ABSTRACT
Objective@#To systematically evaluate the correlation between selenium in the body and the risk of chronic kidney disease (CKD), so as to provide insights into CKD prevention and control.@*Methods@#Publications pertaining to the correlation between selenium level and CKD were retrieved from electronic databases, including CNKI, WanFang Data, PubMed and Web of Science from inception until July 28, 2022. Meta-analysis was performed using the software Stata 16.0, and all measures were expressed with standardized mean difference (SMD) and its 95%CI. The source of heterogeneity was analyzed using subgroup analysis and meta-regression, and sensitivity analysis was performed using the leave-one-out method. In addition, the publication bias was evaluated with d funnel plot, Egger's test and Begg's test, and the robustness of the result was evaluated using the trim and filling method.@*Results@#A total of 2 990 publications were screened, and 63 eligible publications were included in the final analysis, including 18 cross-sectional studies, 40 case-control studies, 2 cohort studies and 3 randomized controlled trials (RCTs), which covered 5 099 CKD patients and 6 334 controls. Meta-analysis showed lower selenium levels in CKD patients than in controls (SMD=-1.828, 95%CI: -2.132 to -1.523, P<0.001). Subgroup analysis showed lower selenium levels among CKD patients than among controls from Asia, Europe and multiple continents (P<0.05), and lower selenium levels were detected in patients undergoing conservative treatment, hemodialysis and peritoneal dialysis than in controls (P<0.05), while the selenium levels were significantly lower in CKD patients than in controls in cross-sectional studies, case-control studies and RCTs (P<0.05). The selenium level was significantly lower among CKD patients than among controls regardless of the study year, sample size and score for quality of publications (P<0.05). Sensitivity analysis showed robustness of this meta-analysis. Publication bias was identified by funnel plot, Begg's test and Egger's test, and the robustness of the result was found using the trim-and-fill method. @*Conclusion @#There may be a possible correlation between selenium and the risk of CKD.
ABSTRACT
OBJECTIVE To investigates the effects of imperatorin on the oxidative stress in the cerebral cortex and hippocampus after focal cerebral ischemia/reperfusion injury. METHODS Transient focal cerebral ischemia/reperfusion model in male Sprague-Dawley rats was induced by 2 h middle cerebral artery occlusion followed by 24 h reperfusion. Imperatorin (1.25 and 2.5 mg·kg- 1) or vehicle were administered intraperitoneally at 1, 5 and 9 h after the onset of ischemia. At 24 h after reperfusion, the biomarkers of oxidative stress such as the levels of reactive oxygen species (ROS), lipid peroxidation products malondialdehyde (MDA), nitric oxide (NO) and total antioxidant capacity (T-AOC), the activities of inducible nitric oxide synthase (iNOS), superoxide dismutase (SOD) and catalase (CAT) in the cerebral cortex and hippocampus were observed. We also assessed the nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and the NAD(P)H-quinone oxidoreductase 1 (NQO-1) protein expression by Western blot. RESULTS As compared to vehicle-treated animals, imperatorin treatment significantly reduced the ROS, MDA, NO levels and iNOS activity, increased T-AOC and the activities of SOD and CAT. Furthermore, imperatorin treatment also significantly induced the nuclear translocation of Nrf2, enhanced the protein expression of HO-1 and NQO-1 in the cerebral cortex and hippocampus. CONCLUSION Our findings indicate that imperatorin can protect the brain against the excessive oxidative stress induced by cerebral ischemia/reperfusion through activation of Nrf2 signaling pathway.