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OBJECTIVE: To explore the clinical value of high mobility group box-1 (HMGB-1), C-reactive protein (CRP), procalcitonin (PCT), and CRP to albumin (Alb) ratio in the diagnosis and evaluation of the severity of sepsis in children. PATIENTS AND METHODS: A total of 90 children, 50 with sepsis and 40 with general infection, whose symptoms did not meet the criteria for diagnosis of sepsis, were admitted to the Pediatrics Department of Jingzhou Central Hospital in Hubei Province between November 2021 and December 2022, were enrolled and selected as experimental and control group, respectively. The serum of two groups was collected within 24 hours after admission, the levels of HMGB-1 were detected by enzyme-linked immunosorbent assay (ELISA), and CRP, PCT, Alb, and hospitalization days were recorded. The differences in indicators between the two groups were compared, and correlation analysis was performed between hospitalization days and various indicators. The receiver operating characteristic (ROC) curve was drawn to evaluate the independent or combined value of CRP, PCT, HMGB-1, and CRP/Alb ratio in the early diagnosis of sepsis in children. RESULTS: These four indicators of children with sepsis were significantly higher than those in the general infection group (all p=0.000). The levels of CRP, PCT and CRP/Alb ratio were significantly positively correlated with the hospitalization days (r=0.329, 0.333, 0.329; p=0.02, 0.01, 0.002). The area under curve (AUC) of CRP, PCT, HMGB-1, and CRP/Alb ratio for the diagnosis of sepsis in children was 0.798, 0.817, 0.838, 0.809, respectively, and that of the combination of four indicators was 0.952. CONCLUSIONS: CRP, PCT, HMGB-1, and CRP/Alb ratio resulted as effective indicators for early diagnosis and evaluation of childhood sepsis, having a higher value in combined diagnosis. [ABSTRACT FROM AUTHOR]

The article presents a study aimed to explore the therapeutic effects of quercetin on rats with encephalitis, especially on cell apoptosis, and the levels of HMGB-1 and TLR-4. The study found Quercetin is effective in treating encephalitis rats possibly through inhibition of neuronal cell apoptosis and level of HMGB-1 and TLR-4.

To determine the effect of green tea with the active ingredient epigallocathechin-3-gallate (EGCG) on the inhibition of apoptosis in the middle cerebral artery occlusion (MCAO) model. Four month old male Rattus norvegicus rats with a body weight of 200–275 g was used for the MCAO model and divided into five groups, and the treatment was carried out for 7 days. Before being sacrificed, the subject had 1 cc of blood drawn for high mobility group box 1 (HMGB-1) examination using enzyme-linked immunosorbent assay (ELISA), and after being sacrificed, the brain tissue specimen was taken to examine caspase-3 and B-cell lymphoma 3 (BCL-3) using immunohistochemistry methods. There was no significant difference in HMGB-1 results for the treatment group compared to the control group (P1: 384.20 ± 231.72 [p = 0.553]; P2: 379.11 ± 268.4 [p = 0.526]; P3: 284, 87 ± 276.19 [p = 0.140]; P4: 435.32 ± 279.95 [p = 0.912]). There is a significant increase in BCL-2 expression between the treatment group compared to the control group (P1: 2.58 ± 0.51 [p = 0.04]; P2: 3.36 ± 0.50 [p<0.001]; P3: 4.00 ± 0.42 [p<0.001]; P4: 3.60 ± 0.52 [p<0.001]). There was a significant difference in caspase-3 expression compared to the control group in the P3 group (P1: 4.33 ± 0.49 [p = 0.652]; P2: 4.09 ± 0.30 [p = 0.136]; P3: 3.58 ± 0.51 [p = 0.01]; P4: 3.89 ± 0.42 [p = 0.063]). There is no correlation between HMGB-1 and caspase-3 (r = −0.063; p = 0.613) or BCL-2 (r = −0.106; p = 0.396). There is significant negative correlation between caspase-3 and BCL-2 (r = −0.459; p = 0.000). Green tea with the active ingredient EGCG can inhibit neuronal cell death through the apoptotic pathway and not through the activation of HMGB-1. [ABSTRACT FROM AUTHOR]

Objective: MicroRNA (miRNA)107 expression is downregulated but high mobility group box 1 (HMGB-1), Toll-like receptors (TLRs), and receptor for advanced glycation end products (RAGE) are upregulated in osteoarthritic (OA) cartilage. We investigated mir-107/HMGB-1 signaling in OA after hyperbaric oxygen (HBO) treatment.Design: MiR-107 mimic was transfected and the HMGB-1 was analyzed in OA chondrocytes. MiRNA targets were identified using bioinformatics and a luciferase reporter assay. After HBO treatment, the mRNA or protein levels of HMGB-1, RAGE, TLR2, TLR4, and inducible nitric oxide (NO) synthase (iNOS) and phosphorylation of mitogen-activated protein kinase (MAPK) were evaluated. The secreted HMGB-1 and matrix metalloproteases (MMPs) levels were quantified. Finally, we detected the HMGB-1 and iNOS expression in rabbit cartilage defects.Results: Overexpression of miR-107 suppressed HMGB-1 expression in OA chondrocytes. The 3'UTR of HMGB-1 mRNA contained a 'seed-matched-sequence' for miR-107. MiR-107 was induced by HBO and a marked suppression of HMGB-1 was observed simultaneously in OA chondrocytes. Knockdown of miR-107 upregulated HMGB-1 expression in hyperoxic cells. HBO downregulated the mRNA and protein expression of HMGB-1, RAGE, TLR2, TLR4, and iNOS, and the secretion of HMGB-1. HBO decreased the nuclear translocation of nuclear factor (NF)-κB, downregulated the phosphorylation of MAPK, and significantly decreased the secretion of MMPs. Morphological and immunohistochemical observation demonstrated that HBO markedly enhanced cartilage repair and the area stained positive for HMGB-1 and iNOS tended to be lower in the HBO group.Conclusions: HBO inhibits HMGB-1/RAGE signaling related pathways by upregulating miR-107 expression in human OA chondrocytes. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To investigate the expression changes of high mobility group box-1 (HMGB-1) and tissue factor (TF) and their correlation in the serum of sepsis rat models. MATERIALS AND METHODS: 30 rats were divided into the sham-operated group, 15 rats were in the control group. The cecal ligation and puncture method was used to make the animal model with abdominal infection induced by sepsis. There were 15 rats in the sepsis group among which they were divided into 3 subgroups at different time points after modeling (after 6 hours, 12 hours, 24 hours). Cardiac function indicators of the rats in each subgroup were monitored, including heart rate (HR), left ventricular end-diastolic pressure (LVEDP) and left ventricular developed pressure (LVDP), and enzyme-linked immunosorbent assay (ELISA) was used to test the changes of the expression levels of HMGB-1 and TF in the serum of the rats after 6 hours, 12 hours, 24 hours. Pearson correlation analysis was used to analyze the correlation between HMGB-1 and TF. RESULTS: HR and LVEDP of the rats in the sepsis group were significantly higher than those of the rats in the control group. The differences were statistically significant (p<0.050). LVDP of the rats in the sepsis group was markedly lower than that of the rats in the control group. The differences were statistically significant (p<0.050). The expressions of HMGB-1 and TF of the rats in the subgroups of the sepsis group were higher than those of the rats in the control group after 6 hours, 12 hours, 24 hours; the expression levels of HMGB-1 and TF of the rats with sepsis increased with time. The differences were statistically significant (p<0.050). When the expressions of HMGB-1 and TF of the rats in the sepsis group were compared with each other within the group the differences were significantly different (p<0.050). The expressions of HMGB-1 and TF in the subgroups at the 24th hour were significantly higher than those at the 6th hour. The differences were statistically significant (p<0.050). The differences in the expression of TF of the rats in the control group were not statistically significant (p>0.050). There was a significant positive correlation between HMGB-1 and TF of the rats in the sepsis group (r=0.772, p=0.002). CONCLUSIONS: The expression levels of HMGB-1 and TF of the rats with sepsis gradually increased with time, and the level of HMGB-1 was positively correlated with the level of TF. [ABSTRACT FROM AUTHOR]

Impaired corneal healing is still a major cause of blindness. As RAGE ( r eceptor for a dvanced g lycation e ndproducts) is involved in inflammation and wound healing in other tissues, we here investigated its relevance for corneal wound healing. Corneal re-epithelialization after alkaline injury was analysed in an ex-vivo approach with cultured, enucleated eyes from mice either of the C57Bl/6 NChR genotype (RAGE+/+) and mice of the same strain lacking the RAGE gene (RAGE−/−). The wound area was determined time dependently by fluorescence imaging using fluorescein staining. The eyes of RAGE−/− mice showed a significantly slower re-epithelialization than eyes of the RAGE+/− and the RAGE+/+ genotype. In immunohistochemistry, RAGE expression was increased in wounded corneas whereas the abundance of the RAGE ligand HMGB1 was unaffected, but an increase in S100b-like proteins was revealed upon injury. However, neither the addition of the RAGE agonist HMGB1 or an HMGB1 antagonising antibody nor bovine S100b protein to the culture medium of the wounded eyes had an effect on corneal wound closure in ex-vivo . Further gene expression analysis by RT-PCR demonstrated an increase in RAGE expression on the mRNA level, no significant regulation of HMGB1 and a differential regulation of the S100 gene family after alkaline burn of the cornea. In conclusion, RAGE is clearly involved in corneal re-epithelialization most probably mediated by signalling via S100 proteins. [ABSTRACT FROM AUTHOR]