Examination of protective and therapeutic effects of ruscogenin on cerulein-induced experimental acute pancreatitis in rats

PURPOSE: To determine the potential protective and therapeutic effects and action mechanism of ruscogenin on cerulein-induced acute pancreatitis (AP) model in rats. METHODS: Overall, 32 rats were attenuated to the sham (2-mL/kg/day isotonic solution for 4 weeks), control (20-µg/kg cerulein-induced AP for 12 hours), prophylaxis groups (cerulein-induced AP following 3-mL/kg/day ruscogenin for 4 weeks) and treatment (3-mL/kg/day ruscogenin following cerulein-induced AP for 12 hours). Blood samples were collected for biochemical analysis of nitric oxide synthase 1 (NOS1/neuronal NOS), malondialdehyde (MDA) and intercellular adhesion molecule 1 (ICAM-1). After sacrification, pancreas tissues were collected and prepared for light microscopic (hematoxylin and eosin), immunohistochemical (nuclear factor kappa B) and biochemical analysis (tumor necrosis factor-alpha [TNF-α], interleukin-6 and 1β [IL-6 and IL-1β], CRP, high-sensitivity CRP [hs-CRP] amylase, lipase, and ICAM-1). Ultrastructural analysis was performed by transmission electron microscopy. RESULTS: The protective and therapeutic actions of ruscogenin were accomplished by improvements in histopathology, by decreasing blood cytokine levels of CRP, hs-CRP levels, TNF-α, IL-6, IL-1β, ICAM-1, by reducing the pancreatic enzymes amylase and lipase in blood, and by suppressing the expression of nuclear factor kappa B, ICAM-1, and NOS-1, but not MDA in pancreatic tissues. Ruscogenin also improved cerulein-induced ultrastructural degenerations in endocrine and exocrine cells, especially in treatment group. CONCLUSION: The present findings have demonstrated the beneficial protective and therapeutical effects of ruscogenin, nominating it as a highly promising supplementary agent to be considered in the treatment of AP, and even as a protective agent against the damages induced by disease.

Association of Insulin Resistance with Overactive Bladder in Female Patients / 대한배뇨장애요실금학회지

PURPOSE: Metabolic syndrome and obesity have been advocated to be risk factors for the development of overactive bladder (OAB). Additionally, insulin resistance is the underlying mechanism of metabolic syndrome. We aimed to investigate the association of insulin resistance with overactive bladder in female patients. METHODS: We prospectively conducted the study in our urology department. Female patients aged between 30 and 76 years old applied to our policlinics with or without OAB symptoms were enrolled. One hundred and twenty-two patients with OAB and 62 age-matched controls without OAB were included into the study. Fasting serum insulin, glucose, high-density lipoprotein (HDL-c), and triglycerides levels were measured. Insulin resistance value was obtained via the homeostasis model assessment of insulin resistance (HOMA-IR) calculator. The chi-square and Mann-Whitney U tests were used to compare differences in variables. RESULTS: Serum insulin level was found higher in female patients with OAB (11.5+/-6.2 microU/mL) relative to controls (6.4+/-2.1 microU/mL), statistically significant (P=0.036). In addition, HOMA-IR was significantly found higher in the OAB group, 2.86 (0.76 to 17.04) in comparison to controls, 1.32 (0.67 to 224), P=0.018. High-density lipoprotein cholesterol levels (HDL-c) were significantly found lower in females with OAB. CONCLUSIONS: Insulin resistance can be associated to overactive bladder and may play significant role in pathogenesis.