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Made available in DSpace on 2019-10-06T16:02:14Z (GMT). No. of bitstreams: 0 Previous issue date: 2018-12-01 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Aims: The objective of this study was to assess the mechanisms underlying pancreatic islet adaptation in diabetic mothers and their pups. Additionally, the influence of pancreatic adaptations on maternal reproductive performance was also investigated. Main methods: Wistar rats were injected with streptozotocin for diabetes induction. At adulthood (3 months), all animals underwent an oral glucose tolerance test (OGTT) for glucose assessment as an inclusion criterion. Following, the animals were mated. At day 18 of pregnancy, the mothers were killed for blood collect ion to determine fasting insulin and glucagon concentrations. The pancreas was removed and processed for the immunohistochemical analysis of insulin, glucagon, somatostatin, Ki-67 and PDX-1, superoxide dismutase 1 (SOD-1), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA). The pregnant uterus was also collected for the evaluation of embryofetal loss. Key findings: The diabetic rats showed increased glucose, serum glucagon and insulin concentrations, and embryofetal loss rates. They also showed a reduction in pancreatic islets area and percentage of cells stained for insulin, increased the percentage of non-β cells (alpha e delta cells) stained for Ki-67, glucagon, and somatostatin. Moreover, the cells stained for somatostatin were spread across the islets and showed stronger staining for MDA and weaker staining for GSH-Px. Significance: Diabetes leads to adaptive responses from the endocrine pancreas in pregnancy that especially involves non-β cells, modifying the mantle-core structure. Nonetheless, these adaptations are not enough for glucose homeostasis and affect the maternal environment, which in turn impairs fetal development. Laboratory of Experimental Research on Gynecology and Obstetrics Gynecology Obstetrics and Mastology Post Graduate Course Botucatu Medical School Univ Estadual Paulista_Unesp DeVry Ruy Barbosa School (DeVry Brazil Group) Laboratory of System Physiology and Reproductive Toxicology Institute of Biological and Health Sciences Federal University of Mato Grosso (UFMT) Department of Morphology Botucatu Bioscience Institute Univ Estadual Paulista_Unesp Biomedical Research Centre Universidad de Valparaíso Laboratory of Experimental Research on Gynecology and Obstetrics Gynecology Obstetrics and Mastology Post Graduate Course Botucatu Medical School Univ Estadual Paulista_Unesp Department of Morphology Botucatu Bioscience Institute Univ Estadual Paulista_Unesp FAPESP: 2011/18519-7

Made available in DSpace on 2019-10-06T16:25:39Z (GMT). No. of bitstreams: 0 Previous issue date: 2019-06-01 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Aim: At performing a temporal analysis of the distribution pattern of islet endocrine cells and antioxidant enzymes in diabetic rats during the post-natal critical development window. Main methods: The newborns received streptozotocin (STZ) at birth for diabetes induction, and control females received the vehicle. The animals were euthanized at different lifetimes: D5, D10, D15, and D30. Morphological analysis of pancreas and biochemical assays was performed. Key findings: The STZ-induced rats presented irregular shape of islet on D5 and there was an attempt to restore of this shape in other life moment studied. There was an increase progressive in islet area, however they maintained smaller than those of control rats, with lower labeling intensity for insulin, higher for glucagon and somatostatin, lower for SOD-1 was lower in the islets of the STZ-induced animals at all times studied and for GSH-Px in D10 and D30. Significance: Although STZ-induced diabetic rats presented compensatory mechanisms to restore the mass of endocrine cells, this was not sufficient since these rats developed the diabetic state. This was confirmed by the oral glucose tolerance test from D30. In addition, the delta (δ)-cells presented ectopic location in islets, indicating a possible relationship for beta (β)-cell mass restoration. There was a response of the pancreas to reduce the hyperglycemia in the first month of life. Furthermore, the cells from the endocrine pancreas of diabetic animals show a decline of antioxidant enzymatic, contributing to the increased susceptibility of cells to hyperglycemia-induced ROS in this postnatal critical development window. Laboratory of Experimental Research of Gynecology and Obstetrics Postgraduate Course of Gynecology Obstetrics and Mastology Botucatu Medical School São Paulo State University (UNESP) DeVry Ruy Barbosa School (DeVry Brazil Group) Department of Pathology National Institute of Medical Sciences and Nutrition “Salvador Zubirán” Department of Pathology School of Veterinary Medicine and Animal Science (FMVZ) São Paulo State University (UNESP) Laboratory of System Physiology and Reproductive Toxicology Institute of Biological and Health Sciences Federal University of Mato Grosso (UFMT) Laboratory of Experimental Research of Gynecology and Obstetrics Postgraduate Course of Gynecology Obstetrics and Mastology Botucatu Medical School São Paulo State University (UNESP) Department of Pathology School of Veterinary Medicine and Animal Science (FMVZ) São Paulo State University (UNESP) FAPESP: 2011/18519-7

Ethnopharmacological relevance Azadirachta indica A. Juss, popularly known as neem, presents medicinal and insecticide properties. However, the repercussions of the neem maternal treatment on fetal development should be investigated. Thus, the aim of this study was to evaluated the effects of Azadirachta indica (neem) on the frequency of congenital malformations in fetuses from rats. Materials and methods Pregnant rats were randomly distributed into three experimental groups: NT=non-treated; TOil=treated with neem seed oil (1.2 mL/day); TAP=treated with active principle of Azadirachta indica (azadirachtin—1.0 mg/mL/day). The neem oil (1.2 mL/day) or azadirachtin (1.0 mg/mL/day) treatments were orally administered throughout pregnancy. Blood samples were collected on days 0, 7, 14 and 20 of pregnancy. Oral glucose test tolerance (OGTT) was performed at day 17 of pregnancy for estimation of total area under the curve (AUC). At term, the fetuses were collected and external and internal (visceral and skeletal) malformations were analyzed. Results The data showed that the dams treated with neem seed oil and Azadirachtin had no significant change in glucose levels and AUC. It was also verified that neem oil treatment contributed to increase the frequency of malformation/variation, in particular the visceral in their fetuses, while neither significant result was observed in TAP group. Conclusion In conclusion, neem seed oil treatment administered during pregnancy caused abnormalities in rat fetuses, showing teratogenic effect but the Azadirachtin (active principle) presented no impairment in the fetuses.

The maternal food supply, nutrition and metabolism leads to lifelong consequences for the health of the infants. Experimental models have been developed to explore these repercussions. We intended (1) to verify the influence of a maternal overnutrition on the maternal oxidative stress in pregnant rat, (2) to evaluate if the maternal oxidative stress interferes on the fetal growth, and (3) to analyze external, skeletal and visceral fetal anomalies. On day 0 of pregnancy, the rats were randomly distributed into two groups (n=21 rats/group): Control group - fed regular diet; Overnutrition group – fed high caloric diet, which was made by mixing the supplemented ingredients to a previously triturated Purina Chow. On day 21 of pregnancy, the rats were euthanized to evaluate reproductive outcomes and fetal development, and to obtain blood samples for maternal metabolic parameters. The fetal weights were significantly reduced after overnutrition treatment during pregnancy. The overnoutrished rats presented higher malonaldehyde-MDA and thiol group concentrations and superoxide dismutase (SOD) activity whereas glutathione peroxidase (GSH-Px) activity was lower. The fetuses from overnutrition group presented higher frequency of skeletal and visceral anomalies. Thus, the overnutrition caused metabolic changes in the maternal organism, particularly in oxidative metabolism, which impaired the fetal growth and development, showing harmful effect of a hypercaloric diet during pregnancy.

We evaluated associations between the concentrations of heat shock proteins (hsp60 and hsp70) and their respective antibodies, alterations in maternal reproductive performance, and fetal malformations in pregnant rats with hyperglycemia. Mild diabetes (MD) or severe diabetes (SD) was induced in Sprague-Dawley rats prior to mating; non-treated non-diabetic rats (ND) served as controls. On day 21 of pregnancy, maternal blood was analyzed for hsp60 and hsp70 and their antibodies; and fetuses were weighed and analyzed for congenital malformations. Hsp and anti-hsp levels were correlated with blood glucose levels during gestation. There was a positive correlation between hsp60 and hsp70 levels and the total number of malformations (R = 0.5908, P = 0.0024; R = 0.4877, P = 0.0134, respectively) and the number of malformations per fetus (R = 0.6103, P = 0.0015; R = 0.4875, P = 0.0134, respectively). The anti-hsp60 IgG concentration was correlated with the number of malformations per fetus (R = 0.3887, P = 0.0451) and the anti-hsp70 IgG level correlated with the total number of malformations (R = 0.3999, P = 0.0387). Moreover, both hsp and anti-hsp antibodies showed negative correlations with fetal weight. The results suggest that there is a relationship between hsp60 and hsp70 levels and their respective antibodies and alterations in maternal reproductive performance and impaired fetal development and growth in pregnancies associated with diabetes.

The expression of HSP70 in embryonic cells of mammals and its role for their normal development and protection is an important aspect to be investigated in pregnancy and/or mild diabetes. In this sense, the present study evaluated the effects of mild diabetes on maternal reproductive parameters and HSP70 levels in Wistar rats at different stages of life and in their offspring. Mild diabetes was induced by a beta-cytotoxic drug (streptozotocin) at birth. Four experimental groups were evaluated: at 90 days of age: nonpregnant nondiabetic (ND90) and nonpregnant mild diabetic (D90) female rats, and at term pregnancy: pregnant female rats of both glycemic status were examined (NDP and DP, respectively). The rats were submitted to oral glucose tolerance test, and blood samples were collected for determination of HSP70 levels. In addition, the reproductive performance of pregnant rats was assessed and HSP70 levels determined in their offspring blood samples. The HSP70 levels and maternal reproductive performance presented no difference between ND and D rats, regardless of the life stage. The HSP70 levels were increased in D90 rats and lower in offspring from D rats. Maternal HSP70 levels were positively correlated to the number of dead embryos. In conclusion, mild diabetes did not affect maternal reproductive performance, but high maternal HSP70 levels compromised embryo development. In addition, offspring from D rats exhibited lower HSP70 levels, showing that this protein can be used as an indicator of metabolic consequences of diabetes and predictor of related disorders in adulthood.

The aim of the present study was at evaluating the effects of oxidative stress in blood and placenta of mild diabetic Wistar rats. At birth, Wistar rats received citrate buffer (nondiabetic group, n = 15) and another group received streptozotocin (100 mg/kg, subcutaneous) to induce mild diabetes (diabetic, n = 15). The glycemia of these pregnant adult female rats were evaluated at days 0, 7, 14, and 21 of pregnancy, and at term pregnancy, the blood and placental samples were collected for oxidative stress measurements. The mild diabetes caused glycemia superior to 120 mg/dL during pregnancy, increased superoxide dismutase, glutathione peroxidase, glutathione reductase activities, and malondialdehyde levels in the blood, and catalase activity in the placenta. Thus, mild diabetes increased activities of antioxidant substances aiming at defending against the exacerbated oxidative stress but were not enough. The placenta also answered to diabetic milieu and increased antioxidant defense, showing that even a mild hyperglycemia was enough to cause placental and maternal blood changes.

Made available in DSpace on 2014-12-03T13:10:33Z (GMT). No. of bitstreams: 0 Previous issue date: 2014-01-01Bitstream added on 2014-12-03T13:23:08Z : No. of bitstreams: 1 WOS000337468100001.pdf: 1280003 bytes, checksum: 10b264a6ba2554b999feb847f11b2369 (MD5) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Glucose homeostasis is controlled by endocrine pancreatic cells, and any pancreatic disturbance can result in diabetes. Because 8% to 12% of diabetic pregnant women present with malformed fetuses, there is great interest in understanding the etiology, pathophysiological mechanisms, and treatment of gestational diabetes. Hyperglycemia enhances the production of reactive oxygen species, leading to oxidative stress, which is involved in diabetic teratogenesis. It has also been suggested that maternal diabetes alters embryonic gene expression, which might cause malformations. Due to ethical issues involving human studies that sometimes have invasive aspects and the multiplicity of uncontrolled variables that can alter the uterine environment during clinical studies, it is necessary to use animal models to better understand diabetic pathophysiology. This review aimed to gather information about pathophysiological mechanisms and fetal outcomes in streptozotocin-induced diabetic rats. To understand the pathophysiological mechanisms and factors involved in diabetes, the use of pancreatic regeneration studies is increasing in an attempt to understand the behavior of pancreatic beta cells. In addition, these studies suggest a new preventive concept as a treatment basis for diabetes, introducing therapeutic efforts to minimize or prevent diabetes-induced oxidative stress, DNA damage, and teratogenesis. Univ Estadual Paulista, UNESP, Grad Program Gynecol Obstet & Mastol, Lab Expt Res Gynecol & Obstet,Botucatu Med Sch, BR-18618970 Botucatu, SP, Brazil Univ Estadual Paulista, UNESP, Botucatu Med Sch, Dept Gynecol & Obstet, BR-18618970 Botucatu, SP, Brazil Univ Estadual Paulista, UNESP, Grad Program Gynecol Obstet & Mastol, Lab Expt Res Gynecol & Obstet,Botucatu Med Sch, BR-18618970 Botucatu, SP, Brazil Univ Estadual Paulista, UNESP, Botucatu Med Sch, Dept Gynecol & Obstet, BR-18618970 Botucatu, SP, Brazil

Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-27T11:29:58Z No. of bitstreams: 0Bitstream added on 2014-05-27T14:43:23Z : No. of bitstreams: 1 2-s2.0-84880090248.pdf: 1487092 bytes, checksum: 9b034a22329b915f71fc84e623c42ecd (MD5) Made available in DSpace on 2014-05-27T11:29:58Z (GMT). No. of bitstreams: 0 Previous issue date: 2013-07-18 The presence of diabetes in pregnancy leads to hormonal and metabolic changes making inappropriate intrauterine environment, favoring the onset of maternal and fetal complications. Human studies that explore mechanisms responsible for changes caused by diabetes are limited not only for ethical reasons but also by the many uncontrollable variables. Thus, there is a need to develop appropriate experimental models. The diabetes induced in laboratory animals can be performed by different methods depending on dose, route of administration, and the strain and age of animal used. Many of these studies are carried out in neonatal period or during pregnancy, but the results presented are controversial. So this paper, addresses the review about the different models of mild diabetes induction using streptozotocin in pregnant rats and their repercussions on the maternal and fetal organisms to propose an adequate model for each approached issue. © 2013 D. C. Damasceno et al. Department of Gynecology and Obstetrics Botucatu Medical School Universidade Estadual Paulista (Unesp), 18618-970 Botucatu, SP Department of Gynecology and Obstetrics Botucatu Medical School Universidade Estadual Paulista (Unesp), 18618-970 Botucatu, SP

Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-27T11:27:23Z No. of bitstreams: 0Bitstream added on 2014-05-27T14:32:03Z : No. of bitstreams: 1 2-s2.0-84874016167.pdf: 154750 bytes, checksum: 82ba0ea3eba705fb9fa2bca1ca066c97 (MD5) Made available in DSpace on 2014-05-27T11:27:23Z (GMT). No. of bitstreams: 0 Previous issue date: 2012-12-01 Background: The aim of this study was to evaluate the changes in testicular function of rats due to cigarette smoke exposure and the possible mechanism by which zinc protects against these alterations. Methods: MaleWistar rats (60 days old) were randomly divided into 3 groups: control (G1, n = 10); exposed to cigarette smoke (G2, n = 10; 20 cigarettes/day/9 weeks) and exposed to cigarette smoke and supplemented with zinc (G3, n = 8; 20 cigarettes/day/9 weeks; 20 mg/kg zinc chloride daily for 9 weeks, by gavage). After the treatment period, the animals were euthanized, and materials were collected for analyses. Results: G2 rats showed a reduction in body mass; impaired sperm concentration, motility, morphology and vitality; and increased malonaldehyde and thiol group levels and superoxide dismutase activity as compared to G1. Zinc prevented the reduction of sperm concentration and the excessive increase of lipid peroxidation and induced an increase in plasma testosterone levels, wet weight of testis and thiol group concentration. Conclusions: Exposure to cigarette smoke led to harmful effects on testicular function at least partially due to the exacerbation of oxidative stress. Supplementary zinc had an important modulator/protector effect on certain parameters. The mechanism of zinc protection can be through an increase of SH concentration. Thus, zinc supplementation may be a promising addition to conventional treatments for male infertility related to smoking. Copyright © 2012 by Institute of Pharmacology Polish Academy of Sciences. Department of Pharmacology Institute of Biosciences UNESP - Univ. Estadual Paulista, 18618-970 Botucatu, Sao Paulo Department of Gynecology and Obstetrics Botucatu Medical School UNESP - Univ. Estadual Paulista, 18618-970 Botucatu, Sao Paulo Department of Pharmacology Institute of Biosciences UNESP - Univ. Estadual Paulista, 18618-970 Botucatu, Sao Paulo Department of Gynecology and Obstetrics Botucatu Medical School UNESP - Univ. Estadual Paulista, 18618-970 Botucatu, Sao Paulo

Made available in DSpace on 2013-08-12T17:58:55Z (GMT). No. of bitstreams: 0 Previous issue date: 2012-09-01 Made available in DSpace on 2013-09-30T18:20:09Z (GMT). No. of bitstreams: 0 Previous issue date: 2012-09-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:35:21Z No. of bitstreams: 1 WOS000309719800008.pdf: 182994 bytes, checksum: f67ace550f0fe880d2a7d27083247d88 (MD5) Made available in DSpace on 2014-05-20T13:35:21Z (GMT). No. of bitstreams: 1 WOS000309719800008.pdf: 182994 bytes, checksum: f67ace550f0fe880d2a7d27083247d88 (MD5) Previous issue date: 2012-09-01 The aim of this work was to evaluate the direct protective action of oral fatty acid supplementation against the deleterious effect of hyperglycemia on maternal reproductive outcomes; fetal growth and development on female Wistar rats. The animals were distributed into four experimental groups: G1= non-diabetic without supplementation (Control group); G2= non-diabetic treated with linoleic (LA) and gammalinolenic acid (GLA) (1 mL of Gamaline-V/day); G3= diabetic without supplementation and G4= diabetic treated with LA and GLA. Diabetes was induced by streptozotocin (40 mg/kg). At day 21 of pregnancy, the gravid uterus was weighed and dissected to count the dead and live fetuses, resorption, implantation, and corpora lutea numbers. The fetuses were analyzed for external and internal anomalies. The treatment with Gamaline-V supplementation to diabetic rats interfered in the maternal reproductive outcome (reduced number of live fetuses and embryonic implantation); however, it protected the deleterious on the incidence of congenital anomalies caused by hyperglycemia. Univ Estadual Paulista, Dept Ginecol & Obstet, Lab Pesquisa Expt Ginecol & Obstet, Botucatu, SP, Brazil Univ Estadual Paulista, Inst Biociencias, Dept Morfol, Botucatu, SP, Brazil Univ Fed Mato Grosso, Inst Ciencias Biol & Saude, Barra do Garcas, MT, Brazil Univ Estadual Paulista, Dept Ginecol & Obstet, Lab Pesquisa Expt Ginecol & Obstet, Botucatu, SP, Brazil Univ Estadual Paulista, Inst Biociencias, Dept Morfol, Botucatu, SP, Brazil

Ethnopharmacological relevance The role of Azadirachta indica (neem) against Chagas disease and its antibiotic and antidiabetic action have been demonstrated in non-pregnant animals. However, the effects of neem on lipid metabolism and oxidative stress during pregnancy remain to be investigated. The objective of this study was to evaluate the effects of Azadirachta indica (neem) on maternal reproductive performance and biochemical parameters in non-diabetic and streptozotocin-induced mild diabetic rats (MD). Materials and methods Pregnant rats were randomly distributed into six experimental groups: ND=non-treated non-diabetic ( n =13); NDOil=non-diabetic treated with 1.2 mL/day neem seed oil ( n =12); NDPA=non-diabetic treated with 1.0 mg/mL/day azadirachtin ( n =12); D=non-treated diabetic ( n =13); DOil: diabetic treated with neem seed oil ( n =12), and DPA=diabetic treated with azadirachtin, n =13. Treatment with either neem oil (1.2 mL/day) or azadirachtin (1.0 mg/mL/day) was orally administered throughout pregnancy. Glucose test tolerance (GTT) was performed at day 17 of pregnancy and used as an inclusion criterion. At term pregnancy, maternal reproductive outcomes, lipid profile and oxidative stress status were assessed. Results Treatment with neem oil and azadirachtin during pregnancy (1) had no hypoglycemic and anti-hyperglycemic effects on non-diabetic and diabetic rats, respectively; (2) affected OGTT glycemic levels in diabetic rats; (3) increased the proportion of fetuses classified as small for pregnancy age (SPA) in all groups; and (4) did not interfere with the lipid profile in non-diabetic dams. Neem oil reduced the rate of total cholesterol and NEFA in diabetic animals. Both neem oil and azadirachtin increased lipoperoxidation, characterized by increased MDA levels in non-diabetic rats. Conclusion Both neem seed oil and azadirachtin impaired intrauterine development and altered antioxidant/oxidative status during pregnancy.

Experimental studies have shown that exposure to cigarette smoke has negative effects on lipid metabolism and oxidative stress status. Cigarette smoke exposure in nonpregnant and pregnant rats causes significant genotoxicity (DNA damage). However, no previous studies have directly evaluated the effects of obesity or the association between obesity and cigarette smoke exposure on genotoxicity. Therefore, the aim of the present investigation was to evaluate DNA damage levels, oxidative stress status and lipid profiles in obese Wistar rats exposed to cigarette smoke.Female rats subcutaneously (s.c.) received a monosodium glutamate solution or vehicle (control) during the neonatal period to induce obesity. The rats were randomly distributed into three experimental groups: control, obese exposed to filtered air, and obese exposed to tobacco cigarette smoke. After a 2-month exposure period, the rats were anesthetized and killed to obtain blood samples for genotoxicity, lipid profile, and oxidative stress status analyses.The obese rats exposed to tobacco cigarette smoke presented higher DNA damage, triglycerides, total cholesterol, free fatty acids, VLDL-c, HDL-c, and LDL-c levels compared to control and obese rats exposed to filtered air. Both obese groups showed reduced SOD activity. These results showed that cigarette smoke enhanced the effects of obesity.In conclusion, the association between obesity and cigarette smoke exposure exacerbated the genotoxicity, negatively impacted the biochemical profile and antioxidant defenses and caused early glucose intolerance. Thus, the changes caused by cigarette smoke exposure can trigger the earlier onset of metabolic disorders associated with obesity, such as diabetes and metabolic syndrome.

Submitted by Guilherme Lemeszenski (guilherme@nead.unesp.br) on 2013-08-22T19:05:30Z No. of bitstreams: 1 S1516-05722011000300017.pdf: 79428 bytes, checksum: 5498c28fd29ad214ea0e2e65f885eb72 (MD5) Made available in DSpace on 2013-08-22T19:05:30Z (GMT). No. of bitstreams: 1 S1516-05722011000300017.pdf: 79428 bytes, checksum: 5498c28fd29ad214ea0e2e65f885eb72 (MD5) Previous issue date: 2011-01-01 Made available in DSpace on 2013-09-30T18:20:53Z (GMT). No. of bitstreams: 2 S1516-05722011000300017.pdf: 79428 bytes, checksum: 5498c28fd29ad214ea0e2e65f885eb72 (MD5) S1516-05722011000300017.pdf.txt: 31755 bytes, checksum: efd100d36370bc319aacf461a2350475 (MD5) Previous issue date: 2011-01-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:35:44Z No. of bitstreams: 2 S1516-05722011000300017.pdf: 79428 bytes, checksum: 5498c28fd29ad214ea0e2e65f885eb72 (MD5) S1516-05722011000300017.pdf.txt: 31755 bytes, checksum: efd100d36370bc319aacf461a2350475 (MD5) Made available in DSpace on 2014-05-20T13:35:44Z (GMT). No. of bitstreams: 2 S1516-05722011000300017.pdf: 79428 bytes, checksum: 5498c28fd29ad214ea0e2e65f885eb72 (MD5) S1516-05722011000300017.pdf.txt: 31755 bytes, checksum: efd100d36370bc319aacf461a2350475 (MD5) Previous issue date: 2011-01-01 Diabetes mellitus (DM) é uma síndrome de etiologia múltipla caracterizada por hiperglicemia crônica. Esta hiperglicemia induz o aumento na produção de espécies reativas de oxigênio (ERO) e diminuição das defesas antioxidantes. Devido às complicações causadas pelo diabete, muitos indivíduos optam por terapias alternativas à base de plantas medicinais para amenizar seus efeitos. Sendo assim, nesta revisão de literatura, foram analisados e descritos diversos trabalhos experimentais com a utilização de animais diabéticos para comprovar os efeitos antioxidantes de algumas dessas plantas e verificar se os títulos e resumos disponibilizados nos artigos são compatíveis aos objetivos de nossa busca. Diabetes mellitus (DM) is a syndrome of multiple etiology characterized by chronic hyperglycemia. This hyperglycemia induces increased production of reactive oxygen species (ROS) and decreased antioxidant defenses. Due to complications caused by diabetes, a large number of people have chosen medicinal plant-based alternative therapies to alleviate its effects. Thus, in this literature review, several experimental studies with the use of diabetic animals were analyzed to demonstrate the antioxidant effects of these plants and to verify if the titles and abstracts provided in the papers are compatible with the aims of our search. Unesp Faculdade de Medicina de Botucatu Departamento de Ginecologia e Obstetrícia Unesp Faculdade de Medicina de Botucatu Departamento de Ginecologia e Obstetrícia

Botucatu Med Sch, Grad Program Gynecol Obstet &Mastol, Lab Expt Res Gynecol &Obstet, Botucatu, SP, Brazil

s / Placenta 36 (2015) 469e521 490 pregnancy morbidity plus vascular thrombosis (PM/VT), pregnancy morbidity without aPL (PM/aPL-) or healthy women (NHS). Drugs were added at the same time with IgG at previous established concentrations. After 24 h, the inserts were removed and trophoblast cell migration across the Matrigel coated membrane was determined using a colorimetric assay. The relative cell invasion value was assessed by comparing the optical densities with no treatment control. STAT-3 activation was determined at same conditions of invasion assays using Western blots. Results: IgGs from patients with APS-associated pregnancy morbidity (PM, PM/VT) induce a significantly decreased invasion in comparison with IgGs from the NHS and PM/aPLgroups. Enoxaparin, aspirin and ATL restore the aPL-decreased invasion and, moreover, ATL has a receptormediated effect as demonstrated by application of its antagonist Boc-2, which reverses the ATL-restored invasion. Additionally, phosphorylation of STAT-3 is reduced by IgGs from PM patients. Conclusion: We show here that some of drugs used in APS-related pregnancy morbidity treatment are involved in the modulation of trophoblast function. They possibly restore some processes essential for normal trophoblast invasion. Moreover, ATL effects may explain the benefits of aspirin treatment observed in patients with obstetric APS. Since STAT-3 is an intracellular signalling molecule involved in migration and invasion processes, our results support the view that aPL from patients with pregnancy morbidity alter the proper function of this pathway. Financial support: CODIUniversidad de Antioquia Grant 91515; Estrategia de sostenibilidad Grupo Reproducci on 2014-2015; Programa de Cooperaci on Cientifica Internacional-Proyectos de Intercambio: Colciencias-Colombia Convocatoria 614-2013, y CONICYT-Chile PCCI 130017. AMA is a fellow of Colciencias. PA.7. MORPHOLOGICAL ANALYSIS OF THE PANCREATIC BETA CELLS OF DIABETIC FEMALE RATS AT DIFFERENT AGES OF LIFE F.Q. Gallego , Y.K. Sinzato , B. Dallaqua , I.L. Iessi , R.L. Amorim , C.E. Fonseca , I.M.P. Calderon , M.V.C. Rudge , D.C. Damasceno . 1 Laboratory of Experimental Research on Gynecology and Obstetrics, Graduate Program on Gynecology, Obstetrics and Mastology, Botucatu Medical School, Brazil; Department of Pathology, Botucatu Veterinary and Zootechnology Medical School, Univ. Estadual Paulista_Unesp, Botucatu, S~ ao Paulo, Brazil Background: Recent studies have shown regeneration of pancreatic islets in physiological and pathological circumstances. We hypothesized that diabetes disturbs insulin-producing b-cell regeneration in laboratory animals. Aim: The objective was to understand the proliferation and death mechanism of pancreatic b-cells in non-diabetic and neonatally streptozotocininduced mild diabetic rats at different stages of life and during pregnancy. Methods: The rats were randomly assigned into the following groups: Non-diabetic (Control1⁄4C, glycemia

Made available in DSpace on 2013-08-28T14:09:48Z (GMT). No. of bitstreams: 1 WOS000294807100001.pdf: 1213498 bytes, checksum: 04f81dbdf7848a204e3b76281faa8d3c (MD5) Made available in DSpace on 2013-09-30T18:20:38Z (GMT). No. of bitstreams: 2 WOS000294807100001.pdf: 1213498 bytes, checksum: 04f81dbdf7848a204e3b76281faa8d3c (MD5) WOS000294807100001.pdf.txt: 34206 bytes, checksum: 004903e674756b84e13c4605be19f97d (MD5) Previous issue date: 2011-08-18 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:35:37Z No. of bitstreams: 2 WOS000294807100001.pdf: 1213498 bytes, checksum: 04f81dbdf7848a204e3b76281faa8d3c (MD5) WOS000294807100001.pdf.txt: 34206 bytes, checksum: 004903e674756b84e13c4605be19f97d (MD5) Made available in DSpace on 2014-05-20T13:35:37Z (GMT). No. of bitstreams: 2 WOS000294807100001.pdf: 1213498 bytes, checksum: 04f81dbdf7848a204e3b76281faa8d3c (MD5) WOS000294807100001.pdf.txt: 34206 bytes, checksum: 004903e674756b84e13c4605be19f97d (MD5) Previous issue date: 2011-08-18 Research Support Centre of the Botucatu Medical School, Universidade Estadual Paulista (UNESP) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Background: The purpose of this study was to evaluate the effects of cigarette smoke exposure before pregnancy on diabetic rats and their offspring development.Methods: Diabetes was induced by streptozotocin and cigarette smoke exposure was conducted by mainstream smoke generated by a mechanical smoking device and delivered into a chamber. Diabetic female Wistar rats were randomly distributed in four experimental groups (n minimum = 13/group): nondiabetic (ND) and diabetic rats exposed to filtered air (D), diabetic rats exposed to cigarette smoke prior to and into the pregnancy period (DS) and diabetic rats exposed to cigarette smoke prior to pregnancy period (DSPP). At day 21 of pregnancy, rats were killed for maternal biochemical determination and reproductive outcomes.Results: The association of diabetes and cigarette smoke in DSPP group caused altered glycemia at term, reduced number of implantation and live fetuses, decreased litter and maternal weight, increased pre and postimplantation loss rates, reduced triglyceride and VLDL-c concentrations, increased levels of thiol groups and MDA. Besides, these dams presented increased SOD and GSH-Px activities. However, the increased antioxidant status was not sufficient to prevent the lipid peroxidation observed in these animals.Conclusion: Despite the benefits stemming from smoking interruption during the pregnancy of diabetic rats, such improvement was insufficient to avoid metabolic alterations and provide an adequate intrauterine environment for embryofetal development. Therefore, these results suggest that it is necessary to cease smoking extensive time before planning pregnancy, since stopping smoking only when pregnancy is detected may not contribute effectively to fully adequate embryofetal development. UNESP Univ Estadual Paulista, Botucatu Med Sch, Dept Gynecol & Obstet, Lab Expt Res Gynecol & Obstet, São Paulo, Brazil Univ Marilia UNIMAR, Dept Pharmacol, Marilia, SP, Brazil Mato Grosso Fed Univ UFMT, Univ Ctr Araguaia, Inst Biol & Hlth Sci, Cuiaba, Mato Grosso, Brazil UNESP Univ Estadual Paulista, Botucatu Med Sch, Dept Gynecol & Obstet, Lab Expt Res Gynecol & Obstet, São Paulo, Brazil FAPESP: 04/01077-8