Acipimox has fewer side effects and can be used. Combined treatment with statins and bile acid compartmentalizers is available for those with extremely elevated TC or LDL-C. Mixed hyperlipidemia: If TC and LDL-C elevation are predominant, statins are available. Rosuvastatin is the most effective statin per unit dose, and fluvastatin has fewer side effects and is safer for elderly patients. Inositol nicotinate is used for the adjuvant treatment of hyperlipidemia, atherosclerosis, and various peripheral vascular disorders (e.g., occlusive atherosclerosis, limb arteriospasm, frostbite, vascular migraine, etc.). Probucol is a strong antioxidant preparation with anti-atherosclerotic effect in addition to lipid regulating effect.