Interferência na barreira intestinal e no metabolismo dos neurônios entéricos no tratamento com Anfotericina B e Ácido Ursólico para leishmaniose visceral
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Data
2022-01-19
Autores
Cavallone, Italo Novais
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Universidade Estadual Paulista (Unesp)
Resumo
A leishmaniose visceral é provocada pela infecção por protozoários do gênero Leishmania em diferentes órgãos como baço, fígado e intestino, que por apresentar associação com o tecido linfoide, torna-se passível dos malefícios da doença. Esta forma clínica é letal se não tratada corretamente. Seu tratamento ocorre através de fármacos como a Anfotericina B, cuja toxicidade, duração e a resistência do protozoário instigam a busca por novos compostos como o Ácido Ursólico. Este estudo objetivou analisar a interferência destes compostos na barreira intestinal e no metabolismo neuronal mioentérico no duodeno de hamsters dourados com leishmaniose visceral. Os hamsters foram divididos em grupos (n = 5): três foram infectados com 2x107 promastigotas de L. infantum, e um foi inoculado com solução salina. Após 45 dias, dois grupos infectados receberam tratamentos com Anfotericina B e Ácido Ursólico, durante 15 dias. Os animais foram sacrificados, o fígado e baço foram destinados para análise de parasitismo. O duodeno foi processado para análise histológica da parede intestinal e morfoquantitativa neuronal. A infecção foi confirmada nos grupos infectados. Os grupos infectados sem tratamento e tratado com Ácido Ursólico apresentaram maiores perfis celular e nuclear. O tratamento com Anfotericina B apresentou perfis celulares menores e maior densidade neuronal. Criptas mais profundas foram observadas no grupo infectado sem tratamento, maior densidade de caliciformes AB+ no tratamento com Ácido Ursólico e vilosidades menores no tratamento com Anfotericna B. Os grupos infectados apresentaram evidências de comprometimento da barreira intestinal, o tratamento com Anfotericina B demonstrou toxicidade relacionada ao metabolismo neuronal entérico.
Visceral leishmaniasis is caused by infection by protozoa of the genus Leishmania in different organs such as the spleen, liver and intestine, which, due to its association with lymphoid tissue, becomes susceptible to the harm of the disease. This clinical form is lethal if not treated correctly. Its treatment occurs through drugs such as Amphotericin B, whose toxicity, duration and protozoan resistance instigate the search for new compounds such as Ursolic Acid. This study aimed to analyze the interference of these compounds on the intestinal barrier and myenteric neuronal metabolism in the duodenum of golden hamsters with visceral leishmaniasis. Hamsters were divided into groups (n = 5): three were infected with 2x107 L. infantum promastigotes, and one was inoculated with saline. After 45 days, two infected groups received treatments with Amphotericin B and Ursolic Acid for 15 days. The animals were sacrificed, the liver and spleen were destined for parasitism analysis. The duodenum was processed for histological analysis of the intestinal wall and neuronal morphoquantitative. Infection was confirmed in the infected groups. The infected groups without treatment and treated with Ursolic Acid had higher cellular and nuclear profiles. Treatment with Amphotericin B showed smaller cell profiles and higher neuronal density. Deeper crypts were observed in the untreated infected group, higher AB+ goblet density in Ursolic Acid treatment and smaller villi in Amphotericin B treatment. Infected groups showed evidence of intestinal barrier impairment, Amphotericin B treatment demonstrated drug-related toxicity. enteric neuronal metabolism.
Visceral leishmaniasis is caused by infection by protozoa of the genus Leishmania in different organs such as the spleen, liver and intestine, which, due to its association with lymphoid tissue, becomes susceptible to the harm of the disease. This clinical form is lethal if not treated correctly. Its treatment occurs through drugs such as Amphotericin B, whose toxicity, duration and protozoan resistance instigate the search for new compounds such as Ursolic Acid. This study aimed to analyze the interference of these compounds on the intestinal barrier and myenteric neuronal metabolism in the duodenum of golden hamsters with visceral leishmaniasis. Hamsters were divided into groups (n = 5): three were infected with 2x107 L. infantum promastigotes, and one was inoculated with saline. After 45 days, two infected groups received treatments with Amphotericin B and Ursolic Acid for 15 days. The animals were sacrificed, the liver and spleen were destined for parasitism analysis. The duodenum was processed for histological analysis of the intestinal wall and neuronal morphoquantitative. Infection was confirmed in the infected groups. The infected groups without treatment and treated with Ursolic Acid had higher cellular and nuclear profiles. Treatment with Amphotericin B showed smaller cell profiles and higher neuronal density. Deeper crypts were observed in the untreated infected group, higher AB+ goblet density in Ursolic Acid treatment and smaller villi in Amphotericin B treatment. Infected groups showed evidence of intestinal barrier impairment, Amphotericin B treatment demonstrated drug-related toxicity. enteric neuronal metabolism.
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Palavras-chave
Intestino, Sistema nervoso entérico, Barreira intestinal, leishmaniose