Objective The 3- N -butylphthalide (NBP) comprises one of the chemical constituents of celery oil. It has a series of pharmacologic mechanisms including reconstructing microcirculation, protecting mitochondrial function, inhibiting oxidative stress, inhibiting neuronal apoptosis, etc. Based on the complex multi-targets of pharmacologic mechanisms of NBP, the clinical application of NBP is increasing and more clinical researches and animal experiments are also focused on NBP. The aim of this review was to comprehensively and systematically summarize the application of NBP on neurologic diseases and briefly summarize its application to non-neurologic diseases. Moreover, recent progress in experimental models of NBP on animals was summarized. Data sources Literature was collected from PubMed and Wangfang database until November 2018, using the search terms including “3- N -butylphthalide,” “microcirculation,” “mitochondria,” “ischemic stroke,” “Alzheimer disease,” “vascular dementia,” “Parkinson disease,” “brain edema,” “CO poisoning,” “traumatic central nervous system injury,” “autoimmune disease,” “amyotrophic lateral sclerosis,” “seizures,” “diabetes,” “diabetic cataract,” and “atherosclerosis.” Study selection Literature was mainly derived from English articles or articles that could be obtained with English abstracts and partly derived from Chinese articles. Article type was not limited. References were also identified from the bibliographies of identified articles and the authors’ files. Results NBP has become an important adjunct for ischemic stroke. In vascular dementia, the clinical application of NBP to treat severe cognitive dysfunction syndrome caused by the hypoperfusion of brain tissue during cerebrovascular disease is also increasing. Evidence also suggests that NBP has a therapeutic effect for neurodegenerative diseases. Many animal experiments have found that it can also improve symptoms in other neurologic diseases such as epilepsy, cerebral edema, and decreased cognitive function caused by severe acute carbon monoxide poisoning. Moreover, NBP has therapeutic effects for diabetes, diabetes-induced cataracts, and non-neurologic diseases such as atherosclerosis. Mechanistically, NBP mainly improves microcirculation and protects mitochondria. Its broad pharmacologic effects also include inhibiting oxidative stress, nerve cell apoptosis, inflammatory responses, and anti-platelet and anti-thrombotic effects. Conclusions The varied pharmacologic mechanisms of NBP involve many complex molecular mechanisms; however, there many unknown pharmacologic effects await further study.

Background: Anti-N-methyl-D-aspartate receptor (NMDAR) immunoglobulin G antibodies which exist on myelin sheaths, composed of oligodendrocytes, especially target GluN1 subunits and are highly characteristic of anti-NMDAR encephalitis which is a newly recognized autoimmune encephalitis (AE) characterized by psychiatric symptoms, behavioral abnormalities, seizures, cognitive impairment and other clinical symptoms. Myelin oligodendrocyte glycoprotein (MOG) is a type of protein which is expressed on the surface of oligodendrocytes and myelin in the central nervous system. Anti-MOG antibodies cause demyelination. In some rare reported cases, these two types of antibodies have been found to co-exist, but the underlying mechanisms remain unknown.Case presentation: Here we report cases of 4 inpatients (median age 31.5 years, age range 27–43 years) from The Second Xiangya Hospital of Central South University between March 2018 and April 2019. Two of the cases were first diagnosed as anti-NMDAR encephalitis and had developed visual impairments in the course of the dosage reduction during corticosteroid therapy. They were found at the time, to have anti-MOG antibody-positive CSF and/or serum. Another patient was diagnosed with anti-MOG inflammatory demyelinating diseases (IDDs) when he tested double positive for both anti-NMDAR and anti-MOG antibodies early in the course of his illness. Over the course of the dosage reduction during corticosteroid therapy, his symptoms deteriorated; however, anti-MOG antibody levels elevated while anti-NDMAR antibody levels remained low. The other patient had initially developed psychiatric symptoms and limb weakness. She was also double positive for anti-NMDAR and anti-MOG antibodies early in the course of her illness. However, over the course of the dosage reduction during corticosteroid therapy, her symptoms worsened and levels of both antibodies elevated.Conclusion: Anti-NMDAR and anti-MOG antibodies may coexist in rare cases. In addition, anti-NMDAR encephalitis and anti-MOG inflammatory demyelinating diseases may occur either simultaneously or in succession. Thus, when a patient is diagnosed with either of these two diseases, but exhibits symptoms of the other disease, the possibility of co-occurrence with both these diseases should be considered and the appropriate antibodies should be accurately detected to enable prompt selection of appropriate treatments by the physicians.