Ulinastatin attenuates renal interstitial inflammation and inhibits fibrosis progression in rats under unilateral ureteral obstruction.

The aim of the present study was to examine the protective effects of the urinary trypsin inhibitor ulinastatin (UTI) on renal interstitial inflammation and fibrosis in rats subjected to unilateral ureteral obstruction (UUO). A total of 24 male Wistar rats were randomly divided into the three groups; the sham operation (SOR) group (n=8), the UUO group (n=8) and the UUO+UTI group (post‑UUO UTI treatment, n=8). UUO was performed with complete ligation of the left ureter.

Ulinastatin inhibits unilateral ureteral obstruction-induced renal interstitial fibrosis in rats via transforming growth factor β (TGF-β)/Smad signalling pathways.

This study aims to explore the protective effects and mechanisms of ulinastatin (UTI), which is a urinary trypsin inhibitor, of the renal interstitial fibrosis of rats subjected to unilateral ureteral obstruction (UUO). A total of 36 male Wistar rats were divided in random into three groups, namely, the sham operation (SOR) group (n=12), the UUO group (n=12), and the UTI treatment group (n=12). Six rats from each group were euthanised after unilateral ureteral obstruction operation on the seventh and fourteenth days, respectively.

Parathyroid hormone(1-34)-induced apoptosis in neuronal rat PC12 cells: implications for neurotoxicity.

Based on accumulated evidence, we speculate that a high concentration of parathyroid hormone (PTH) may cause neurotoxicity in patients with uremia through apoptosis-induced neuropathy. In this study, we demonstrated that in vitro stimulation with PTH(1-34) induced a significant decrease in PC12 cell numbers in both dosage- and time-dependent fashions when these cells were treated with PTH(1-34) at concentrations of 0.01, 0.

[Parathyroid hormone 1-34 induce cardiac myocytes hypertrophy via extracellular regulated protein kinase 1/2 pathway].

Objective: To investigate the role of mitogen activated protein kinase kinase 1 (MAPKK, MEK1) and regulated kinase1/2 (ERK1/2) on cardiac hypertrophy induced by rat parathyroid hormone1-34 (rPTH1-34).

Method: Neonatal rat cardiomyocytes was treated with or without 10(-7) mol/L rPTH1-34 in the absence or presence 2 x 10(-5) mol/L PD98059, a MEK1 inhibitor. Cellular diameter was measured by Motic Images Advanced 3.