Abstract Objective: the purpose of this study was to assess the impact of 14 treatments including a total of 10 dietary antioxidants on the risk of prostate cancer. Material and methods: we searched PubMed, Embase, the Cochrane Library, and the Web of Science for only randomized controlled trials (RCTs) to investigate the effect of these 10 antioxidants on the risk of getting prostate cancer. Using the Cochrane Risk of Bias Assessment Tool, the methodological quality of the included studies was evaluated. Data extraction: studies were appraised by two investigators and data were extracted. Using a surface under cumulative ranking (SUCRA) probability, a Bayesian network meta-analysis was undertaken to evaluate the relative ranking of agents. Results: from the earliest accessible date through August 2022, RCTs were gathered. A total of 14 randomized controlled trials were included with a total sample size of 73,365 males. The results of the network meta-analysis showed that green tea catechins (GTCs) significantly reduced the risk of prostate cancer (SUCRA, 88.6 %) followed by vitamin D (SUCRA, 55.1 %), vitamin B6 (54.1 %), and folic acid was the lowest (22.0 %). Conclusion: based on the Ranking Plot of the Network, we can state that GTCs might have an impact on the prevention of prostate cancer compared to other dietary antioxidants, but we still need quality literature to further prove it.

Resumen Objetivo: el propósito de este estudio fue evaluar el impacto de 14 tratamientos que incluyen un total de 10 antioxidantes dietéticos sobre el riesgo de cáncer de próstata. Material y métodos: buscamos en PubMed, Embase, la Biblioteca Cochrane y Web of Science solo ensayos controlados aleatorizados (ECA) para investigar el efecto de estos 10 antioxidantes sobre el riesgo de contraer cáncer de próstata. Se evaluó la calidad metodológica de los estudios incluidos mediante la herramienta Cochrane de evaluación del riesgo de sesgo. Extracción de datos: dos investigadores evaluaron los estudios y extrajeron los datos. Utilizando una probabilidad de clasificación acumulativa de superficie (SUCRA) se llevó a cabo un metanálisis de red bayesiano para evaluar la clasificación relativa de los agentes. Resultados: desde la primera fecha accesible hasta agosto de 2022, se recopilaron ECA. Se incluyeron 14 ensayos controlados aleatorizados con un tamaño de muestra total de 73.365 varones. Los resultados del metanálisis en red mostraron que las catequinas del té verde (GTC) redujeron significativamente el riesgo de cáncer de próstata (SUCRA, 88,6 %), seguidas de la vitamina D (SUCRA, 55,1 %), la vitamina B6 (54,1 %) y el ácido fólico fue el más bajo (22,0 %). Conclusión: según el diagrama de clasificación de la red, podemos afirmar que los GTC podrían tener un impacto en la prevención del cáncer de próstata en comparación con otros antioxidantes dietéticos, pero aún necesitamos literatura de calidad para demostrarlo.

ABSTRACT Purpose: Traumatic brain injury (TBI) remains a major public health problem and cause of death. Ulinastatin (UTI), a serine protease inhibitor, has been reported to have an anti-inflammatory effect and play a role in immunoregulation and organ protection by reducing reactive oxygen species (ROS) production, oxidative stress and inflammation. However, the neuroprotective of UTI in TBI has not been confirmed. Therefore, this study aimed to investigate the neuroprotection and potential molecular mechanisms of UTI in TBI-induced EBI in a C57BL/6 mouse model. Methods: The neurological score and brain water content were evaluated. Enzyme-linked immunosorbent assay was used to detect neuroinflammatory cytokine levels, ROS and malondialdehyde detection to evaluate oxidative stress levels, and TUNEL staining and western blotting to examine neuronal damages and their related mechanisms. Results: Treatment with UTI markedly increased the neurological score; alleviated brain oedema; decreased the inflammatory cytokine tumour necrosis factor a, interleukin-1β (IL-1β), IL-6 and nuclear factor kappa B (NF-kB) levels; inhibited oxidative stress; decreased caspase-3 and Bax protein expressions; and increased the Bcl-2 levels, indicating that UTI-mediated inhibition of neuroinflammation, oxidative stress and apoptosis ameliorated neuronal death after TBI. The neuroprotective capacity of UTI is partly dependent on the TLR4/NF-kB/p65 signalling pathway. Conclusions: Therefore, this study reveals that UTI improves neurological outcomes in mice and reduces neuronal death by protecting against neural neuroinflammation, oxidative stress and apoptosis.

ABSTRACT Purpose: Spontaneous intracerebral hemorrhage (ICH) is still a major public health problem, with high mortality and disability. Ulinastatin (UTI) was purified from human urine and has been reported to be anti-inflammatory, organ protective, and antioxidative stress. However, the neuroprotection of UTI in ICH has not been confirmed, and the potential mechanism is unclear. In the present study, we aimed to investigate the neuroprotection and potential molecular mechanisms of UTI in ICH-induced early brain injury in a C57BL/6 mouse model. Methods: The neurological score, brain water content, neuroinflammatory cytokine levels, oxidative stress levels, and neuronal damage were evaluated. Results: UTI treatment markedly increased the neurological score, alleviated brain edema, decreased the levels of the inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and NF-κB, decreased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and upregulated the levels of glutathione (GSH), superoxide dismutase (SOD), and Nrf2. This finding indicated that UTI-mediated inhibition of neuroinflammation and oxidative stress alleviated neuronal damage after ICH. The neuroprotective capacity of UTI is partly dependent on the ROS/MAPK/Nrf2 signaling pathway. Conclusions: UTI improves neurological outcomes in mice and reduces neuronal death by protecting against neural neuroinflammation and oxidative stress.

ABSTRACT Purpose To evaluate the effects of controlled decompression and rapid decompression, explore the potential mechanism, provide the theoretical basis for the clinical application, and explore the new cell death method in intracranial hypertension. Methods Acute intracranial hypertension was triggered in rabbits by epidural balloon compression. New Zealand white rabbits were randomly put into the sham group, the controlled decompression group, and the rapid decompression group. Brain water content, etc., was used to evaluate early brain injury. Western blotting and double immunofluorescence staining were used to detect necroptosis and apoptosis. Results Brain edema, neurological dysfunction, and brain injury appeared after traumatic brain injury (TBI). Compared with rapid decompression, brain water content was significantly decreased, neurological scores were improved by controlled decompression treatment. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining and Nissl staining showed neuron death decreased in the controlled decompression group. Compared with rapid decompression, it was also found that apoptosis-related protein caspase-3/ tumor necrosis factor (TNF)-a was reduced markedly in the brain cortex and serum, and the expression levels of necroptosis-related protein, receptor-interacting protein 1 (RIP1)/receptor-interacting protein 1 (RIP3) reduced significantly in the controlled decompression group. Conclusions Controlled decompression can effectively reduce neuronal damage and cerebral edema after craniocerebral injury and, thus, protect the brain tissue by alleviating necroptosis and apoptosis.