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Results: 6

1.
Fig. 6.

Fig. 6. From: Transient receptor potential ankyrin 1 mediates chronic pancreatitis pain in mice.

TRPA1 mediates TNBS-induced CP hypersensitivity. CP was induced by intraductal injection of TNBS in trpa1+/+ and trpa1-/- mice: trpa1 -/- mice showed no mechanical sensitivity, as suggested by lack of increase in referred abdominal (A) hypersensitivity and hindpaw sensitivity threshold (B) compared with trpa1+/+ mice. These findings suggest that TRPA1 is involved in activating pain pathways in this model of CP. Values are means ± SE (n = 6–10). ****P < 0.0001 vs. trpa1+/+ TNBS.

Fiore Cattaruzza, et al. Am J Physiol Gastrointest Liver Physiol. 2013 June 1;304(11):G1002-G1012.
2.
Fig. 2.

Fig. 2. From: Transient receptor potential ankyrin 1 mediates chronic pancreatitis pain in mice.

TNBS-induced CP reduced amylase activity (A) and pancreas size (B) in mice. Mice with TNBS-induced CP had significantly less amylase activity than control groups (A), consistent with loss of exocrine functionality of the pancreas. TNBS caused a significant decrease in pancreas size, as quantified (B and D) and shown in representative images (C), consistent with the presence of atrophy in the gland. Spleen size was similar among all experimental groups (D). Values are means ± SE (n = 5–15). **P < 0.05, ****P < 0.0001 vs. sham. ##P < 0.01, ###P < 0.001 vs. saline. +P < 0.05, +++P < 0.001, ++++P < 0.0001 vs. vehicle.

Fiore Cattaruzza, et al. Am J Physiol Gastrointest Liver Physiol. 2013 June 1;304(11):G1002-G1012.
3.
Fig. 5.

Fig. 5. From: Transient receptor potential ankyrin 1 mediates chronic pancreatitis pain in mice.

Transient receptor potential ankyrin 1 (TRPA1) mediates TNBS-induced CP. CP was induced by intraductal injection of TNBS in trpa1+/+ and trpa1-/- mice. HSS was decreased (A and D) and amylase activity was increased (B) in trpa1-/- compared with trpa1+/+ mice, suggesting that TRPA1 is involved in mediating inflammation in this CP model. C: no significant differences between the 2 genotypes were detected when pancreatic atrophy was measured. Values are means ± SE (n = 5–10). **P < 0.01 vs. trpa1+/+ TNBS.

Fiore Cattaruzza, et al. Am J Physiol Gastrointest Liver Physiol. 2013 June 1;304(11):G1002-G1012.
4.
Fig. 3.

Fig. 3. From: Transient receptor potential ankyrin 1 mediates chronic pancreatitis pain in mice.

TNBS-induced CP increased pancreatic fibrosis in mice. Fibrosis was measured by immunohistochemistry and Western blotting: picrosirius red was used to stain collagen deposition (A and B), and Western blotting to α-smooth muscle actin (α-SMA) was used to measure activation of pancreatic stellate cells (PSCs, C), which have been shown top play a major role in promoting pancreatic fibrosis. Mice with TNBS-induced CP had robust pancreatic collagen deposition, which was absent in all control groups, as shown in representative images in A. EtOH, ethanol. Superficial area of stained collagen was significantly increased in mice with CP (B). Mice with TNBS-induced CP also had increased activation of PSCs compared with vehicle-treated controls (C). Values are means ± SE (n = 7–9). *P < 0.05, ***P < 0.001 vs. sham. #P < 0.05 vs. saline. +++P < 0.001 vs. vehicle.

Fiore Cattaruzza, et al. Am J Physiol Gastrointest Liver Physiol. 2013 June 1;304(11):G1002-G1012.
5.
Fig. 1.

Fig. 1. From: Transient receptor potential ankyrin 1 mediates chronic pancreatitis pain in mice.

Trinitrobenzene sulfonic acid (TNBS)-induced chronic pancreatitis (CP) decreased body weight (A) and increased histological damage score (B and C) in mice. Mice with TNBS-induced CP lost more body weight (A) and had higher histological severity score (B and C) than did ethanol, saline, and sham-operated control groups. Values are means ± SE (n = 6–10). *P < 0.05, **P < 0.01, ****P < 0.0001 vs. sham. ####P < 0.0001 vs. saline. +P < 0.05, ++++P < 0.0001 vs. vehicle. C: representative hematoxylin-eosin (H & E)-stained histological sections of the pancreas 21 days after instillation of TNBS, vehicle, or saline into the pancreatic duct. Striking features of this CP model were fat replacement, fibrosis, and presence of inflammatory cells.

Fiore Cattaruzza, et al. Am J Physiol Gastrointest Liver Physiol. 2013 June 1;304(11):G1002-G1012.
6.
Fig. 4.

Fig. 4. From: Transient receptor potential ankyrin 1 mediates chronic pancreatitis pain in mice.

TNBS-induced CP decreases voluntary wheel-running activity (A) and increases pain behaviors (B–D). In mice with TNBS-induced CP, voluntary wheel-running activity decreased dramatically within the first 2 wk compared with control groups (A). Mechanical sensitivity was measured with calibrated (0.07, 0.16, and 1 g) Von Frey filaments (VFFs). Mice were probed on the abdomen (B) and hindpaw (C). In both cases, mice with TNBS-induced CP had increased mechanical sensitivity compared with control groups. D: mice with CP also showed significantly more catalepsy (immobility measured over a 10-min period using the open-field apparatus) than sham-operated controls at all time points. Thus all the behavioral end points strongly support the presence of abdominal and generalized hypersensitivity in mice with TNBS-induced CP. Values are means ± SE (n = 6–10). *P < 0.5, **P < 0.01, ***P < 0.001, ****P < 0.0001 vs. sham-operated.

Fiore Cattaruzza, et al. Am J Physiol Gastrointest Liver Physiol. 2013 June 1;304(11):G1002-G1012.

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