M2 macrophages attenuate sepsis-induced AKI, presumably by upregulating IL-10 expression and suppressing TNF-α secretion.
Stroke is a leading cause of cardiovascular morbidity, economic and social burden and mortality. Novel approaches are needed to address stroke prevention and treatment. The purpose of this study was to explore the effects of aloe polysaccharide on caspase-3 expression following cerebral ischemia reperfusion injury in rats. Male Wistar rats were randomly divided into 5 groups (16 rats in each group): aloe polysaccharide, ginkgo leaf tablet, nimodipine, model and sham surgery groups. The rats were administered the appropriate drug or normal saline for 7 days by gavage. A rat model of cerebral ischemia and reperfusion injury was established using the middle cerebral artery occlusion (MCAO) model. Caspase-3 protein and mRNA expression levels in the cerebral cortex were detected by immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR), respectively. Results showed that caspase-3 protein and mRNA expression levels in the cerebral cortex in the aloe polysaccharide, ginkgo leaf tablet and nimodipine groups were significantly lower compared with the model group and were higher than the sham surgery group (P<0.05). No significant difference was observed in caspase-3 protein and mRNA expression among the aloe polysaccharide, the ginkgo leaf tablet and the nimodipine groups (P>0.05). In conclusion, aloe polysaccharide has a protective effect on cerebral ischemia that may be due to the inhibition of neuronal cell apoptosis.
Single nucleotide polymorphisms in the promoter region of interleukin-18 (IL-18), an inflammatory cytokine, have been linked to susceptibility to many diseases, including cancer and immune dysfunction. Here, we explored the potential association between the IL-18 -607C/A (rs1946518) promoter region polymorphism and susceptibility to ischemic stroke (IS). This locus was amplified from peripheral blood samples of 386 IS patients (cases) and 364 healthy individuals (controls) by the polymerase chain reaction with sequence-specific primers. Significant differences were observed by the χ2 test in the -607C/A (rs1946518) genotype and allele frequencies between cases and controls (P < 0.05). Furthermore, after excluding for age, gender, smoking status, and hypertension, logistic regression indicated that IS susceptibility of -607C carriers increased 1.6 times (OR = 1.601, 95%CI = 1.148-2.233, P = 0.006) compared to -607A carriers. Additionally, similar increases in IS risk were noted for male patients or patients less than 65 years old. In conclusion, IL-18 -607C/A (rs1946518) promoter polymorphism is associated with IS susceptibility, and the C allele may confer increased IS risk.
Supplemental oxygen is commonly used to treat severe respiratory failure, while prolonged exposure to hyperoxia can induce acute lung injury characterized by the accumulation of reactive oxygen species (ROS) and pulmonary inflammation. Dysregulation of microRNAs contributes to multiple diseases, including hyperoxia-induced acute lung injury (HALI). In this study, we explored the roles of miR-20b in mediating the response of type II alveolar epithelial cells (ACE IIs) to hyperoxia and the potential underlying mechanisms. We found that miR-20b was significantly decreased in the lung tissues of HALI models and H2O2-treated ACE IIs. Hyperoxia induced the release of TNF-α, decreased the mitochondrial membrane potential, and led to excessive ROS production and cell apoptosis. Overexpression of miR-20b suppressed the hyperoxia-induced biological effects in ACE IIs. miR-20b negatively regulated the expression levels of Mitofusin 1 (MFN1) and MFN2, the two key proteins of mitochondrial fusion, via complementarily binding to the 3ʹ-untranslated regions of mRNAs. Furthermore, both in vivo and in vitro, upregulation of MFN1 and MFN2 aggravated lung damage and cell apoptosis that were alleviated by miR-20b overexpression. These results provided new insights into the involvement of the miR-20b/MFN1/2 signaling pathway in HALI.
Background: As an immune marker, serum soluble programmed cell death ligand-1 (sPD-L1) is significantly increased in sepsis and is predictive of mortality. We investigated the prognostic value of sPD-L1 in postseptic immunosuppression and progression to chronic critical illness (CCI). Methods: Adults with sepsis in intensive care units (ICUs) for the first time were screened and assigned to either a CCI group (ICU stay ≥14 days with persistent organ dysfunction) or a rapid recovery (RAP) group based on clinical outcome. Data regarding basic admission information and clinical parameters were collected and compared across the two groups. Serum sPD-L1 levels were detected by enzyme-linked immunosorbent assay at admission and on the seventh day (D7). Logistic regression analysis was used to determine the factors affecting septic patients' lymphocytopenia diagnosis on day 7 and CCI progression during hospitalization. The receiver operating characteristic curve and DeLong test were used to assess variable predictive power. Results: During the study period, a total of 166 septic patients were admitted to the ICU, and 91 septic patients were enrolled after screening. Compared with those in healthy individuals, the sPD-L1 levels in septic patients were significantly higher and positively correlated with traditional inflammatory markers and disease severity scores (P < 0.05). In a multivariate regression analysis, sPD-L1 alone predicted lymphocytopenia on day 7 (P < 0.05). In the sepsis cohort, 59 patients (64.8%) experienced RAP, and 32 patients (35.2%) developed CCI. Compared with the RAP group, the patients in the CCI group had a higher mean age, greater severity of disease, and higher mortality (P < 0.05). D7-sPD-L1 remained higher in the CCI group, and the area under the curve that predicted the occurrence of CCI was equivalent to the APACHE II score, with areas under the curve of 0.782 and 0.708, respectively. Conclusions: The severity of infection and immunosuppression in sepsis may be linked to serum sPD-L1. D7-sPD-L1 is valuable in predicting the progression of CCI in patients.
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