RESUMO
The aim of the present study was to detect the expression of resistin in rats with acute pancreatitis (AP) and investigate its significance in the pathogenesis of AP. In total, 40 Sprague-Dawley rats were randomly divided into four groups (n=10), including the normal control, sham-operated, acute edematous pancreatitis (AEP) and acute necrotizing pancreatitis (ANP) groups. Following the establishment of animal models, the levels of serum resistin, C-reactive protein (CRP), tumor necrosis factor-α (TNF-α) and interleukin (IL)-1ß were measured using ELISA. Resistin expression in the pancreatic tissues was detected using an immunohistochemical method. In addition, the mRNA expression of resistin in the pancreatic tissues was analyzed with quantitative polymerase chain reaction. The levels of serum amylase, serum resistin, TNF-α, IL-1ß and CRP were all significantly higher in the AEP and ANP groups when compared with the control and sham-operated groups (P<0.01), as were the pancreas/body weight ratios and pathological scores of the pancreas. These increases were more significant in the ANP group than in the AEP group (P<0.05). The mRNA expression levels of resistin in the pancreatic tissues were markedly higher in the AEP and ANP groups when compared with the control and sham-operated groups (P<0.01), particularly in the pancreatic tissues of the ANP group, which exhibited notably higher levels compared with the AEP group. The serum resistin level was found to positively correlate with the serum levels of CRP, TNF-α and IL-1ß, and the pathological scores of the pancreatic tissues. In conclusion, the results indicated that resistin may be associated with the occurrence and development of AP; thus, the protein may be a valuable indicator for assessing the severity of AP.
RESUMO
BACKGROUND: Several polymorphisms have been identified in the vitamin D receptor (VDR) gene, while their roles in the incidence of ulcerative colitis (UC) and Crohn's disease (CD) are conflicting. This meta-analysis was designed to clarify the impact of these polymorphisms on UC and CD risk. METHODS: The PubMed, Embase, and Cochrane electronic databases were searched from February 1995 to August 2011 for studies on the four VDR polymorphisms: TaqI, BsmI, FokI, and ApaI. Data were extracted and pooled odd ratios (ORs) and 95% confidence intervals (95% CIs) were calculated. RESULTS: Nine studies were included. In Asians, the ff genotype of FokI was associated with increased UC risk (OR = 1.65; 95% CI, 1.11- 2.45). The "a" allele carrier status of ApaI appeared to be a protective factor for CD (OR = 0.81; 95% CI, 0.67-0.97). The tt genotype increased the risk of CD in Europeans (OR = 1.23; 95% CI, 1.02-1.49). Moreover, the tt genotype of TaqI in males had a moderate elevated risk of UC (OR = 1.56; 95% CI, 1.02-2.39) and CD (OR = 1.84; 95% CI, 1.19-2.83). CONCLUSIONS: The meta-analysis reveals a significant increase in CD risk for Europeans carrying TaqI tt genotype and a significant decrease in CD risk for all carriers of the Apal "a" allele. For Asians, the VDR FokI polymorphism appears to confer susceptibility to UC. For males, the TaqI tt genotype is associated with susceptibilities to both UC and CD. Our study explored the genetic risk prediction in UC and CD, and may provide valuable insights into IBD therapy.
