Given an abstract from a research paper, your task is to identify and label relationships between chemical compounds and genes mentioned in the abstract.

The relationship type must be one of ['DOWNREGULATOR', 'SUBSTRATE', 'INDIRECT-REGULATOR', 'PART-OF', 'MODULATOR-ACTIVATOR', 'REGULATOR', 'INHIBITOR', 'COFACTOR', 'UPREGULATOR', 'ACTIVATOR', 'ANTAGONIST', 'NOT', 'INDIRECT-DOWNREGULATOR', 'SUBSTRATE_PRODUCT-OF', 'INDIRECT-UPREGULATOR', 'AGONIST', 'PRODUCT-OF', 'MODULATOR', 'DIRECT-REGULATOR', 'UNDEFINED', 'AGONIST-INHIBITOR', 'AGONIST-ACTIVATOR', 'MODULATOR-INHIBITOR'].

Please format your output as a JSON array. Each entry in the array should express a single relation, formatted as ["<Entity_A>", "<RELATION_A_B>", "<Entity_B>"]. If no relations can be found, please output an empty JSON array [].

Abstract:

Mechanisms of lipid-lowering agents. Lipid-lowering agents are used with the purpose of ameliorating hyperlipoproteinemias, in order to prevent arterial disease. Lipid-lowering drugs can be classified into absorbable agents and into nonabsorbable compounds, acting within the gastrointestinal lumen. Absorbable drugs (fibric acids, nicotinic acid, probucol, HMG-CoA reductase inhibitors) reduce plasma very-low-density lipoproteins (VLDL) and/or low-density lipoproteins (LDL) by a variety of mechanisms. Fibric acids, in particular, act by stimulating the catabolism of VLDL and also, as a consequence, improving LDL delipidation, thus favoring receptor uptake. Nicotinic acid and acipimox interfere with the biosynthesis of LDL and can also improve the clearance of VLDL/LDL. Probucol acts by a newly described mechanism, i.e. accelerating reverse transport of cholesteryl esters from high-density lipoproteins to lower-density lipoproteins. Finally, HMG-CoA reductase inhibitors, interfering with the biosynthesis of cholesterol, can induce an increased expression of liver high-affinity lipoprotein receptors. Nonabsorbable agents (anion-exchange resins, neomycin, beta-sitosterol) interrupt the recirculation of bile acids and/or reduce the absorption of cholesterol with the gut. They display a selective activity on hypercholesterolemia, again by increasing LDL receptor expression. The choice of one or more lipid-lowering agents will depend upon the patient 's phenotype, determining responsiveness to the pharmacological treatment.
[["probucol", "INDIRECT-DOWNREGULATOR", "plasma very-low-density lipoproteins"], ["probucol", "INDIRECT-DOWNREGULATOR", "LDL"], ["Probucol", "REGULATOR", "lower-density lipoproteins"], ["nicotinic acid", "INDIRECT-DOWNREGULATOR", "low-density lipoproteins"], ["nicotinic acid", "INDIRECT-DOWNREGULATOR", "LDL"], ["Nicotinic acid", "INDIRECT-REGULATOR", "LDL"], ["fibric acids", "INDIRECT-DOWNREGULATOR", "LDL"], ["Fibric acids", "INDIRECT-DOWNREGULATOR", "VLDL"], ["cholesteryl esters", "SUBSTRATE", "lower-density lipoproteins"], ["cholesteryl esters", "SUBSTRATE", "high-density lipoproteins"], ["fibric acids", "INDIRECT-DOWNREGULATOR", "VLDL"], ["fibric acids", "INDIRECT-DOWNREGULATOR", "plasma very-low-density lipoproteins"], ["nicotinic acid", "INDIRECT-DOWNREGULATOR", "plasma very-low-density lipoproteins"], ["fibric acids", "INDIRECT-DOWNREGULATOR", "low-density lipoproteins"], ["probucol", "INDIRECT-DOWNREGULATOR", "low-density lipoproteins"], ["probucol", "INDIRECT-DOWNREGULATOR", "VLDL"], ["Fibric acids", "INDIRECT-REGULATOR", "LDL"], ["nicotinic acid", "INDIRECT-DOWNREGULATOR", "VLDL"], ["Probucol", "REGULATOR", "high-density lipoproteins"]]