Hermine Boukeng Jatsa1, Remo Castro Russo2, Cintia Aparecida de Jesus Pereira3, Edenil Costa Aguilar4, Cristiana Couto Garcia5, Emília Souza Araújo6, Jailza Lima Rodrigues Oliveira7, Vanessa Fernandes Rodrigues8, Vinícius Gustavo de Oliveira9, Jacqueline Isaura Alvarez-Leite10, Fernão Castro Braga11, Pierre Kamtchouing12, Deborah Aparecida Negrão-Corrêa13, Mauro Martins Teixeira14. 1. Laboratory of Animal Physiology, Department of Animal Biology and Physiology, Faculty of Science, University of Yaoundé I, P.O. Box 812, Yaoundé, Cameroon; Laboratory of Immunopharmacology, Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil; Laboratory of Schistosomiasis, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil; Laboratory of Arterosclerosis and Nutritional Biochemistry, Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil. Electronic address: mjatsa@yahoo.fr. 2. Laboratory of Immunopharmacology, Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil; Laboratory of Pulmonary Immunology and Mechanics, Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil. Electronic address: russorc@gmail.com. 3. Laboratory of Schistosomiasis, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil. Electronic address: monjoloci@yahoo.com. 4. Laboratory of Arterosclerosis and Nutritional Biochemistry, Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil. Electronic address: edenilcostaaguilar@yahoo.com.br. 5. Laboratory of Immunopharmacology, Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil. Electronic address: criscoutog@yahoo.com.br. 6. Laboratory of Schistosomiasis, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil. Electronic address: emilhotas@yahoo.com.br. 7. Laboratory of Schistosomiasis, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil. Electronic address: jailzalima@yahoo.com.br. 8. Laboratory of Schistosomiasis, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil. Electronic address: rfvannessa@gmail.com. 9. Laboratory of Schistosomiasis, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil. Electronic address: vgo1990@gmail.com. 10. Laboratory of Arterosclerosis and Nutritional Biochemistry, Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil. Electronic address: jalvarezleite@gmail.com. 11. Laboratory of Phytochemistry, Department of Pharmaceutical Products, Faculty of Pharmacy, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil. Electronic address: fernao@netuno.lcc.ufmg.br. 12. Laboratory of Animal Physiology, Department of Animal Biology and Physiology, Faculty of Science, University of Yaoundé I, P.O. Box 812, Yaoundé, Cameroon. Electronic address: pikam55@yahoo.fr. 13. Laboratory of Schistosomiasis, Department of Parasitology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil. Electronic address: denegrao@icb.ufmg.br. 14. Laboratory of Immunopharmacology, Department of Biochemistry and Immunology, Institute of Biological Sciences, Federal University of Minas Gerais, Av. Antônio Carlos 2267, Belo Horizonte, Brazil. Electronic address: mmtex@icb.ufmg.br.
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE: Sida pilosa Retz (Malvaceae) is a plant used in Africa for the treatment of intestinal helminthiasis, lower abdominal pains and dysmenorrhea. AIM OF THE STUDY: In order to determine the potential use of S. pilosa in the treatment of schistosomiasis mansoni, we evaluated the schistosomicidal, antioxidant and anti-fibrotic properties of the aqueous extract and the n-butanol fraction of its aerial parts. MATERIAL AND METHODS: S. pilosa aqueous extract (SpAE) at 100, 200 and 400mg/kg and n-butanol fraction (SpBF) at 50, 100 and 200mg/kg were administered per os to Schistosoma mansoni-infected mice for 4 weeks. Praziquantel (100mg/kg × 5 days) was used as reference drug. After sacrifice, worm burden and egg count, transaminases and proteins levels were evaluated. Malondialdehyde (MDA), lipid hydroperoxydes (LOOH), catalase (CAT), superoxide dismutase (SOD), eosinophil peroxidase (EPO) and myeloperoxidase (MPO) were also measured. The anti-fibrotic effect of the plant was evaluated by the determination of hydroxyproline and γ-interferon (IFN-γ). RESULTS: The treatment of S. mansoni-infected mice by SpAE or SpBF resulted in a moderate reduction of worm burden and egg load in the liver and intestine. Both SpAE and SpBF significantly reversed the increasing liver proteins, MDA, LOOH and CAT levels induced by the infection. Moreover, SOD activity was improved by SpAE and SpBF. Schistosomiasis mansoni considerably increased the EPO (p<0.001) and MPO activities (p<0.001). SpAE treatment significantly reduced EPO and MPO activities at all doses. SpBF failed to reduce the increasing MPO and decreased EPO only at the highest dose. S. mansoni-infection induced an increase in hydroxyproline content (p<0.001) and a decrease in IFN-γ level (p<0.001). Both SpAE and SpBF significantly reduced hepatic hydroxyproline content, while only SpAE (p<0.05) improved IFN-γ level. CONCLUSION: These results suggest that the liver pathology in schistosomiasis mansoni is improved by S. pilosa aqueous extract, which disclosed a moderate schistosomicidal, but strong antioxidant and anti-fibrotic activities. The n-butanol fraction was however less active than the aqueous extract.
ETHNOPHARMACOLOGICAL RELEVANCE: Sida pilosa Retz (Malvaceae) is a plant used in Africa for the treatment of intestinal helminthiasis, lower abdominal pains and dysmenorrhea. AIM OF THE STUDY: In order to determine the potential use of S. pilosa in the treatment of schistosomiasis mansoni, we evaluated the schistosomicidal, antioxidant and anti-fibrotic properties of the aqueous extract and the n-butanol fraction of its aerial parts. MATERIAL AND METHODS:S. pilosa aqueous extract (SpAE) at 100, 200 and 400mg/kg and n-butanol fraction (SpBF) at 50, 100 and 200mg/kg were administered per os to Schistosoma mansoni-infectedmice for 4 weeks. Praziquantel (100mg/kg × 5 days) was used as reference drug. After sacrifice, worm burden and egg count, transaminases and proteins levels were evaluated. Malondialdehyde (MDA), lipid hydroperoxydes (LOOH), catalase (CAT), superoxide dismutase (SOD), eosinophil peroxidase (EPO) and myeloperoxidase (MPO) were also measured. The anti-fibrotic effect of the plant was evaluated by the determination of hydroxyproline and γ-interferon (IFN-γ). RESULTS: The treatment of S. mansoni-infectedmice by SpAE or SpBF resulted in a moderate reduction of worm burden and egg load in the liver and intestine. Both SpAE and SpBF significantly reversed the increasing liver proteins, MDA, LOOH and CAT levels induced by the infection. Moreover, SOD activity was improved by SpAE and SpBF. Schistosomiasis mansoni considerably increased the EPO (p<0.001) and MPO activities (p<0.001). SpAE treatment significantly reduced EPO and MPO activities at all doses. SpBF failed to reduce the increasing MPO and decreased EPO only at the highest dose. S. mansoni-infection induced an increase in hydroxyproline content (p<0.001) and a decrease in IFN-γ level (p<0.001). Both SpAE and SpBF significantly reduced hepatic hydroxyproline content, while only SpAE (p<0.05) improved IFN-γ level. CONCLUSION: These results suggest that the liver pathology in schistosomiasis mansoni is improved by S. pilosa aqueous extract, which disclosed a moderate schistosomicidal, but strong antioxidant and anti-fibrotic activities. The n-butanol fraction was however less active than the aqueous extract.