Probucol will become a New Model for Treating Cerebral Infarction with a High Risk of Hemorrhage.

Antiplatelet, antihypertensive, and lipid-lowering agents are the three foundational agents for secondary prevention of ischemic stroke, among which lipid-lowering is one of the most important cornerstones. Probucol is a potent antioxidative lipid-lowering drug used to prevent and treat atherosclerotic cardiovascular diseases and xanthomas. However, it has faded from Western markets by lowering LDL-C and HDL-C levels. Probucol alleviates atherosclerosis improving high-density lipoprotein function, and does not increase the risk of cardiovascular events. Probucol-induced pharmacological changes in HDL-C may not be a reliable prognostic marker for cardiovascular risk. Q-T interval prolongation is a rare adverse reaction as described in the manufacturer's instructions, but prolonged Q-T interval may only be an intermediate pharmacological phenomenon of electrophysiological changes, and as a result, probucol has a strong benefit for secondary prevention of cardiovascular events and can reduce mortality without increasing the risk of cardiovascular and cerebrovascular adverse events. The new mechanism is that probucol penetrates the core of lowdensity lipoprotein particles, enhancing the activity of plasma cholesteryl ester transfer protein and liver scavenger receptor type I activity, thereby reducing LDH; at the same time, increasing the activity of paraoxonase 1, strengthened the antioxidant function of HDL, and reduced the serum HDL-C. If clinical or imaging findings suggest a high risk of recurrence of cerebral ischemia with a high risk of cerebral hemorrhage, probucol may be selected for prevention. This article focuses on basic research and clinical evidence and provides new insights into the low bioavailability.

Probucol will become a new model for treating cerebral infarction with a high risk of hemorrhage: A narrative review.

Lipid-lowering agents are relevant in stroke prevention. Probucol (PU) is an antioxidative and lipid-lowering drug that has been used to treat atherosclerotic cardiovascular diseases and xanthomas. The drug penetrates the core of low-density lipoprotein cholesterol (LDL-C) particles, enhancing the activity of plasma cholesterol l ester transfer protein (CETP) and strengthening the liver scavenger receptor type I, resulting in reducing LDL-C; by increasing the activity of paraoxonase 1, upregulating the antioxidant function of high-density lipoprotein (HDL), and it decreases the serum HDL-cholesterol (HDL-C) level. This drug has been retired from the Western markets for lowering HDL-C levels and Q-interval prolongation. The latter side effect has been rarely reported and may be transient. Recent clinical evidence supports the effectiveness of PU in preventing cardiovascular events and in reducing mortality, irrespective of the reduction of HDL-C. Based on basic research and clinical studies, it appears that PU might be a valuable alternative when statins are ineffective or contraindicated, in patients at high risk of recurrence of cerebral ischemia and hemorrhage.