Xanthoceraside induces cell apoptosis through downregulation of the PI3K/Akt/Bcl-2/Bax signaling pathway in cell lines of human bladder cancer.

BACKGROUND: Xanthoceraside is a component obtained in the husks of Xanthoceras sorbifolia Bunge. Series of researches proved that xanthoceraside had functions of anti-inflammation and anti-tumor effects. However, the mechanisms of xanthoceraside against bladder cancer are unclear. Accordingly, we proposed to investigate xanthoceraside's impacts and potential mechanisms in cells of bladder cancer. METHODS: By using the CCK-8 assay, we measured the viability of cells. With the use of 4,6-diamidino-2-phenylindole (DAPI) staining, we examined nuclear fragmentation and chromatin condensation in the nuclei of apoptotic cells. By using flow cytometry, we measured cell apoptosis. By using Western blotting, we tested the expressions of Caspase-9, Caspase-8, Caspase-3, Bcl-xL, P53, and PI3K/Akt/Bcl-2/Bax. RESULTS: The proliferation of cell lines of human bladder cancer T24 and 5637 was suppressed by xanthoceraside significantly in a time- and concentration-dependent way. When cell lines 5637 and T24 were incubated as the xanthoceraside dose increased, the rates of cell apoptosis were upregulated, which was dependent on dose. According to further analysis, xanthoceraside induced apoptosis by upregulating Bax and downregulating the expression of Bcl-xL and Bcl-2. However, xanthoceraside did not change the expression of Caspase-9, Caspase-8, and Caspase-3. Interestingly, xanthoceraside also downregulated the expression of p-PI3K and p-Akt, and upregulated P53. CONCLUSIONS: Xanthoceraside induces cell apoptosis through downregulation of the PI3K/Akt/Bcl-2/Bax signaling pathway in cell lines of human bladder cancer.

Baseline Serum Cystatin C Is a Potential Predictor for Acute Kidney Injury in Patients with Acute Pancreatitis.

AIMS: The study is aimed at studying the incidence of acute kidney injury (AKI) and exploring the potential predictor for AKI in patients with acute pancreatitis. METHODS: A retrospective study adopting a stratified cohort sampling design was performed in a cohort of patients (n = 237) diagnosed with acute pancreatitis without any renal injury. The following information including age, gender, serum creatinine, serum urea nitrogen, serum uric acid, serum cystatin C, fasting serum glucose, serum amylase, serum lipase, serum choline esterase, total protein, albumin, globulin, total bilirubin, direct bilirubin, total bile acids, glutamic-pyruvic transaminase, glutamic-oxaloacetic transaminase, gamma glutamyl transpeptidase, and alkaline phosphatase were collected from each patient when they were diagnosed with acute pancreatitis. Student t-test was conducted to figure out the difference between patients with and without AKI. Univariate and multivariate logistic regression analyses were used for investigating the predictors for AKI in patients with acute pancreatitis. RESULTS: 18 (7.6%) patients in total had developed AKI among the study group. Compared with patients without AKI (1.01 ± 0.26 mg/L), the level of baseline serum cystatin C (CYS-C) was significantly higher in patients with AKI (3.64 ± 2.17 mg/L, P < 0.001). Baseline serum CYS-C (OR = 203.594, P < 0.001) was the independent and significant predictor for AKI in patients with acute pancreatitis. AKI in patients with acute pancreatitis could be identified with a sensitivity of 88.9% at specificity of 100% (AUC = 0.948, 95% CI 0.879-1.000) by baseline serum CYS-C (cut-off value = 1.865 mg/L). CONCLUSIONS: Baseline serum CYS-C shall be adopted to predict the potential risk of AKI in patients with acute pancreatitis.

A systematic review of the epidemiological literature on the risk of urological cancers in systemic lupus erythematosus.

PURPOSE: A grow body of studies has evaluated the risk of development of urological cancer in systemic lupus erythematosus (SLE) with inconclusive results. To clarify the association, a meta-analysis approach was performed to assess the published evidence on urological cancers and SLE. METHODS: Relevant English electronic databases were systematic searched for published studies characterizing the risk of developing urological cancer as a result of SLE. Standardized incidence rate (SIR) with its 95 % confidence interval (CI) of each study was combined using a fixed-/random-effect model in STATA software. RESULTS: A total of 12 papers including 68366 SLE patients were suitable for meta-analysis. Of these, 9 reported the SIR for prostate cancer, 7 for bladder cancer and 6 for kidney cancer. Summary SIRs were 0.77 (95 % CI 0.69-0.87, P < 0.001); 1.75 (95 % CI 0.94-3.23, P = 0.075) and 2.29 (95 % CI 1.25-4.18, P = 0.007), respectively. Significant heterogeneity was noticed in subgroups of bladder and kidney cancer. No obvious publication bias was detected. CONCLUSIONS: Findings from this meta-analysis indicate that SLE is associated with a decreased risk of prostate cancer and an increased risk of kidney cancer.