Silencing information regulator 1 ameliorates lipopolysaccharide-induced acute lung injury in rats via the upregulation of caveolin-1.

BACKGROUND: Acute lung injury (ALI) is an intractable medical problem linked with to high morbidity and mortality all over the worldglobally. The prognosis of advanced acute lung injury remains persistently poor due to its underlying mechanisms remain unclear.Despite advancements in medical research, the its prognosis of advanced ALI remains persistently poor due to unclear underlying mechanisms. We aimed to investigate the protective effects of silencing information regulator 1 (SIRT1) on lipopolysaccharide (LPS)-induced acute lung injuryALI and to reveal its underlying molecular mechanism. METHODS: Male Sprague--Dawley rats were divided grouped into 4 groupsfour: normal saline group (group NS), lipopolysaccharide group (group L), SIRT1 activator SRT1720-pretreated group (group S), and SIRT1 inhibitor EX527- pretreated group (group E). Rats They were intranasally dripped with LPS to establish the model of ALI modelsacute lung injury respectively. We investigated the effect of SIRT1 on acute lung injury by analysing We analyzed the CT images of the rat lungs and used, HE staining, lung wet-to-dry ratio, inflammatory factor expression, lung injury marker expression, immunohistochemistry, and related mRNA expression to determine the effect of SIRT1 on ALI. RESULTS: Our results show that LPS induction produced resulted in acute lung injury, ALI and disrupting disrupted normal SIRT1 expression, which led to the overexpression of STAT3, TLR4, TNF-ɑ, and IL-6 and suppression of Cav-1 expression. Upregulation The upregulation of Cav-1 protein and mRNA following the administration of an SIRT1 agonist resulted in reduced lung injury. SRT1720 pretreatment was closely associated with reduced expressions of STAT3,TLR4, TNF-ɑ, and IL-6. ALI lung injury was more severeworsened after administration of SIRT1 inhibitors, and the changes in the above indicators were reversed. CONCLUSIONS: These results suggest that SIRT1 may protect against LPS-induced acute lung injuryALI via by counteracting inflammatory remissionion, and this protective effect might may be mediated by suppressing STAT3 to activate the expression ofinduce Cav-1 expression.

Meta-analysis of correlationship between HLA-G 3'UTR 14-bp Ins/Del polymorphism and virus susceptibility.

BACKGROUND: There is a considerable amount of literature on the potential relationship between human leukocyte antigen-G 14-bp Ins/Del polymorphism and virus infection; however, results from these studies were inconclusive. OBJECTIVES: A meta-analysis was carried out to determine whether the 14-bp Ins/Del polymorphism is a susceptible factor for virus infection. METHODS: Data were extracted from PubMed and Web of Science databases, and included 10 case-control studies (1835 patients and 2357 controls). RESULTS: A total of 177 records from 10 studies were retrieved. Overall, no significant correlation was found between HLA-G 14-bp Ins/Del polymorphism and total viruses under all genetic models (dominant model: OR = 0.93, 95% CI = 0.68-1.29; recessive model: OR = 1.12, 95% CI = 0.84-1.48; deletion/deletion (DD) vs insertion/insertion (II): OR = 1.03, 95% CI = 0.71-1.49; deletion (D) vs insertion (I): OR = 1.01, 95% CI = 0.81-1.25). However, further subgroup analyses by virus type and ethnicity revealed that HLA-G 14-bp Ins/Del polymorphism was significantly associated with HTLV-1 infection in mixed population under the dominant model. CONCLUSIONS: Our study demonstrated that HLA-G 14-bp Ins/Del polymorphism may not have any effect on susceptibility to viruses.