The results indicate that chronic HFD increased pancreatic FFA and lipid peroxidation associated with pancreatic injuries and collagen synthesis by activated pancreatic stellate cells in rats.

Background: Mast cells (MCs) in the nasal respiratory mucosa (NRM) play a triggering role in the pathogenesis of allergic rhinitis (AR). Recent research evidence in mouse models of AR suggests an underlying MC-related allergic response in mouse nasal olfactory mucosa (NOM). Objective: We soughtto investigate the phenotypic characteristics of nasal MCs in a mouse model of AR. Methods: By MC-specific staining and immunohistochemistry, we analyzed the subset, protease and IgE-binding phenotypes of nasal MCs in ovalbumin (OVA)-sensitized unchallenged and challenged mice. Results: In OVA-sensitized challenged mice, increased serum OVA-specific IgE levels (p < 0.001) and eosinophil infiltration confirmed AR induction. In addition to constitutive connective tissue MCs, mucosal MCs were induced in NRM and NOM of OVA-sensitized challenged mice. Connective tissue MCs and mucosal MCs in mouse NRM and NOM were positive for mouse MC protease-1, -4, -5, -6, -7 and carboxypeptidase-A3. In line with MCs in NRM, there were increased numbers (p = 0.019) and proportions (p = 0.027) of MCs with surface-bound IgE in NOM of OVA-sensitized challenged mice. Conclusion: In the setting of AR, MCs in mouse NOM exhibit the same subset, protease and IgE-binding phenotypes as MCs in mouse NRM.

Background Pancreatic stellate cells (PSCs) activation plays a critical role in the development of chronic pancreatitis. Previous studies confirmed that thromboxane A2 receptor (TxA 2 r) was overexpressed in activated PSCs in rats. The purpose of this study was to investigate the role of TxA 2 r in the activation of PSCs induced by 8-epi-prostaglandin F 2α (8-epi-PGF 2α ). Methods TxA 2 r expression in both quiescent and activated PSCs was detected by immunocytochemistry and immunoblot assay. Isolated PSCs were treated with 8-epi-PGF 2α (10 −6 , 10 −7 , 10 −8 mol/L) for 48 h, and SQ29548 (10 −4 , 10 −6 , and 10 −7 mol/L), a TxA 2 r-specific antagonist for 48 h, respectively, to identify the drug concentration with the best biological effect and the least cytotoxicity. Then isolated PSCs were treated with SQ29548 (10 −4 mol/L) for 2 h, followed by 10 −7 mol/L 8-epi-PGF 2α for 48 h. Real-time polymerase chain reaction was performed to detect the messenger RNA (mRNA) levels of α-smooth muscle actin (α-SMA) and collagen I. Comparisons between the groups were performed using Student's t test. Results TxA 2 r was up-regulated in activated PSCs in vitro compared with quiescent PSCs (all P < 0.001). Compared with the control group, different concentrations of 8-epi-PGF 2α significantly increased mRNA levels of α-SMA (10 −6 mol/L: 2.23 ± 0.18 vs. 1.00 ± 0.07, t = 10.70, P < 0.001; 10 −7 mol/L: 2.91 ± 0.29 vs. 1.01 ± 0.08, t = 10.83, P < 0.001; 10 −8 mol/L, 1.67 ± 0.07 vs. 1.00 ± 0.08, t = 11.40, P < 0.001) and collagen I (10 −6 mol/L: 2.68 ± 0.09 vs. 1.00 ± 0.07, t = 24.94, P < 0.001; 10 −7 mol/L: 2.12 ± 0.29 vs. 1.01 ± 0.12 , t = 6.08, P < 0.001; 10 −8 mol/L: 1.46 ± 0.15 vs. 1.00 ± 0.05, t = 4.93, P = 0.008). However, different concen...