Myocardial protective effects of Munziq in myocardial ischemia-reperfusion injury rats with abnormal savda syndrome.

This study evaluated the influence and mechanism of different Munziq doses on myocardial ischemia reperfusion injury (MIRI) rats with abnormal savda. Wistar rats (N = 96) were divided into the following 8 groups (12 rats each): ischemia-reperfusion (I/R) model group, high-dose, medium-dose, and low-dose Munziq groups, normal I/R group, sham model group, normal sham group, and Atorvastatin group. Changes in heart physiology and myocardial morphology after injury with MIRI were monitored in each group. Heat shock protein 70 (HSP70) and calcitonin gene-related peptide (CGRP) protein expression and serum concentrations of superoxide dismutase (SOD), malondialdehyde (MDA), interleukin (IL)-6, and IL-8 were detected by using western blot and ELISA methods, respectively. The large-dose Munziq group showed the most significant changes. The VPC incurring time was not delayed in the small-dose group, but the accumulative time was significantly reduced (P < 0.01). The ventricular tachycardia incurring time did not differ significantly between groups. Compared with the normal sham surgical group, the I/R groups showed significant increases in HSP70 and CGRP expression (P < 0.01) and MDA, IL-6, and IL-8 concentrations (P < 0.05) and a significant decrease in the SOD concentration (P < 0.05). Compared with the I/R groups, Munziq intervention significantly enhanced HSP70 and CGRP expression (P < 0.01), significantly decreased MDA, IL-6, and IL-8 concentrations (P < 0.05), and significantly increased the SOD concentration (P < 0.05). In conclusion, Munziq intervention improves cardiac physiological function, increases the expression of HSP70 and CGRP, and decreases the inflammatory reaction in MIRI model rats.

A new non-uremic rat model of long-term peritoneal dialysis.

Together with the development of peritoneal dialysis (PD), appropriate animal models play an important role in the investigation of physiological, pathophysiological and clinical aspects of PD. However, there is still not an ideal experimental PD animal model. In this study, 45 Sprague-Dawley rats were divided into three groups. Group 1 (n=15) was receiving daily peritoneal injection through the catheter connected to the abdominal cavity, using PD solution containing 3.86 % D-glucose. Group 2 (n=15) was receiving daily peritoneal injection of 0.9 % physiological saline through a catheter. Group 3 (n=15), which was subjected to sham operation, served as controls. Our results showed that WBC counts in peritoneal effluent of Group 1 were slightly higher than those of Group 2 and control group, respectively (p<0.05). However, there was no episode of infection in any group. In addition, there was no significant difference in neutrophils fractions among these three groups. Hematoxylin-eosin and Masson's trichrome staining demonstrated a dramatic increase in thickness of the mesothelium-to-muscle layer of peritoneum exposed to high glucose (Group 1) compared to Group 2 and controls (p<0.01). These data indicated that we established a novel rat model of PD with a modified catheter insertion method. This model is more practical, easy to operate, not too expensive and it will facilitate the investigate of long-term effects of PD.