RESUMENEl objetivo de este estudio fue evaluar la distribución de mastocitos en el ovario y el útero durante el ciclo estral de ratas. Se utilizaron cuarenta ratas Albino de Wistar hembras, de 10 a 12 semanas de edad. Se tomaron muestras de los tejidos del ovario y útero para luego ser fijadas en Mota por 48 horas y parafina, luego se cortaron secciones de 6 μm de espesor las cuales fueron teñidas con Azul de Toluidina (1% de solución acuosa) y Alcian safranina-azul (pH: 1,0, utilizando 0,1 HCl N como tampón). En el ovario, los mastocitos se presentaron principalmente en la túnica albugínea, en las áreas intersticiales entre folículos o cuerpos lúteos y en la proximidad de vasos sanguíneos en la médula. El número de mastocitos en la médula y la corteza ovárica y en el endometrio y miometrio uterino fueron mayores durante el estro, metaestro, las fases de estro y metaestro, respectivamente. Se encontró que el número de mastocitos fue mayor en la médula (7,4 ± 0,52) y la corteza ovárica (2,1 ± 0,30) de hembras en estro, en comparación a otras fases del ciclo estral (P<0,05), con un mayor número en el endometrio de hembras en estro y metaestro (6,8 ± 0,45 para el estro, 6,2 ± 0,56 para el metaestro) y en el miometrio (7,1 ± 0,63 para el estro, 7,5 ± 0,33 para el metaestro) comparado a otras fases del ciclo (P < 0,05). Durante todas las etapas del ciclo estral, excepto el proestro, los mastocitos teñidos con safranina se mostraron numerosos en todos los tejidos. Los mastocitos resultaron safranina positivos en el miometrio sólo en el proestro. Se concluyó que algunos cambios fisiológicos podrían ser responsables de la variación en la distribución de mastocitos en los tejidos ováricos y uterinos de la rata durante el ciclo estral.Palabras clave: mastocitos, ciclo estral, rata.

This study investigated the effects of royal jelly (RJ) on acetic acid-induced colitis in rats. Twenty adult female Wistar albino rats were divided into four treatment groups of 5 animals each, including a control group (Group I); Group II was treated orally with RJ (150 mg kg−1 body weight); Group III had acetic acid-induced colitis; and Group IV had acetic acid-induced colitis treated orally with RJ (150 mg kg−1 body weight) for 4 weeks. Colitis was induced by intracolonic instillation of 4% acetic acid; the control group received physiological saline (10 mL kg−1). Colon samples were obtained under deep anaesthesia from animals in all groups. Tissues were fixed in 10% formalin neutral buffer solution for 24 h and embedded in paraffin. Six-micrometre-thick sections were stained with Mallory’s triple stain and toluidine blue in 1% aqueous solution at pH 1.0 for 5 min (for Mast Cells). RJ was shown to protect the colonic mucosa against the injurious effect of acetic acid. Colitis (colonic damage) was confirmed histomorphometrically as significant increases in the number of mast cells (MC) and colonic erosions in rats with acetic acid-induced colitis. The RJ treatment significantly decreased the number of MC and reduced the area of colonic erosion in the colon of RJ-treated rats compared with rats with untreated colitis. The results suggest that oral treatment with RJ could be used to treat colitis.

This study was designed to evaluate the effects of Cd exposure on morphological aspects of beta-cell and weights of fetus and placenta in streptozotocin (STZ)-induced diabetic pregnant rats. Ninety-nine virgin female Wistar rats (200-220 g) were mated with 33 males for at least 12 h. From the onset of pregnancy, the rats were divided into four experimental groups (control, Cd treated, STZ treated, and Cd+STZ treated). The Cd-treated group was injected subcutaneously daily with CdCl2 dissolved in isotonic NaCl, starting at the onset of pregnancy throughout the experiment. Diabetes was induced on the 13th d of pregnancy by a single intraperitoneal injection of STZ in STZ-treated group. In addition to the daily injection of Cd, a single intraperitoneal injection of STZ was also given on the 13th d of pregnancy in the Cd+STZ-treated group. The rats received the last injection 24 h before being sacrificed and 10 randomly selected rats in each group were sacrificed on the 15th and 20th d of pregnancy. Blood samples were taken for the determination of the serum glucose and insulin levels. Maternal pancreases, fetuses, and placentas of sacrificed rats in all groups were harvested (fetal pancreas was also harvested only on the 20th d of pregnancy) for morphological and immunohistochemical examinations. Cd exposure alone caused a degeneration, necrosis, and weak degranulation, but Cd exposure with STZ caused a severe degeneration, necrosis, and degranulation in the beta-cells of the pancreatic islets. No morphological or immunohistochemical differences were found in beta-cells of fetal pancreatic islets of control or other treatment groups. Cd exposure alone also decreased the fetal and placental weights. The administration of STZ alone, on the other hand, increased the placental weight. Cd, STZ, and Cd+STZ administration increased the glucose and decreased the insulin level. The increase in glucose and decrease in insulin levels were higher when Cd and STZ were given together. All of these changes were more severe on the 20th d than those on the 15th d of the pregnancy. It is concluded that Cd exposure during pregnancy may reduce the birth and placental weights and produce necrosis, degeneration, and degranulation in beta-cells of pancreatic islets, causing an increase in the serum glucose level. These changes might be severe in diabetic pregnant mothers.

The physiological distribution of mast cells (MCs) in the reproductive tract and ovary of 12 Angora goats was determined using light microscopic histochemical techniques. Uterus (corpus uteri and cornu uteri), uterine cervix, uterine tubes (isthmus and ampulla) and ovary samples were obtained by laparatomy from groups of animals during metoestrus, dioestrus and proestrus (days 5, 10 and 16 of the oestrous cycle). Tissues were fixed in Mota's fixative (basic lead acetate) for 48 h and embedded in paraffin. Six-micrometre-thick sections were stained with toluidine blue in 1% aqueous solution at pH 1.0 for 5 min and alcian blue-Safranin at pH 1.0 for 30 min. MCs were generally associated with blood vessels in all reproductive organs. In the uterus, they were concentrated mainly in the close of the uterine gland and deep stroma in the endometrium. Higher MC numbers were observed by toluidine blue staining in the uterus, uterine cervix and uterine tubes on days 10 (corpus uterine: 4.7 +/- 3.8 and cornu uterine: 4.9 +/- 3.5) and 16 (corpus uterine: 5.9 +/- 4.5 and cornu uterine: 5.4 +/- 2.4) of the oestrous cycle compared with day 5 (p < 0.05). Mast cells were not observed in the follicles, the corpus luteum and the underside of the surface epithelium of the ovarian cortex, but were observed in the interstitial cortical stroma and the ovarian medulla. In the ovary, MC numbers were significantly higher on day 16 of the oestrous cycle (cortex: 3.4 +/- 2.4 and medulla: 5.7 +/- 4.5, p < 0.05). Safranin-positive connective tissue MCs were not observed in the uterine tube on any occasion. These results indicate oestrous cycle-related changes in the number and location of MCs in goat reproductive organs.

This study has shown that RJ has anti-inflammatory and cell regeneration effect in the colon of rats with acetic acid induced colitis.