Neuroprotective mechanisms of 3-n-butylphthalide in neurodegenerative diseases

Since 3-n-butylphthalide (NBP) was approved by the China Food and Drug Administration for the treatment of acute ischemia stroke in 2002, a number of studies have investigated NBP worldwide. In recent years, NBP has also demonstrated potential as treatment of several neurodegenerative diseases, which has increased the interest in its mechanisms of protection and action. Clinical studies and studies that used cell or animal models, have directly demonstrated neuroprotective effects of NBP via the following mechanisms: i) Inhibiting the inflammatory reaction; ii) reducing mitochondrial oxidative stress; iii) regulating apoptosis and autophagy; iv) inducing resistance to endoplasmic reticulum stress; and v) decreasing abnormal protein deposition. Therefore, NBP may be a potential drug for neurodegenerative diseases, and it is particularly important to identify the mechanism of NBP as it may assist with the development of new drugs for neurodegeneration. The present review summarizes the neuroprotective mechanisms of NBP and discusses new perspectives and prospects. The aim of the current review is to provide a new summary regarding NBP and its associated mechanisms.