Baicalein shows anti-inflammatory effects in human rheumatoid arthritis fibroblast-like synoviocytes (RAFLS). Considering its anti-proliferatory effects on various cancer cells, we investigated the effects of baicalein on interleukin-1 beta (IL-1β)-induced proliferation of human RAFLS. Cell proliferation was examined by (3)H-thymidine incorporation assay. Western blot analysis was performed to assess the phosphorylation of extracellular regulating kinase (ERK), p38, and c-Jun N-terminal kinase, and nuclear translocation of nuclear factor kappa B (NF-κB) subunit p65. Notably, baicalein significantly suppressed IL-1β-mediated RAFLS proliferation (P < 0.05), along with reduced ERK1/2 and p38 phosphorylation. The IL-1β-induced p65 nuclear translocation and NF-κB DNA binding activity was significantly decreased by baicalein. Additionally, the inhibitory effects of baicalein on IL-1β-induced proliferation of RAFLS were dose-dependently reversed by the addition of recombinant macrophage migration inhibitory factory (MIF). Our results indicate that baicalein inhibits IL-1β-induced RAFLS proliferation, which involves suppression of NF-κB transcriptional activity and MIF-mediated signaling.

Brain injury is the most common intracranial injury in human cerebrovascular disease, which may lead to ischemic stroke. Resveratrol induces ameliorative effects in the treatment of certain human diseases by regulating different signaling pathways. The present study assessed the therapeutic effects of resveratrol and its potential mechanism of action in the neurons from rats with ischemia/reperfusion-induced cerebral hemorrhage. The rat model of cerebral hemorrhage was established and reverse transcription-quantitative polymerase chain reaction, western blotting, immunohistochemistry and terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assays were subsequently performed to assess the therapeutic effects of resveratrol. The results demonstrated that treatment with resveratrol (10 mg/kg/day) decreased cerebral water content, hippocampal cell apoptosis and cerebral infarct volume compared with the PBS-treated group. Resveratrol treatment also increased neuronal cell viability, improved neurological function and blood brain barrier disruption compared with the PBS group following 21 days of treatment. The administration of resveratrol was demonstrated to decrease the levels of certain inflammatory factors, including ionized calcium binding adaptor molecule 1 and myeloperoxidase, in rats with cerebral hemorrhage. The results revealed that treatment with resveratrol regulated neuronal apoptosis by downregulating the transforming growth factor-β (TGF-β)-mediated extracellular signal-regulated kinase (ERK) signaling pathway. In conclusion, these results indicate that resveratrol decreases ischemia/reperfusion-induced neuronal apoptosis by downregulating the TGF-β-mediated ERK pathway in a rat model of cerebral hemorrhage and may serve as a potential agent for the treatment of cerebral hemorrhage.

Rationale: Intracranial small aneurysm is a rare cause of ischemic stroke, and been described only in sparse case reports. The exact pathophysiology, treatment strategies, and prognosis remain incompletely understood. Patient concerns: A 42-year-old man presented with an acute onset weakness of the right limbs. Diagnoses: Neuroimaging evaluation confirmed a diagnosis of acute ischemic stroke and left internal carotid artery (ICA) small aneurysm. Interventions: The patient underwent oral anti-platelet therapy (100 mg aspirin daily). Outcomes: The patient recovered to normal status within 4 weeks following antiplatelet treatment. During a follow-up period of 1 year, he remained neurologically asymptomatic and led a virtually normal life. Lessons: It is crucial for clinicians to be aware of this entity, as cerebral infarction caused by small cerebral aneurysm is extremely rare.