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DESONIDA: DESENVOLVIMENTO E ESTUDO DE ESTABILIDADE DE FORMULAÇÕES DE USO TÓPICO / DESONIDE: DEVELOPMENT AND STABILITY STUDY OF TOPICAL FORMULATIONSRosa, Priscila 09 October 2013 (has links)
Desonide is a corticoid used topically in the treatment of dermatological diseases
of inflammatory or allergic origin. In Brazil, is available as cream (0.05%), creamy lotion
(0.05%), gel cream (0.05%), ointment (0.05%) and hair lotion (0.1%). Recent studies
demonstrated the photoinstability of some marketed formulations of desonide (hair
lotion, creamy lotion and gel cream), upon direct exposure to UVA radiation. Thus, the
aim of this work was to develop desonide hair solution and desonide gel cream, seeking
to obtain products with higher photostability than the marketed products. Capillary
solutions with similar composition to the one commercially available were prepared and
they were added of excipients such as antioxidants and ultraviolet filter benzophenone-3
(BZ-3). The antioxidants used were not able to avoid desonide fotodegradation upon
UVA light exposure (15h), being the residual content of desonide between 43.2 and
61.8%. The antioxidants used were not able to avoid the desonide fotodegradation when
the formulations were exposed to UVA for 15 hours (residual levels between 43.2% and
61.8%). BZ-3 at 0.3% prevented desonide photolysis, since after 15 hours of exposure
to direct UVA radiation, the residual content of desonide was 98.61%. The photostability
of the hair solution with BZ-3 was also evaluated against UVC radiation, and their results
compared to the formulation without this adjuvant. It was observed that desonide in hair
solution with BZ-3 degraded slowly (t 90 1.41 h) than the formulation without BZ-3 (t90
0.64 h). The BZ-3 was also used as adjuvant in the gel cream developed, but at the
concentration of 0.1%. This formulation was characterized with respect to its rheological
properties, spreadability, pH, in vitro release profile and content, presenting satisfactory
physicochemical characteristics and being suitable for topical application. The
photostability study conducted by direct exposure to UVA radiation demonstrated the
stability of the desonide gel cream, which was indicated by the residual content around
95% after 48 hours of evaluation. The stability study performed at 20°C and 40°C
showed that the capillary solution formulation was stable under both conditions for 70
days. Under the same conditions, the gel cream proved to be stable at a temperature of
20°C for 60 days. / A desonida é um corticosteroide de uso tópico, utilizada no tratamento de
doenças dermatológicas de origem alérgica ou inflamatória. No Brasil, encontra-se
disponível sob as formas de creme (0,05%), loção cremosa (0,05%), loção capilar
(0,1%), pomada (0,05%) e gel creme (0,05%). Estudos de estabilidade recentes
demonstraram a fotoinstabilidade da desonida nas formulações de loção capilar, loção
cremosa e gel creme comercializadas após exposição direta à radiação UVA. Dessa
forma, o objetivo desse trabalho foi desenvolver solução capilar e gel creme de
desonida, buscando obter produtos com maior fotoestabilidade do que os produtos
comercializados. Prepararam-se soluções capilares com composição semelhante à
disponível no comércio nacional, porém contendo excipientes como antioxidantes e o
filtro ultravioleta benzofenona-3 (BZ-3). Os antioxidantes usados não evitaram a
fotodegradação da desonida quando as formulações foram expostas à radiação UVA
durante 15 horas (teores residuais entre 43,2% e 61,8%). O uso da BZ-3 na
concentração de 0,3% preveniu a fotólise da desonida, visto que após 15 horas de
exposição direta à radiação UVA, o teor residual de desonida foi 98,61%. A
fotoestabilidade da solução capilar com BZ-3 também foi avaliada frente à radiação
UVC, e seus resultados comparados à formulação sem o adjuvante. Observou-se que
na formulação com BZ-3 a desonida degradou mais lentamente (t90 1,41h) do que na
formulação sem BZ-3 (t90 0,64 h). O gel creme desenvolvido também contém a BZ-3 em
sua composição, porém na concentração de 0,1%. Essa formulação foi caracterizada
quanto às suas propriedades reológicas, espalhabilidade, pH, perfil de liberação in vitro
e teor, apresentando características físico-químicas satisfatórias e adequadas à
aplicação tópica. O estudo de fotoestabilidade, realizado através da exposição direta da
formulação à radiação UVA demonstrou a estabilidade da desonida na formulação,
sendo obtido teor residual em torno de 95% após 48 horas de avaliação. O estudo de
estabilidade realizado a 20ºC e a 40ºC demonstrou que a formulação de solução capilar
manteve-se estável em ambas as condições durante 70 dias. Nas mesmas condições, o
gel creme demonstrou ser estável em temperatura de 20ºC durante 60 dias.
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Pharmaceutical and Natural (Exercise) Mechanisms to Mitigate the Negative Impact of PTSD and Chronic Stress on Synaptic Plasticity and MemoryMiller, Roxanne M 01 November 2017 (has links)
Synapses can be altered due to experiences in a process called synaptic plasticity, which causes memory formations. Synapses can be strengthened through methods known as long-term potentiation (LTP) or weakened through long-term depression (LTD). Stresses can cause changes by altering synapses through either LTP or LTD. Rats were used to study the effects of post-traumatic stress disorder (PTSD)-like symptoms and a prophylactic treatment using pharmaceuticals. The first model used was the single prolonged stress (SPS) with two weeks of chronic light, which was not as effective for causing changes in synaptic plasticity. The second model, seven days of social defeat (SD) with two weeks of chronic light was more effective at inducing PTSD-like behavior symptoms and causing changes in LTP levels in the ventral hippocampus, amygdala, and prefrontal cortex between stressed and non-stressed rats. For the prophylactic treatment, propranolol and mifepristone were administered one week prior to and throughout the two weeks of the social defeat protocol. The drugs were able to prevent the changes due to stress on LTP in the three aforementioned brain regions, but did not change the anxious behavior of the rats. An enzyme-linked immunosorbent assay (ELISA) was used to determine corticosterone and norepinephrine levels between the different groups of rats. No significant differences were detected between SD and control rats, but SD injected rats were different from controls indicating that the injections were causing added stress. Reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) was used to detect changes in the adrenergic, corticoid, AMPA, and NMDA receptors. There were a few significant changes to some of the targets indicating that the stress protocol and drugs were having an effect on the mRNA expression. Propranolol and mifepristone could possibly be used as a prophylactic treatment for traumatic stress. In a separate study, techniques were used to determine the negative effects chronic stress (non-PTSD-like) has on synaptic plasticity in the dorsal hippocampus and to show how exercise was able to mitigate some of those negative stress effects. Electrophysiology showed differences in LTP between four groups of mice: sedentary no stress (SNS), sedentary with stress (SWS), exercise with stress (EWS), and exercise no stress (ENS). SWS had the lowest amount of LTP, whereas ENS had the highest. SNS and EWS had similar levels of LTP, which were in between the SWS and ENS groups. Corticosterone blood levels measured by an ELISA showed significant increases in the stressed groups compared to the non-stressed groups. The radial arm maze showed that both groups of exercise mice made fewer reference memory errors the second week of testing compared to the sedentary groups. RT-qPCR determined that brain-derived neurotrophic factor (BDNF) and corticoid and dopamine 5 receptors were likely causing some of the memory changes.
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Pharmaceutical and Natural (Exercise) Mechanisms to Mitigate the Negative Impact of PTSD and Chronic Stress on Synaptic Plasticity and MemoryMiller, Roxanne M 01 November 2017 (has links)
Synapses can be altered due to experiences in a process called synaptic plasticity, which causes memory formations. Synapses can be strengthened through methods known as long-term potentiation (LTP) or weakened through long-term depression (LTD). Stresses can cause changes by altering synapses through either LTP or LTD. Rats were used to study the effects of post-traumatic stress disorder (PTSD)-like symptoms and a prophylactic treatment using pharmaceuticals. The first model used was the single prolonged stress (SPS) with two weeks of chronic light, which was not as effective for causing changes in synaptic plasticity. The second model, seven days of social defeat (SD) with two weeks of chronic light was more effective at inducing PTSD-like behavior symptoms and causing changes in LTP levels in the ventral hippocampus, amygdala, and prefrontal cortex between stressed and non-stressed rats. For the prophylactic treatment, propranolol and mifepristone were administered one week prior to and throughout the two weeks of the social defeat protocol. The drugs were able to prevent the changes due to stress on LTP in the three aforementioned brain regions, but did not change the anxious behavior of the rats. An enzyme-linked immunosorbent assay (ELISA) was used to determine corticosterone and norepinephrine levels between the different groups of rats. No significant differences were detected between SD and control rats, but SD injected rats were different from controls indicating that the injections were causing added stress. Reverse transcriptase quantitative polymerase chain reaction (RT-qPCR) was used to detect changes in the adrenergic, corticoid, AMPA, and NMDA receptors. There were a few significant changes to some of the targets indicating that the stress protocol and drugs were having an effect on the mRNA expression. Propranolol and mifepristone could possibly be used as a prophylactic treatment for traumatic stress. In a separate study, techniques were used to determine the negative effects chronic stress (non-PTSD-like) has on synaptic plasticity in the dorsal hippocampus and to show how exercise was able to mitigate some of those negative stress effects. Electrophysiology showed differences in LTP between four groups of mice: sedentary no stress (SNS), sedentary with stress (SWS), exercise with stress (EWS), and exercise no stress (ENS). SWS had the lowest amount of LTP, whereas ENS had the highest. SNS and EWS had similar levels of LTP, which were in between the SWS and ENS groups. Corticosterone blood levels measured by an ELISA showed significant increases in the stressed groups compared to the non-stressed groups. The radial arm maze showed that both groups of exercise mice made fewer reference memory errors the second week of testing compared to the sedentary groups. RT-qPCR determined that brain-derived neurotrophic factor (BDNF) and corticoid and dopamine 5 receptors were likely causing some of the memory changes.
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