Ursodeoxycholic acid (UDCA) can be used to prevent atherosclerosis. However, the molecular mechanism of UDCA on carotid atherosclerosis is not known. A combination of bioinformatics, network pharmacology, and molecular docking was used to unravel the potential molecular mechanisms of UDCA in alleviating carotid atherosclerosis. The results of weighted gene co-expression network analysis (WGCNA) combined with differential expression analysis were used to screen for potent targets in carotid atherosclerosis. A typical target for UDCA in the treatment of carotid atherosclerosis was obtained by network pharmacology, and a protein-protein interaction network was constructed. Nine core targets were obtained using four algorithms of the cytoHubba plugin of Cytoscape 3.9.0, and molecular docking was completed using Autodock Vina 1.1.2. GO, and KEGG enrichment pathway analysis was performed based on the Metascape platform. The results showed that CD4, PTPRC, CCL5, MMP9, CD38, CASP1, CCR2, EGFR, and SYK were the targets of action of UDCA in the treatment of carotid atherosclerosis. The enrichment analysis results showed that these targets were significantly enriched in pathways associated with inflammation. In conclusion, this study highlights some of the molecular mechanisms of UDCA in the treatment of carotid atherosclerosis and provides a theoretical basis for future studies.
Rationale: Todd paralysis (a stroke-like presentation in some patients with epilepsy) caused by limbic encephalitis (LE) is not easily distinguished from acute ischemic stroke by clinicians in the emergency room. Patient concerns: We report a contactin-associated protein-like 2-antibody (CASPR2-Ab)-positive patient who presented with atypical LE. Diagnoses: CASPR2-Ab-positive LE was the presumed diagnosis. Re-evaluation of cerebrospinal fluid (CSF) samples revealed autoantibodies targeting CASPR2 at an immunoglobulin G titer of 1:1. The clinical presentation of subacute onset seizures, abnormal electroencephalography, hypermetabolism on positron emission tomography, good immunotherapy response, and the presence of specific antibodies in serum supports a diagnosis of autoimmune LE. Intervention: The patient received glucocorticoids (1 g for 3 days and 500 mg for 3 days), immunoglobulin (25 g for 3 days), sodium valproate (1 g for 3 days), and clonazepam (1 mg for 3 days). Outcomes: Remission of temporal lobe epilepsy symptoms and cognitive dysfunction was observed. Follow-up analysis of CSF and serological examination were not approved by the patient. His Mini-Mental State Examination score improved to 21/30. Stable remission of symptoms was achieved throughout the follow-up period of 50 days. Lessons: Autoimmune encephalitis (AE) should be considered in cases of late-onset epilepsy following meningioma peritumoral brain edema and resection. A diagnosis of AE should be considered in patients presenting with stroke-like symptoms if the magnetic resonance imaging abnormality does not match a known vascular territory. Early and correct diagnosis is crucial because immunotherapy is usually effective for this disease.
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