Search

Objectives: There are conflicting results for the association between vitamin B6 intake with reduced pancreatic carcinoma risk. Thus, a meta-analysis was performed to summarize the evidences from epidemiological studies. Methods: We searched documents from PubMed-Medline, Web of Science, and Cochrane Library. The results were analyzed by using Stata software. Results: A total of nine studies were included. The multivariate-adjusted results found that the total RR values of pancreatic carcinoma was 0.65 (95% CI: 0.53–0.80) for the highest vitamin B6 intake vs the lowest vitamin B6 intake, and there was no significant heterogeneity among studies (I2 = 42.0%, P = 0.087). Sensitivity analysis indicated that no single study leaded to an excessive change for the relation between vitamin B6 intake and pancreatic carcinoma risk. Conclusions: This meta-analysis suggested that vitamin B6 intake could significantly decrease pancreatic carcinoma risk. However, further study is needed based on the limitations of the current analysis. [ABSTRACT FROM AUTHOR]

Pancreatic fibrosis increases pancreatic cancer risk in chronic pancreatitis (CP). Pancreatic stellate cells (PSCs) play a critical role in pancreatic fibrosis by transforming growth factor-β (TGFβ) has been shown to inhibit transforming growth factor-β receptor (TGFβR)-mediated Smad and no-Smad signaling pathways. Thus, the effects of Hsp90 inhibitor on pancreatic fibrosis are evaluated in CP mice, and the association between Hsp90 and biological functions of PSCs is further investigated in vitro. The effects of Hsp90 inhibitor 17AAG on pancreatic fibrosis were assessed in caerulein-induced CP mice, and primary PSCs were used to determine the role of Hsp90 inhibitor 17AAG in vitro. We observed increased expression of Hsp90 in pancreatic tissues of caerulein-induced CP mice. Hsp90 inhibitor 17AAG ameliorated pancreatic inflammation and fibrosis in caerulein-induced CP mice. In vitro, Hsp90 inhibitor 17AAG inhibited TGFβ1-induced activation and extracellular matrix accumulation of PSCs by blocking TGFβR-mediated Smad2/3 and PI3K /Akt/GSK-3β signaling pathways.Hsp90 inhibitor 17AAG degraded TGFβRII by a ubiquitin-proteasome pathway, co-immunoprecipitation showed an interaction between Hsp90 and TGFβRII in PSCs. The study suggests that an Hsp90 inhibitor 17AAG remarkable prevents the development of pancreatic fibrosis in caerulein-induced CP mice, and suppresses activation and extracellular matrix accumulation of PSCs in vitro. The current results provide a potential treatment strategy based on Hsp90 inhibition for pancreatic fibrosis in CP. • Hsp90 inhibitor 17AAG has beneficial effects on pancreatic inflammation in chronic pancreatitis mice. • Hsp90 inhibitor 17AAG prevents the development of pancreatic damage and fibrosis in chronic pancreatitis mice. • Hsp90 inhibitor 17AAG degrades TGFRβII with a ubiquitin-proteasome mechanism in pancreatic stellate cells. [ABSTRACT FROM AUTHOR]

The serum level of IL-33 was upregulated in systemic lupus erythematosus (SLE), which may be used as biomarkers and/or therapeutic targets for SLE. The aim of this study was to investigate the association of four novel polymorphisms of IL-33 with risk of SLE. The study population comprised 540 Chinese individuals, including 257subjects with SLE and 283 healthy controls. The gene polymorphism was measured using Snapshot SNP genotyping assays and confirmed by sequencing. Serum IL-33 (sIL-33) levels were measured by ELISA. The serum SLE levels were significantly higher in the group of patients with SLE than those in the control group ( P < 0.001). The rs1891385C allele was associated with a significantly increased risk of SLE as compared with the rs1891385 A allele ( OR = 1.405, 95% CI , 1.052–1.875, P = 0.021). The C-T-T-G haplotype was significantly increased the risk of SLE ( OR = 1.411; 95% CI , 1.021–1.948; P = 0.036). IL-33 gene rs1891385 polymorphism was significantly associated with the expression of sIL-33 in the SLE patients. Besides, in our study, we found that the unregulated sIL-33 level was significantly associated with the abnormal changed CRP and ESR. This is the first study reporting the IL-33 gene polymorphisms and SLE, which may help refine the SLE risk profile. [ABSTRACT FROM AUTHOR]