Background Aloin exerts considerable protective effects in various disease models, and its effect on hepatic ischemia-reperfusion (HIR) injury remains unknown. This research is aimed at conducting an in-depth investigation of the antioxidant, anti-inflammatory, and antiapoptosis effects of aloin in HIR injury and explain the underlying molecular mechanisms. Methods In vivo, different concentrations of aloin were intraperitoneally injected 1 h before the establishment of the HIR model in male mice. The hepatic function, pathological status, oxidative stress, and inflammatory and apoptosis markers were measured. In vitro, aloin (AL, C21H22O9) or lipopolysaccharide (LPS) was added to a culture of mouse primary hepatocytes before it underwent hypoxia/reoxygenation (H/R), and the apoptosis in the mouse primary hepatocytes was analyzed. Results We found that 20 mg/kg was the optimum concentration of aloin for mitigating I/R-induced liver tissue damage, characterized by decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Aloin pretreatment substantially suppressed the generation of hepatic malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), and IL-6 and enhanced the hepatic superoxide dismutase (SOD) activities as well as glutathione (GSH) and IL-10 levels in the liver tissue of I/R mice; this indicated that aloin ameliorated I/R-induced liver damage by reducing the oxidative stress and inflammatory response. Moreover, aloin inhibited hepatocyte apoptosis and inflammatory response that was caused by the upregulated expression of Bcl-2, the downregulated expression of cleaved caspase3(C-caspase3), Bax, Toll-like receptor 4 (TLR4), FADD, MyD88, TRAF6, phosphorylated IKKα/β (p-IKKα/β), and phosphorylated nuclear factor κB p65 (p-NF-κB p65).

BackgroundAccurate and early prognosis of disease is essential to clinical decision making, particularly in diseases, such as HCC, that are typically diagnosed at a late stage in the course of disease and therefore carry a poor prognosis. CDCA5 is a cell cycle regulatory protein that has shown prognostic value in several cancers.MethodsWe retrospectively evaluated 178 patients with HCC treated with curative liver resection between September 2009 and September 2012 at Nanchong Central Hospital in Nanchong, Sichuan Province, China. Patients were screened for their CDCA5 expression levels and assigned to either the high or low expression group. Patient demographics, comorbidities, clinicopathologic data, such as tumor microvascular invasion status and size, and long-term outcomes were compared between the two groups. The effect of CDCA5 on the proliferation of liver cancer cells was analyzed using in vitro and in vivo assays.ResultsThe present study found that increased CDCA5 expression was associated with increased tumor diameter and microvascular invasion in HCC. It was also found that CDCA5 overexpression may be associated with liver cancer cells. Additionally, this study confirmed that CDCA5 expression was increased in HCC tissue versus normal liver tissue, that CDCA5 expression was associated with decreased survival and that CDCA5 knockdown using shRNA led to cell cycle arrest in the G2/M phase.ConclusionsThese findings suggest that CDCA5 expression is associated with poor prognosis in patients with hepatocellular carcinoma.

Acetaminophen (APAP) is one of the safest and most effective over-the-counter (OTC) analgesics and antipyretics, but excessive doses of which will induce hepatotoxicity with high morbidity and mortality worldwide. Kaempferol...

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Long non-coding RNAs (lncRNAs) play a significant role in multiple human cancers as competing endogenous RNAs (ceRNAs). However, a systematic mRNA-microRNA (miRNA)-lncRNA network linked to kidney renal clear cell carcinoma (KIRC) prognosis has not been described. In this study, we aimed to identify the prognosis-related ceRNA regulatory network and analyzed its relationship with immune cell infiltration to predict KIRC patient survival. The MMP25-AS1/hsa-miR-10a-5p/SERPINE1 ceRNA network related to the prognosis of KIRC was obtained through bioinformatics analysis based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Meanwhile, we constructed a three-gene-based survival predictor model, which could be referential for future clinical research. Methylation analyses suggested that the abnormal upregulation of the SERPINE1 likely resulted from hypomethylation. Furthermore, the immune infiltration analysis showed that the MMP25-AS1/hsa-miR-10a-5p/SERPINE1 axis could affect the changes in the tumor immune microenvironment and the development of KIRC by affecting the expression of chemokines (CCL4, CCL5, CXCL13, and XCL2). Tumor Immune Dysfunction and Exclusion (TIDE) analysis indicated that the high expression of SERPINE1 might be related to tumor immune evasion in KIRC. In summary, the current study constructing the MMP25-AS1/hsa-miR-10a-5p/SERPINE1 ceRNA network might be a novel significant prognostic factor associated with the diagnosis and prognosis of KIRC.