Immune response plays an important role in the development of hepatic fibrosis. In the present study, we investigated the effects of quercetin on hepatitis and hepatic fibrosis induced by immunological mechanism. In the acute hepatitis model, quercetin (2.5 mg/kg) was injected iv into mice 30 min after concanavalin A (Con A) challenge. Mice were sacrificed 4 or 24 h after Con A injection, and aminotransferase tests and histopathological sections were performed. Treatment with quercetin significantly decreased the levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Consistent with this observation, treatment with quercetin markedly attenuated the pathologic changes in the liver. A hepatic fibrosis model was also generated in mice by Con A challenge once a week for 6 consecutive weeks. Mice in the experimental group were treated with daily iv injections of quercetin (0.5 mg/kg). Histopathological analyses revealed that treatment with quercetin markedly decreased collagen deposition, pseudolobuli development, and hepatic stellate cells activation. We also examined the effects of quercetin on the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and transforming growth factor beta (TGF-β) pathways by immunohistochemistry and real-time reverse transcriptase-polymerase chain reaction (RT-PCR). NF-κB and TGF-β production was decreased after treatment with quercetin, indicating that the antifibrotic effect of quercetin is associated with its ability to modulate NF-κB and TGF-β production. These results suggest that quercetin may be an effective therapeutic strategy in the treatment of patients with liver damage and fibrosis.

ABSTRACT. Studies examining the role of interleukin (IL)-1β -511C/ T promoter polymorphism in the pathogenesis of chronic obstructive pulmonary disease (COPD) have shown inconsistent results. This metaanalysis was performed to assess the association between the IL-1β -511C/T promoter polymorphism and COPD susceptibility. Published case-control, cross-sectional, and cohort studies from Pubmed, Embase, and China National Knowledge Infrastructure databases were retrieved. Data were extracted and pooled odds ratios (ORs) with 95% confidence intervals (CIs) were calculated. Twelve studies with 1692 cases and 2009 controls were included in this meta-analysis. Pooled effect size showed an overall but not significantly decreased risk of IL-1β -511 C/T with COPD susceptibility (OR = 0.89, 95%CI = 0.78-1.01) in a complete overdominant genetic model (TT+CC vs CT), indicating that homozygous individuals (CC and TT) have a decreased risk for COPD compared with heterozygotes (2015) (CT). In subgroup analysis by ethnicity, IL-1β -511C/T was significantly correlated with a decreased risk of COPD in Asians (OR = 0.73, 95%CI = 0.60-0.88, P = 0.001), but not in Caucasians (OR = 1.02, 95%CI = 0.83-1.24, P = 0.46), confirming a protective role of IL-1β -511C/T in COPD in Asians. Moreover, after excluding studies that included populations not in Hardy-Weinberg equilibrium, the pooled results were robust and no publication bias was observed. This meta-analysis suggests that the IL-1β -511C/T promoter polymorphism deceases the risk of COPD in Asians.