The Experts below are selected from a list of 69 Experts worldwide ranked by ideXlab platform
Zhenguo Liu - One of the best experts on this subject based on the ideXlab platform.
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People’s Republic of China
2016Co-Authors: Yunpeng Cai, Xinxin Yang, Zhenguo Liu, Weien Yuan, Ruiyuan Zheng, Meiling Liao, Correspondence Zhenguo LiuAbstract:which permits unrestricted noncommercial use, provided the original work is properly cited. International Journal of Nanomedicine 2012:7 2077–2086 International Journal of Nanomedicine Controlled-release Levodopa Methyl Ester/ benserazide-loaded nanoparticles ameliorate Levodopa-induced dyskinesia in rat
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controlled release Levodopa Methyl Ester benserazide loaded nanoparticles ameliorate Levodopa induced dyskinesia in rats
International Journal of Nanomedicine, 2012Co-Authors: Xinxin Yang, Yunpeng Cai, Weien Yuan, Ruiyuan Zheng, Meiling Liao, Zhenguo LiuAbstract:Background Levodopa remains the most effective drug in the treatment of Parkinson's disease. However, long-term administration of Levodopa induces motor complications, such as Levodopa-induced dyskinesia. The mechanisms underlying Levodopa-induced dyskinesia are not fully understood. Methods In this study, we prepared Levodopa Methyl Ester (LDME)/benserazide-loaded nanoparticles, which can release LDME and benserazide in a sustained manner. Dyskinesia was induced in rats by repeated administration of Levodopa then treated with LDME plus benserazide or the same dose of LDME/benserazide-loaded nanoparticles. Apomorphine- induced rotations and abnormal involuntary movements (AIMs) were measured on treatment days 1, 5, 10, 15, and 20. In addition, the levels of phosphorylated dopamine- and cyclic adenosine monophosphate- regulated phosphoprotein of 32 kDa, extracellular signal-regulated kinases 1/2, and ΔfosB were determined by WEstern blot. Tau levels were determined by WEstern blot and immunohistochemistry. Dynorphin levels in the striatum and cortex of rats were measured using enzyme-linked immunosorbent assay. Results Over the course of Levodopa treatment, the rats developed abnormal AIMs, classified as locomotive, axial, orolingual, and forelimb dyskinesia. The degree of reduction of apomorphine-induced rotations was comparable in dyskinetic rats treated with LDME plus benserazide or LDME/benserazide-loaded nanoparticles. The axial, limb, and orolingual (ALO) AIMs of dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 14 ± 2.5, 9 ± 2.0, and 10 ± 2.1 on treatment days 10, 15, and 20, respectively, which were significantly reduced compared with dyskinetic rats treated with LDME plus benserazide (25 ± 3.7, 27 ± 3.8, and 25 ± 3.5, respectively). The locomotive AIMs of dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 2.3 ± 0.42, 1.7 ± 0.35, and 1.6 ± 0.37 on treatment days 10, 15, and 20, respectively, which were also reduced compared with dyskinetic rats treated with LDME plus benserazide (4.4 ± 0.85, 4.7 ± 0.95 and 4.8 ± 0.37, respectively). WEstern blot showed that the levels of phosphorylated dopamine- and cyclic adenosine monophosphate-regulated phosphoprotein of 32 kDa, extracellular signal-regulated kinases 1/2, tau, and ΔfosB in dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 134.6 ± 14.1, 174.9 ± 15.1, 134.2 ± 19.3, and 320.5 ± 32.8, respectively, which were significantly reduced compared with those of dyskinetic rats treated with LDME plus benserazide (210.3 ± 19.7, 320.8 ± 21.9, 340.4 ± 27.1, and 620.7 ± 48.3, respectively). Immunohistochemistry indicated that the level of phosphorylated tau was (7.2 ± 1.1) × 10(4) in dyskinetic rats treated with LDME/benserazide-loaded nanoparticles. However, the tau level was only (14.6 ± 2.3) × 10(4) in LDME plus benserazide-treated dyskinetic rats. There was a significant difference between the two groups. Enzyme-linked immunosorbent assay showed that dynorphin levels in the striatum and cortex of dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 5.7 ± 1.2 and 4.8 ± 0.87, respectively, which were significantly reduced compared with LDME plus benserazide-treated dyskinetic rats (13.3 ± 2.1 and 8.1 ± 1.1 for the striatum and cortex, respectively). Conclusion Results suggest that LDME/benserazide-loaded nanoparticles can be used to reduce the expression of dyskinesia in dyskinetic rats.
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sustained release formulation of Levodopa Methyl Ester benserazide for prolonged suppressing dyskinesia expression in 6 ohda leisoned rats
Neuroscience Letters, 2011Co-Authors: Tiantian Ren, Xinxin Yang, Yunpeng Cai, Zhenguo Liu, Weien YuanAbstract:Abstract Although Levodopa remains the most effective drug in the treatment of Parkinson's disease (PD), chronic administration of Levodopa in the treatment of PD usually caused Levodopa-induced dyskinesia (LID), the pathogenesis of which is poorly understood. It has been demonstrated that continuous dopamine stimulation reduces the expression of LID in PD. In the present study, Levodopa Methyl Ester (LDME) and benserazide were microencapsulated into poly (lactide-co-glycolide) (PLGA) microspheres and then administrated to PD model of rats, which were induced by 6-hydroxydopamine injections. We found that both LDME/benserazide-loaded microspheres achieved sustained-release without burst release during the first day. LDME and benserazide had the same release slope from the second day on in vivo though benserazide released faster than LDME during the whole process. In our pharmacodynamic study, LDME/benserazide-loaded microspheres decreased apomorphine-induced turns and improved stepping of the lesioned forepaw in PD rats. Moreover, wEstern blot analysis showed that the levels of ΔfosB, phosphorylated dopamine, cAMP-regulated phosphoprotein of 32 kDa at threonine 34 and extracellular signal-regulated kinases 1 and 2 were decreased by LDME/benserazide-loaded microspheres in PD rats. These data showed that LDME/benserazide-loaded microspheres could be used to treat PD motor symptoms and ameliorate the expression of LID in this rat model of PD.
Weien Yuan - One of the best experts on this subject based on the ideXlab platform.
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People’s Republic of China
2016Co-Authors: Yunpeng Cai, Xinxin Yang, Zhenguo Liu, Weien Yuan, Ruiyuan Zheng, Meiling Liao, Correspondence Zhenguo LiuAbstract:which permits unrestricted noncommercial use, provided the original work is properly cited. International Journal of Nanomedicine 2012:7 2077–2086 International Journal of Nanomedicine Controlled-release Levodopa Methyl Ester/ benserazide-loaded nanoparticles ameliorate Levodopa-induced dyskinesia in rat
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controlled release Levodopa Methyl Ester benserazide loaded nanoparticles ameliorate Levodopa induced dyskinesia in rats
International Journal of Nanomedicine, 2012Co-Authors: Xinxin Yang, Yunpeng Cai, Weien Yuan, Ruiyuan Zheng, Meiling Liao, Zhenguo LiuAbstract:Background Levodopa remains the most effective drug in the treatment of Parkinson's disease. However, long-term administration of Levodopa induces motor complications, such as Levodopa-induced dyskinesia. The mechanisms underlying Levodopa-induced dyskinesia are not fully understood. Methods In this study, we prepared Levodopa Methyl Ester (LDME)/benserazide-loaded nanoparticles, which can release LDME and benserazide in a sustained manner. Dyskinesia was induced in rats by repeated administration of Levodopa then treated with LDME plus benserazide or the same dose of LDME/benserazide-loaded nanoparticles. Apomorphine- induced rotations and abnormal involuntary movements (AIMs) were measured on treatment days 1, 5, 10, 15, and 20. In addition, the levels of phosphorylated dopamine- and cyclic adenosine monophosphate- regulated phosphoprotein of 32 kDa, extracellular signal-regulated kinases 1/2, and ΔfosB were determined by WEstern blot. Tau levels were determined by WEstern blot and immunohistochemistry. Dynorphin levels in the striatum and cortex of rats were measured using enzyme-linked immunosorbent assay. Results Over the course of Levodopa treatment, the rats developed abnormal AIMs, classified as locomotive, axial, orolingual, and forelimb dyskinesia. The degree of reduction of apomorphine-induced rotations was comparable in dyskinetic rats treated with LDME plus benserazide or LDME/benserazide-loaded nanoparticles. The axial, limb, and orolingual (ALO) AIMs of dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 14 ± 2.5, 9 ± 2.0, and 10 ± 2.1 on treatment days 10, 15, and 20, respectively, which were significantly reduced compared with dyskinetic rats treated with LDME plus benserazide (25 ± 3.7, 27 ± 3.8, and 25 ± 3.5, respectively). The locomotive AIMs of dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 2.3 ± 0.42, 1.7 ± 0.35, and 1.6 ± 0.37 on treatment days 10, 15, and 20, respectively, which were also reduced compared with dyskinetic rats treated with LDME plus benserazide (4.4 ± 0.85, 4.7 ± 0.95 and 4.8 ± 0.37, respectively). WEstern blot showed that the levels of phosphorylated dopamine- and cyclic adenosine monophosphate-regulated phosphoprotein of 32 kDa, extracellular signal-regulated kinases 1/2, tau, and ΔfosB in dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 134.6 ± 14.1, 174.9 ± 15.1, 134.2 ± 19.3, and 320.5 ± 32.8, respectively, which were significantly reduced compared with those of dyskinetic rats treated with LDME plus benserazide (210.3 ± 19.7, 320.8 ± 21.9, 340.4 ± 27.1, and 620.7 ± 48.3, respectively). Immunohistochemistry indicated that the level of phosphorylated tau was (7.2 ± 1.1) × 10(4) in dyskinetic rats treated with LDME/benserazide-loaded nanoparticles. However, the tau level was only (14.6 ± 2.3) × 10(4) in LDME plus benserazide-treated dyskinetic rats. There was a significant difference between the two groups. Enzyme-linked immunosorbent assay showed that dynorphin levels in the striatum and cortex of dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 5.7 ± 1.2 and 4.8 ± 0.87, respectively, which were significantly reduced compared with LDME plus benserazide-treated dyskinetic rats (13.3 ± 2.1 and 8.1 ± 1.1 for the striatum and cortex, respectively). Conclusion Results suggest that LDME/benserazide-loaded nanoparticles can be used to reduce the expression of dyskinesia in dyskinetic rats.
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sustained release formulation of Levodopa Methyl Ester benserazide for prolonged suppressing dyskinesia expression in 6 ohda leisoned rats
Neuroscience Letters, 2011Co-Authors: Tiantian Ren, Xinxin Yang, Yunpeng Cai, Zhenguo Liu, Weien YuanAbstract:Abstract Although Levodopa remains the most effective drug in the treatment of Parkinson's disease (PD), chronic administration of Levodopa in the treatment of PD usually caused Levodopa-induced dyskinesia (LID), the pathogenesis of which is poorly understood. It has been demonstrated that continuous dopamine stimulation reduces the expression of LID in PD. In the present study, Levodopa Methyl Ester (LDME) and benserazide were microencapsulated into poly (lactide-co-glycolide) (PLGA) microspheres and then administrated to PD model of rats, which were induced by 6-hydroxydopamine injections. We found that both LDME/benserazide-loaded microspheres achieved sustained-release without burst release during the first day. LDME and benserazide had the same release slope from the second day on in vivo though benserazide released faster than LDME during the whole process. In our pharmacodynamic study, LDME/benserazide-loaded microspheres decreased apomorphine-induced turns and improved stepping of the lesioned forepaw in PD rats. Moreover, wEstern blot analysis showed that the levels of ΔfosB, phosphorylated dopamine, cAMP-regulated phosphoprotein of 32 kDa at threonine 34 and extracellular signal-regulated kinases 1 and 2 were decreased by LDME/benserazide-loaded microspheres in PD rats. These data showed that LDME/benserazide-loaded microspheres could be used to treat PD motor symptoms and ameliorate the expression of LID in this rat model of PD.
Xinxin Yang - One of the best experts on this subject based on the ideXlab platform.
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People’s Republic of China
2016Co-Authors: Yunpeng Cai, Xinxin Yang, Zhenguo Liu, Weien Yuan, Ruiyuan Zheng, Meiling Liao, Correspondence Zhenguo LiuAbstract:which permits unrestricted noncommercial use, provided the original work is properly cited. International Journal of Nanomedicine 2012:7 2077–2086 International Journal of Nanomedicine Controlled-release Levodopa Methyl Ester/ benserazide-loaded nanoparticles ameliorate Levodopa-induced dyskinesia in rat
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controlled release Levodopa Methyl Ester benserazide loaded nanoparticles ameliorate Levodopa induced dyskinesia in rats
International Journal of Nanomedicine, 2012Co-Authors: Xinxin Yang, Yunpeng Cai, Weien Yuan, Ruiyuan Zheng, Meiling Liao, Zhenguo LiuAbstract:Background Levodopa remains the most effective drug in the treatment of Parkinson's disease. However, long-term administration of Levodopa induces motor complications, such as Levodopa-induced dyskinesia. The mechanisms underlying Levodopa-induced dyskinesia are not fully understood. Methods In this study, we prepared Levodopa Methyl Ester (LDME)/benserazide-loaded nanoparticles, which can release LDME and benserazide in a sustained manner. Dyskinesia was induced in rats by repeated administration of Levodopa then treated with LDME plus benserazide or the same dose of LDME/benserazide-loaded nanoparticles. Apomorphine- induced rotations and abnormal involuntary movements (AIMs) were measured on treatment days 1, 5, 10, 15, and 20. In addition, the levels of phosphorylated dopamine- and cyclic adenosine monophosphate- regulated phosphoprotein of 32 kDa, extracellular signal-regulated kinases 1/2, and ΔfosB were determined by WEstern blot. Tau levels were determined by WEstern blot and immunohistochemistry. Dynorphin levels in the striatum and cortex of rats were measured using enzyme-linked immunosorbent assay. Results Over the course of Levodopa treatment, the rats developed abnormal AIMs, classified as locomotive, axial, orolingual, and forelimb dyskinesia. The degree of reduction of apomorphine-induced rotations was comparable in dyskinetic rats treated with LDME plus benserazide or LDME/benserazide-loaded nanoparticles. The axial, limb, and orolingual (ALO) AIMs of dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 14 ± 2.5, 9 ± 2.0, and 10 ± 2.1 on treatment days 10, 15, and 20, respectively, which were significantly reduced compared with dyskinetic rats treated with LDME plus benserazide (25 ± 3.7, 27 ± 3.8, and 25 ± 3.5, respectively). The locomotive AIMs of dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 2.3 ± 0.42, 1.7 ± 0.35, and 1.6 ± 0.37 on treatment days 10, 15, and 20, respectively, which were also reduced compared with dyskinetic rats treated with LDME plus benserazide (4.4 ± 0.85, 4.7 ± 0.95 and 4.8 ± 0.37, respectively). WEstern blot showed that the levels of phosphorylated dopamine- and cyclic adenosine monophosphate-regulated phosphoprotein of 32 kDa, extracellular signal-regulated kinases 1/2, tau, and ΔfosB in dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 134.6 ± 14.1, 174.9 ± 15.1, 134.2 ± 19.3, and 320.5 ± 32.8, respectively, which were significantly reduced compared with those of dyskinetic rats treated with LDME plus benserazide (210.3 ± 19.7, 320.8 ± 21.9, 340.4 ± 27.1, and 620.7 ± 48.3, respectively). Immunohistochemistry indicated that the level of phosphorylated tau was (7.2 ± 1.1) × 10(4) in dyskinetic rats treated with LDME/benserazide-loaded nanoparticles. However, the tau level was only (14.6 ± 2.3) × 10(4) in LDME plus benserazide-treated dyskinetic rats. There was a significant difference between the two groups. Enzyme-linked immunosorbent assay showed that dynorphin levels in the striatum and cortex of dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 5.7 ± 1.2 and 4.8 ± 0.87, respectively, which were significantly reduced compared with LDME plus benserazide-treated dyskinetic rats (13.3 ± 2.1 and 8.1 ± 1.1 for the striatum and cortex, respectively). Conclusion Results suggest that LDME/benserazide-loaded nanoparticles can be used to reduce the expression of dyskinesia in dyskinetic rats.
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sustained release formulation of Levodopa Methyl Ester benserazide for prolonged suppressing dyskinesia expression in 6 ohda leisoned rats
Neuroscience Letters, 2011Co-Authors: Tiantian Ren, Xinxin Yang, Yunpeng Cai, Zhenguo Liu, Weien YuanAbstract:Abstract Although Levodopa remains the most effective drug in the treatment of Parkinson's disease (PD), chronic administration of Levodopa in the treatment of PD usually caused Levodopa-induced dyskinesia (LID), the pathogenesis of which is poorly understood. It has been demonstrated that continuous dopamine stimulation reduces the expression of LID in PD. In the present study, Levodopa Methyl Ester (LDME) and benserazide were microencapsulated into poly (lactide-co-glycolide) (PLGA) microspheres and then administrated to PD model of rats, which were induced by 6-hydroxydopamine injections. We found that both LDME/benserazide-loaded microspheres achieved sustained-release without burst release during the first day. LDME and benserazide had the same release slope from the second day on in vivo though benserazide released faster than LDME during the whole process. In our pharmacodynamic study, LDME/benserazide-loaded microspheres decreased apomorphine-induced turns and improved stepping of the lesioned forepaw in PD rats. Moreover, wEstern blot analysis showed that the levels of ΔfosB, phosphorylated dopamine, cAMP-regulated phosphoprotein of 32 kDa at threonine 34 and extracellular signal-regulated kinases 1 and 2 were decreased by LDME/benserazide-loaded microspheres in PD rats. These data showed that LDME/benserazide-loaded microspheres could be used to treat PD motor symptoms and ameliorate the expression of LID in this rat model of PD.
Yunpeng Cai - One of the best experts on this subject based on the ideXlab platform.
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People’s Republic of China
2016Co-Authors: Yunpeng Cai, Xinxin Yang, Zhenguo Liu, Weien Yuan, Ruiyuan Zheng, Meiling Liao, Correspondence Zhenguo LiuAbstract:which permits unrestricted noncommercial use, provided the original work is properly cited. International Journal of Nanomedicine 2012:7 2077–2086 International Journal of Nanomedicine Controlled-release Levodopa Methyl Ester/ benserazide-loaded nanoparticles ameliorate Levodopa-induced dyskinesia in rat
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controlled release Levodopa Methyl Ester benserazide loaded nanoparticles ameliorate Levodopa induced dyskinesia in rats
International Journal of Nanomedicine, 2012Co-Authors: Xinxin Yang, Yunpeng Cai, Weien Yuan, Ruiyuan Zheng, Meiling Liao, Zhenguo LiuAbstract:Background Levodopa remains the most effective drug in the treatment of Parkinson's disease. However, long-term administration of Levodopa induces motor complications, such as Levodopa-induced dyskinesia. The mechanisms underlying Levodopa-induced dyskinesia are not fully understood. Methods In this study, we prepared Levodopa Methyl Ester (LDME)/benserazide-loaded nanoparticles, which can release LDME and benserazide in a sustained manner. Dyskinesia was induced in rats by repeated administration of Levodopa then treated with LDME plus benserazide or the same dose of LDME/benserazide-loaded nanoparticles. Apomorphine- induced rotations and abnormal involuntary movements (AIMs) were measured on treatment days 1, 5, 10, 15, and 20. In addition, the levels of phosphorylated dopamine- and cyclic adenosine monophosphate- regulated phosphoprotein of 32 kDa, extracellular signal-regulated kinases 1/2, and ΔfosB were determined by WEstern blot. Tau levels were determined by WEstern blot and immunohistochemistry. Dynorphin levels in the striatum and cortex of rats were measured using enzyme-linked immunosorbent assay. Results Over the course of Levodopa treatment, the rats developed abnormal AIMs, classified as locomotive, axial, orolingual, and forelimb dyskinesia. The degree of reduction of apomorphine-induced rotations was comparable in dyskinetic rats treated with LDME plus benserazide or LDME/benserazide-loaded nanoparticles. The axial, limb, and orolingual (ALO) AIMs of dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 14 ± 2.5, 9 ± 2.0, and 10 ± 2.1 on treatment days 10, 15, and 20, respectively, which were significantly reduced compared with dyskinetic rats treated with LDME plus benserazide (25 ± 3.7, 27 ± 3.8, and 25 ± 3.5, respectively). The locomotive AIMs of dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 2.3 ± 0.42, 1.7 ± 0.35, and 1.6 ± 0.37 on treatment days 10, 15, and 20, respectively, which were also reduced compared with dyskinetic rats treated with LDME plus benserazide (4.4 ± 0.85, 4.7 ± 0.95 and 4.8 ± 0.37, respectively). WEstern blot showed that the levels of phosphorylated dopamine- and cyclic adenosine monophosphate-regulated phosphoprotein of 32 kDa, extracellular signal-regulated kinases 1/2, tau, and ΔfosB in dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 134.6 ± 14.1, 174.9 ± 15.1, 134.2 ± 19.3, and 320.5 ± 32.8, respectively, which were significantly reduced compared with those of dyskinetic rats treated with LDME plus benserazide (210.3 ± 19.7, 320.8 ± 21.9, 340.4 ± 27.1, and 620.7 ± 48.3, respectively). Immunohistochemistry indicated that the level of phosphorylated tau was (7.2 ± 1.1) × 10(4) in dyskinetic rats treated with LDME/benserazide-loaded nanoparticles. However, the tau level was only (14.6 ± 2.3) × 10(4) in LDME plus benserazide-treated dyskinetic rats. There was a significant difference between the two groups. Enzyme-linked immunosorbent assay showed that dynorphin levels in the striatum and cortex of dyskinetic rats treated with LDME/benserazide-loaded nanoparticles were 5.7 ± 1.2 and 4.8 ± 0.87, respectively, which were significantly reduced compared with LDME plus benserazide-treated dyskinetic rats (13.3 ± 2.1 and 8.1 ± 1.1 for the striatum and cortex, respectively). Conclusion Results suggest that LDME/benserazide-loaded nanoparticles can be used to reduce the expression of dyskinesia in dyskinetic rats.
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sustained release formulation of Levodopa Methyl Ester benserazide for prolonged suppressing dyskinesia expression in 6 ohda leisoned rats
Neuroscience Letters, 2011Co-Authors: Tiantian Ren, Xinxin Yang, Yunpeng Cai, Zhenguo Liu, Weien YuanAbstract:Abstract Although Levodopa remains the most effective drug in the treatment of Parkinson's disease (PD), chronic administration of Levodopa in the treatment of PD usually caused Levodopa-induced dyskinesia (LID), the pathogenesis of which is poorly understood. It has been demonstrated that continuous dopamine stimulation reduces the expression of LID in PD. In the present study, Levodopa Methyl Ester (LDME) and benserazide were microencapsulated into poly (lactide-co-glycolide) (PLGA) microspheres and then administrated to PD model of rats, which were induced by 6-hydroxydopamine injections. We found that both LDME/benserazide-loaded microspheres achieved sustained-release without burst release during the first day. LDME and benserazide had the same release slope from the second day on in vivo though benserazide released faster than LDME during the whole process. In our pharmacodynamic study, LDME/benserazide-loaded microspheres decreased apomorphine-induced turns and improved stepping of the lesioned forepaw in PD rats. Moreover, wEstern blot analysis showed that the levels of ΔfosB, phosphorylated dopamine, cAMP-regulated phosphoprotein of 32 kDa at threonine 34 and extracellular signal-regulated kinases 1 and 2 were decreased by LDME/benserazide-loaded microspheres in PD rats. These data showed that LDME/benserazide-loaded microspheres could be used to treat PD motor symptoms and ameliorate the expression of LID in this rat model of PD.
Fabrizio Stocchi - One of the best experts on this subject based on the ideXlab platform.
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Fluctuating parkinsonism: a pilot study of single afternoon dose of Levodopa Methyl Ester
Journal of Neurology, 1996Co-Authors: Fabrizio Stocchi, Luca Barbato, Lucia Bramante, Giampietro Nordera, Laura Vacca, Stefano RuggieriAbstract:Thirty-four patients with idiopathic fluctuating Parkinson's disease and early afternoon “delayed on” or severely resistant “off” periods, in spite of long-term antiparkinsonian therapy, were studied. The first afternoon Levodopa administration was substituted with an equimolar dosage of the liquid formulation Levodopa Methyl Ester (LDME). The major end-points for efficacy were latency to “on” and duration of “on” periods. The patients were divided into five subgroups according to their baseline treatment and they were evaluated monthly for 6 months using the Unified Parkinson's Disease Rating Scale. The patients completed weekly self-evaluation using an “on-off” chart. LDME was well tolerated by all the patients. A statistically significant reduction in latency to “on” was observed in all patients. The clinical effect of LDME remained stable during the treatment period (repeat measures ANOVA). The more rapid clinical effect of LDME and its stable and predictable antiparkinsonian activity represents a new and useful approach for treating patients with complicated Parkinson's disease.
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the clinical efficacy of a single afternoon dose of Levodopa Methyl Ester a double blind cross over study versus placebo
Functional Neurology, 1994Co-Authors: Fabrizio Stocchi, Luca Barbato, L Bramante, A Bonamartini, S RuggieriAbstract:Levodopa Methyl Ester (LDME) is a highly water soluble derivative produced by Esterification of the carboxilic acid moiety of the L-Dopa molecule that is rapidly hydrolyzed to L-Dopa and can be administered orally in an easily dosable liquid form. In this study the relative efficacy and tolerability of a single dose of an oral solution of 250 mg of LDME was compared to that of placebo in reversing afternoon off period. A controlled double-blind cross-over study versus placebo had previously been carried out in 25 idiopathic parkinsonian patients with predictable fluctuations in motor performances. The study design stipulated the sequential administration of LDME and placebo in group A and placebo and LDME in group B on two consecutive days. All patients turned "on" with LDME and none with placebo solution. The mean latency to "on" was 25.3 +/- 13.5 min for the A group and 27.6 +/- 3.9 min for group B (Fig. 2) and the "on" duration was 147.7 +/- 50.3 min and 163.3 +/- 39.3 min for the A and B groups respectively. Five patients suffering from drug resistant "off" phenomena turned "on" with LDME solution showing a mean latency to "on" of 31.4 +/- 6.2 min.
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the clinical efficacy of single morning doses of Levodopa Methyl Ester dispersible madopar and sinemet plus in parkinson disease
Clinical Neuropharmacology, 1992Co-Authors: M J Steiger, Fabrizio Stocchi, S Ruggieri, L Bramante, Niall QuinnAbstract:For many patients with Parkinson disease and Levodopa-related motor fluctuations, the latency to onset of action of a single dose of a Levodopa preparation may be both long and variable, In an effort to find a more rapidly acting and reliable preparation of Levodopa, we therefore studied the efficacy of single doses of an oral solution of 250 mg of Levodopa Methyl Ester (ME) with benserazide, 50 mg and of a molar equivalent dose of dispersible Madopar (DM) (50/200) in 13 patients in the fasting state after overnight drug withdrawal. The response of seven of these patients was compared to that after two Sinemet 25/100. The latency to "on" was equally fast with ME and DM, and significantly faster than after standard Sinemet. The duration of "on" was similar with all three. Because of this more rapid relief of "off" periods, both ME and DM offer a potential clinical advantage over standard preparations of Levodopa.
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the clinical efficacy of oral Levodopa Methyl Ester solution in reversing afternoon off periods in parkinson s disease
Clinical Neuropharmacology, 1991Co-Authors: M J Steiger, Fabrizio Stocchi, A Carta, S Ruggieri, A Agnoli, Niall Quinn, C D MarsdenAbstract:We compared the efficacy of a single dose of an oral solution of Levodopa Methyl Ester (ME) to that of standard Levodopa, in the form of a single dose of Madopar, in reversing afternoon "off" periods in 12 patients with Parkinson's disease (PD). The highly soluble ME solution led to a significantly more rapid reversal of "off" periods. This preparation may therefore convey a clinical advantage in patients experiencing motor fluctuations whilst taking multiple daily dosages of Levodopa, particularly in those with long or highly variable latency to the next "on" period.