Search

Intracerebral hemorrhage (ICH) induces a complex sequence of apoptotic cascades and inflammatory responses, leading to neurological impairment. Transient receptor potential vanilloid 1 (TRPV1), a nonselective cation channel with high calcium permeability, has been implicated in neuronal apoptosis and inflammatory responses. This study used a mouse ICH model and neuronal cultures to examine whether TRPV1 activation exacerbates brain damage and neurological deficits by promoting neuronal apoptosis and neuroinflammation. ICH was induced by injecting collagenase in both wild‐type (WT) C57BL/6 mice and TRPV1−/− mice. Capsaicin (CAP; a TRPV1 agonist) or capsazepine (a TRPV1 antagonist) was administered by intracerebroventricular injection 30 min before ICH induction in WT mice. The effects of genetic deletion or pharmacological inhibition of TRPV1 using CAP or capsazepine on motor deficits, histological damage, apoptotic responses, blood–brain barrier (BBB) permeability, and neuroinflammatory reactions were explored. The antiapoptotic mechanisms and calcium influx induced by TRPV1 inactivation were investigated in cultured hemin‐stimulated neurons. TRPV1 expression was upregulated in the hemorrhagic brain, and TRPV1 was expressed in neurons, microglia, and astrocytes after ICH. Genetic deletion of TRPV1 significantly attenuated motor deficits and brain atrophy for up to 28 days. Deletion of TRPV1 also reduced brain damage, neurodegeneration, microglial activation, cytokine expression, and cell apoptosis at 1 day post‐ICH. Similarly, the administration of CAP ameliorated brain damage, neurodegeneration, brain edema, BBB permeability, and cytokine expression at 1 day post‐ICH. In primary neuronal cultures, pharmacological inactivation of TRPV1 by CAP attenuated neuronal vulnerability to hemin‐induced injury, suppressed apoptosis, and preserved mitochondrial integrity in vitro. Mechanistically, CAP reduced hemin‐stimulated calcium influx and prevented the phosphorylation of CaMKII in cultured neurons, which was associated with reduced activation of P38 and c‐Jun NH2‐terminal kinase mitogen‐activated protein kinase signaling. Our results suggest that TRPV1 inhibition may be a potential therapy for ICH by suppressing mitochondria‐related neuronal apoptosis. [ABSTRACT FROM AUTHOR]

BACKGROUND: Improved access to media and medical knowledge has elicited stronger public health awareness. OBJECTIVE: This study developed a smart drug interaction reminder system for patients to increase knowledge and reduce nurse workload. METHODS: This study used a single-group pre-test/post-test design and applied mining techniques to analyze the weight and probability of interaction among various medicines. Data were collected from 258 participants at a teaching hospital in northern Taiwan using convenience sampling. An app was used to give patients real-time feedback to obtain access to information and remind them of their health issues. In addition to guiding the patients on medications, this app measured the nurses' work satisfaction and patients' knowledge of drug interaction. RESULTS: The results indicate that using information technology products to assist the app's real-time feedback system promoted nurses' work satisfaction, improved their health education skills, and helped patients to better understand drug interactions. CONCLUSION: Using information technology to provide patients with real-time inquiring functions has a significant effect on nurses' load reduction. Thus, smart drug interaction reminder system apps can be considered suitable nursing health education tools and the SDINRS app can be integrated into quantitative structure-activity relationship intelligence in the future. [ABSTRACT FROM AUTHOR]