Histopathological and biochemical studies on pancreatic fibrosis in WBN/Kob rats

Abstract

We investigated the time-course of changes in pancreatic fibrosis accompanied with pancreatitis in WBN/Kob rats. The areas of fibrosis and fatty replacement were analysed morphometrically, and biochemical measurements of pancreatic and plasma prolyl hydroxylase and of pancreatic collagenase were assessed. Male rats showed acute pancreatitis at 2-3 months of age, lesions that later underwent a transition to widespread fibrosis. The fibrosis then decreased, and the fibrotic tissue was replaced with adipose tissue. Morphometrically, the fibrotic area reached its maximal size when the rats were 4 months old, diminishing thereafter. The fibrosis occurred mainly in the intralobular space, and was principally attributable to type-III collagen. Type-I collagen scarcely appeared throughout the experimental period. Alpha-Smooth muscle actin appeared in and around myofibroblasts that developed in an early stage and diminished later in accordance with the progressive manner of fibrosis. The plasma prolyl hydroxylase level was higher in males than in females from 4 through 10 months of age. Pancreatic collagenase activity in the males also increased during the same period. These findings suggest that pancreatic fibrosis in male WBN/Kob rats is affected by the balance between prolyl hydroxylase and collagenase.

Cytoglobin/STAP, its unique localization in splanchnic fibroblast-like cells and function in organ fibrogenesis

“…In the WBN/Kob rats developing chronic spontaneous pancreatitis, 31,32 numerous Cygb/STAP-positive cells appeared in the fibrotic tissues. These cells were regarded as fibroblast-like cells by their morphological features and results of double-immunostaining analysis for anti-HSP47 and anti-ED1 or OX62 antibodies.…”

“…31,32 In fact, 20-week-old WBN/Kob rats showed degeneration and necrosis of acinar cells, proliferation of pancreatic ductules, inflammatory cell infiltration, and fibrosis ( …”

Postrest Contraction in the Ventricular Papillary Muscle of Spontaneously Diabetic WBN/Kob Rat.

“…Tsuchida et al [41] demonstrated abnormal ventricular function in 8 to 19-month-old male WBN/Kob rats, and showed that these rats resemble the NIDDM model, to some extent, in terms of the slow progression of pathophysiological change and a long span without insulin administration. Furthermore, Kakinuma et al [18] investigated the time-course of changes in pancreatic fibrosis in WBN/Kob rats. The male rats showed acute pancreatitis at 2-3 months of age, lesions that later underwent a transition to widespread fibrosis.…”

“…In STZ-induced diabetic rats, it is well known that diabetes depresses the contractility of isolated ventricular muscles (e.g., [8,12,40]) and myocytes [18,36,47]. The speed of the contraction of the papillary muscles from diabetic animals decreased while their relaxation was delayed (e.g., [12]).…”

“…It has been reported that male WBN/Kob rats spontaneously develop DM between the ages of 9 and 15 months [41,42,44]. However, acute pancreatitis and the pancreatic fibrosis were found even in 2-3 month-old WBN/Kob rats [18,43]. In the ventricle, necrosis of the cardiomyocytes was found in 3-month-old WBN/Kob rats [44].…”