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There was a correlation between CHF and the dysfunction of CD4(+) T cells showing immune activation phenomenons of deviations from the Th1/Th2 balance towards Th1 and from the Th17/Treg balance towards Th17, which was also related to the types, severity and prognosis of the disease.

Objective This study aimed to investigate the incidence and related risk factors of cerebral microbleeds (CMBs) in young and middle-aged patients with hypertension. Methods The study included 232 young and middle-aged (18-59 years-old) patients with hypertension from September 2014 to December 2016 in the Department of Neurology, Affiliated Hospital of Guizhou Medical University, China. The data were recorded which included demographics, vascular risk factors, medication history, and imaging data of patients. CMBs were evaluated based on the microbleeds anatomical rating scale. Results Of the enrolled participants, 115 were CMB positive, accounting for 49.6%. CMBs were more prone to occur in deep regions than in others (39.13%). Multiple cerebral microbleeds were associated with white matter hyperintensities(WMH), dyslipidemia, hyperhomocysteine, and uric acid. Moreover, WMH, dyslipidemia, ever smoker, antiplatelets use, and hyperhomocysteine were found to be risk factors for deep or infratentorial CMBs in young and middle-aged patients with hypertension. However, the lobar CMBs only had an independent correlation with dyslipidemia in these participants. Conclusions The incidence of CMBs in patients with hypertension was relatively high. It mostly occurred in a deep or infratentorial area with more vascular-associated risk factors. However, in patients with lobar CMBs, factors associated with lipid metabolism, such as amyloid deposition and unidentified genotype variation, may be crucial. Screening and regular follow-ups of CMBs by Susceptibility Weighted Imaging and active prevention in young and middle-aged patients with hypertension have clinical significance for timely understanding and predicting the occurrence and development of related cerebrovascular disease events.

Ischemic stroke exhibits high morbidity, disability, and mortality, and treatments for ischemic stroke are limited despite intensive research. The potent neuroprotective benefits of Epimedium against ischemic stroke have gained lots of interest. Nevertheless, systematic research on the direct role and mechanisms of Epimedium in ischemic stroke is still lacking. Network pharmacology analysis coupled with experimental verification was utilized to systematically evaluate the potential pharmacological mechanism of Epimedium against ischemic stroke. The TCMSP database was used to mine the bioactive ingredients and Epimedium’s targets. The DrugBank, OMIM, and GeneCards databases were employed to identify potential targets of ischemic stroke. GO and KEGG pathway analyses were also carried out. The interaction between active components and hub targets was confirmed via molecular docking. An experimental ischemic stroke model was used to evaluate the possible therapeutic mechanism of Epimedium. As a result, 23 bioactive compounds of Epimedium were selected, and 30 hub targets of Epimedium in its function against ischemic stroke were identified, and molecular docking results demonstrated good binding. The IL-17 signaling pathway was revealed as a potentially significant pathway, with the NF-κB and MAPK/ERK signaling pathways being involved. Furthermore, in vivo experiments demonstrated that Epimedium treatment could improve neurological function and reduce infarct volume. Additionally, Epimedium reduced the activation of microglia and astrocytes in both the ischemic penumbra of the hippocampus and cerebral cortex following ischemic stroke. Western blot and RT–qPCR analyses demonstrated that Epimedium not only depressed the expression of IL-1β, TNF-α, IL-6, and IL-4 but also inhibited the NF-κB and MAPK/ERK signaling pathways. This study applied network pharmacology and in vivo experiment to explore possible mechanism of Epimedium’s role against ischemic stroke, which provides insight into the treatment of ischemic stroke.