Crataeva tapia is a plant popularly used for diabetes treatment, in Brazil. Progressive decline in renal and hepatic functions has been described in patients with diabetes mellitus, and mortality rate is increased in patients with chronic liver and renal disease. This study aimed to evaluate whether Crataeva tapia bark lectin (CrataBL) improves hyperglycemia and renal and hepatic damage in diabetic mice. CrataBL was purified by ion exchange chromatography on CM-cellulose, and intraperitoneal administration of CrataBL to alloxan-induced diabetic mice at dose of 10 mg/Kg/day and 20 mg/Kg/day for 10 days significantly reduced serum glucose levels by 14.9% and 55.9%, respectively. Serum urea, creatinine, aspartate aminotransferase, and alanine aminotransferase were also significantly reduced after treatment with both doses of CrataBL. Furthermore, histological analysis of liver, kidney, and pancreas revealed an improvement in the tissue morphology upon treatment with CrataBL. The results suggest that CrataBL has a beneficial hypoglycemic activity and improves the renal and hepatic complications of diabetes. Therefore, this lectin may be a promising agent for the treatment of diabetes, and this might be the basis for its use in the folk medicine as an alternative treatment to manage diabetes-related complications such as hyperglycemia and tissue damage.
The multiple control of gonadotropin releasing hormone (GnRH)/luteinizing hormone (LH) secretion involves locus coeruleus (LC) and neuropeptide Y (NPY). The objective of the present study was to analyze the possible contribution of the LC to the control of NPY activity in the medial basal hypothalamus (MBH) and medial preoptic area (MPOA) during the LH surge induced by estrogen (E(2)) and progesterone (P(4)). Ovariectomized adult Wistar rats were submitted to the hormone replacement and to the LC bilateral lesion (lesioned groups) or sham surgery (control groups). On the day of the experiment the rats were decapitated at 11:00, 13:00, 15:00 and 17:00 h for plasma and brain collection. Plasma LH was determined by radioimmunoassay. MBH and MPOA were microdissected for the measurement of NPY by enzyme immunoassay. NPY mRNA levels in MBH were assessed by the ribonuclease protection assay. The results showed that LC lesion: decreased the plasma LH; increased the content of NPY in the MBH and reduced the increase of NPY content in the MPOA during afternoon in which LH surge was induced. The increased NPY content in MBH was not associated with an increase of the respective mRNA content, suggesting the action of postranscriptional and/or postranslational mechanisms. In conclusion, the NPY activity in the MPOA on LH surge induced by estrogen and progesterone could be controlled by LC through two ways, at least: one direct way, by the release of NPY from LC neurons terminals that innervate the MPOA and they release NA and NPY; one indirect way, by the control of release but not synthesis of NPY from neurons in the MBH which innervate the MPOA.
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