The Experts below are selected from a list of 285 Experts worldwide ranked by ideXlab platform
Kartik T. Nakhate - One of the best experts on this subject based on the ideXlab platform.
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Phloridzin ameliorates type 2 diabetes‐induced depression in mice by mitigating oxidative stress and modulating brain‐derived neurotrophic factor
Journal of Diabetes & Metabolic Disorders, 2021Co-Authors: Sandesh P. Kamdi, Amit Raval, Kartik T. NakhateAbstract:Type 2 diabetes (T2D) is linked with depression due to insulin resistance, oxidative stress and disruption of neurotrophic factors. We evaluated potential benefits of Phloridzin in ameliorating depressive symptoms in T2D. Adult male Swiss-albino mice (25–30 g) on high-fat-diet (HFD) for 2 weeks were administered with streptozotocin (STZ; 35 mg/kg, intraperitoneal) to induce T2D. Seven days after STZ administration, diabetic mice on HFD were distributed into different groups. Animals were subjected daily to oral treatment of saline (0.25 ml), fluoxetine (10-20 mg/kg) or Phloridzin (10-20 mg/kg) for a period of 4 weeks. One hour after last dose, the immobility time of animals was evaluated in forced swim test (FST) and tail suspension test (TST). To further confirm the mechanisms involved in antidepressant effect of Phloridzin, biochemical parameters like brain derived neurotropic factor (BDNF), glutathione (GSH), extracellular signal-regulated kinase (ERK), tyrosine receptor kinase B (TrkB) and cAMP-response element binding protein (CREB) were estimated in the brain. Animals with T2D showed a significant increase in immobility as compared to control in FST and TST. However, 4 weeks administration of fluoxetine or Phloridzin attenuated this effect. A significant decline in GSH, BDNF, TrkB, CREB and ERK levels were noticed in the brain of mice with T2D. These changes were also attenuated by administration of Phloridzin. Phloridzin may ameliorates T2D-induced depression by mitigating the oxidative stress, and up-regulation of neurotrophins in the brain. Therefore, Phloridzin can be used as a therapeutic intervention for the management of depression co-morbid with T2D.
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Phloridzin ameliorates type 2 diabetes induced depression in mice by mitigating oxidative stress and modulating brain derived neurotrophic factor
Journal of diabetes and metabolic disorders, 2021Co-Authors: Sandesh P. Kamdi, Amit Raval, Kartik T. NakhateAbstract:Type 2 diabetes (T2D) is linked with depression due to insulin resistance, oxidative stress and disruption of neurotrophic factors. We evaluated potential benefits of Phloridzin in ameliorating depressive symptoms in T2D. Adult male Swiss-albino mice (25–30 g) on high-fat-diet (HFD) for 2 weeks were administered with streptozotocin (STZ; 35 mg/kg, intraperitoneal) to induce T2D. Seven days after STZ administration, diabetic mice on HFD were distributed into different groups. Animals were subjected daily to oral treatment of saline (0.25 ml), fluoxetine (10-20 mg/kg) or Phloridzin (10-20 mg/kg) for a period of 4 weeks. One hour after last dose, the immobility time of animals was evaluated in forced swim test (FST) and tail suspension test (TST). To further confirm the mechanisms involved in antidepressant effect of Phloridzin, biochemical parameters like brain derived neurotropic factor (BDNF), glutathione (GSH), extracellular signal-regulated kinase (ERK), tyrosine receptor kinase B (TrkB) and cAMP-response element binding protein (CREB) were estimated in the brain. Animals with T2D showed a significant increase in immobility as compared to control in FST and TST. However, 4 weeks administration of fluoxetine or Phloridzin attenuated this effect. A significant decline in GSH, BDNF, TrkB, CREB and ERK levels were noticed in the brain of mice with T2D. These changes were also attenuated by administration of Phloridzin. Phloridzin may ameliorates T2D-induced depression by mitigating the oxidative stress, and up-regulation of neurotrophins in the brain. Therefore, Phloridzin can be used as a therapeutic intervention for the management of depression co-morbid with T2D.
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Phloridzin ameliorates type 2 diabetes‐induced depression in mice by mitigating oxidative stress and modulating brain‐derived neurotrophic factor
Journal of Diabetes & Metabolic Disorders, 2021Co-Authors: Sandesh P. Kamdi, Amit Raval, Kartik T. NakhateAbstract:Purpose Type 2 diabetes (T2D) is linked with depression due to insulin resistance, oxidative stress and disruption of neurotrophic factors. We evaluated potential benefits of Phloridzin in ameliorating depressive symptoms in T2D. Methods Adult male Swiss-albino mice (25–30 g) on high-fat-diet (HFD) for 2 weeks were administered with streptozotocin (STZ; 35 mg/kg, intraperitoneal) to induce T2D. Seven days after STZ administration, diabetic mice on HFD were distributed into different groups. Animals were subjected daily to oral treatment of saline (0.25 ml), fluoxetine (10-20 mg/kg) or Phloridzin (10-20 mg/kg) for a period of 4 weeks. One hour after last dose, the immobility time of animals was evaluated in forced swim test (FST) and tail suspension test (TST). To further confirm the mechanisms involved in antidepressant effect of Phloridzin, biochemical parameters like brain derived neurotropic factor (BDNF), glutathione (GSH), extracellular signal-regulated kinase (ERK), tyrosine receptor kinase B (TrkB) and cAMP-response element binding protein (CREB) were estimated in the brain. Results Animals with T2D showed a significant increase in immobility as compared to control in FST and TST. However, 4 weeks administration of fluoxetine or Phloridzin attenuated this effect. A significant decline in GSH, BDNF, TrkB, CREB and ERK levels were noticed in the brain of mice with T2D. These changes were also attenuated by administration of Phloridzin. Conclusions Phloridzin may ameliorates T2D-induced depression by mitigating the oxidative stress, and up-regulation of neurotrophins in the brain. Therefore, Phloridzin can be used as a therapeutic intervention for the management of depression co-morbid with T2D.
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Phloridzin attenuates lipopolysaccharide-induced cognitive impairment via antioxidant, anti-inflammatory and neuromodulatory activities.
Cytokine, 2021Co-Authors: Sandesh P. Kamdi, Amit Raval, Kartik T. NakhateAbstract:Abstract Background Lipopolysaccharide (LPS) is known to produce neuroinflammation and memory impairment. Although Phloridzin (a phenolic phytoconstituent) shows antioxidant- and anti-inflammatory activities, its ameliorative potential in LPS-mediated neuroinflammation and memory dysfunction remains unexplored. Objectives To investigate the protective effect of Phloridzin against LPS-mediated memory impairment and neuroinflammation in mice. Methods Different groups of mice were treated with LPS (250 μg/kg) via intraperitoneal (ip) route to induce cognitive impairments. The animals were administered with Phloridzin (10–20 mg/kg, oral) or donepezil (1 mg/kg, intraperitoneal), and memory functions were evaluated by Morris water maze (MWM) and Y-maze. At the end of the behavioral experiments, the animals were sacrificed and different biochemical parameters like acetylcholinesterase (AChE), brain derived neurotropic factor (BDNF), tumor necrosis factor (TNF-α), interleukin-6 (IL-6), superoxide dismutase (SOD) and glutathione (GSH) concentration in the hippocampus and the cerebral cortex were estimated. Results While LPS administered animals showed significantly decreased memory retention in both MWM and Y maze, a significant reversal in all the parameters were observed following treatment with Phloridzin. LPS-treated animals showed significantly decreased level of antioxidants (SOD and GSH), neurotropic factor (BDNF) and cholinergic transmission (increased AChE) and increased levels of inflammatory/oxidative markers (TNF-α, IL-6 and MDA) in hippocampus and cortex. These changes were alleviated after the treatment with Phloridzin. Conclusions Phloridzin may have neuroprotective role against LPS-induced neuroinflammation and memory impairment by virtue of its antioxidant, anti-inflammatory, and enhanced cholinergic signalling activity in the hippocampus and cerebral cortex.
Kurt Kalcher - One of the best experts on this subject based on the ideXlab platform.
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highly selective electrochemical determination of phlorizin using square wave voltammetry at a boron doped diamond electrode
Food Analytical Methods, 2017Co-Authors: Eda Mehmeti, Dalibor M Stankovic, Astrid Ortner, Janez Zavasnik, Kurt KalcherAbstract:A boron-doped diamond electrode was used as an electrochemical sensor for the determination of phlorizin (aka Phloridzin, phlorrhizin) using square wave voltammetry (SWV). Phlorizin (Phl) exhibited a well-defined oxidation peak at +0.9 V (versus Ag/AgCl electrode 3 M KCl) in solutions with a pH value of 6.0. Parameters such as pH value and scan rate were optimized for cyclic voltammetry as well as amplitude and frequency for SWV. The sensor gave excellent response with a wide linear dynamic range for concentrations of phlorizin from 3 to 100 μM with a detection limit of 0.23 μM and a good repeatability (± 0.9%, n = 7 measurements, c = 10 μM). The effect of interferences by most common compounds was tested, and the method was successfully applied to the determination of the title compound in apple root extracts and urine samples with satisfactory recovery.
Sandesh P. Kamdi - One of the best experts on this subject based on the ideXlab platform.
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Phloridzin ameliorates type 2 diabetes‐induced depression in mice by mitigating oxidative stress and modulating brain‐derived neurotrophic factor
Journal of Diabetes & Metabolic Disorders, 2021Co-Authors: Sandesh P. Kamdi, Amit Raval, Kartik T. NakhateAbstract:Type 2 diabetes (T2D) is linked with depression due to insulin resistance, oxidative stress and disruption of neurotrophic factors. We evaluated potential benefits of Phloridzin in ameliorating depressive symptoms in T2D. Adult male Swiss-albino mice (25–30 g) on high-fat-diet (HFD) for 2 weeks were administered with streptozotocin (STZ; 35 mg/kg, intraperitoneal) to induce T2D. Seven days after STZ administration, diabetic mice on HFD were distributed into different groups. Animals were subjected daily to oral treatment of saline (0.25 ml), fluoxetine (10-20 mg/kg) or Phloridzin (10-20 mg/kg) for a period of 4 weeks. One hour after last dose, the immobility time of animals was evaluated in forced swim test (FST) and tail suspension test (TST). To further confirm the mechanisms involved in antidepressant effect of Phloridzin, biochemical parameters like brain derived neurotropic factor (BDNF), glutathione (GSH), extracellular signal-regulated kinase (ERK), tyrosine receptor kinase B (TrkB) and cAMP-response element binding protein (CREB) were estimated in the brain. Animals with T2D showed a significant increase in immobility as compared to control in FST and TST. However, 4 weeks administration of fluoxetine or Phloridzin attenuated this effect. A significant decline in GSH, BDNF, TrkB, CREB and ERK levels were noticed in the brain of mice with T2D. These changes were also attenuated by administration of Phloridzin. Phloridzin may ameliorates T2D-induced depression by mitigating the oxidative stress, and up-regulation of neurotrophins in the brain. Therefore, Phloridzin can be used as a therapeutic intervention for the management of depression co-morbid with T2D.
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Phloridzin ameliorates type 2 diabetes induced depression in mice by mitigating oxidative stress and modulating brain derived neurotrophic factor
Journal of diabetes and metabolic disorders, 2021Co-Authors: Sandesh P. Kamdi, Amit Raval, Kartik T. NakhateAbstract:Type 2 diabetes (T2D) is linked with depression due to insulin resistance, oxidative stress and disruption of neurotrophic factors. We evaluated potential benefits of Phloridzin in ameliorating depressive symptoms in T2D. Adult male Swiss-albino mice (25–30 g) on high-fat-diet (HFD) for 2 weeks were administered with streptozotocin (STZ; 35 mg/kg, intraperitoneal) to induce T2D. Seven days after STZ administration, diabetic mice on HFD were distributed into different groups. Animals were subjected daily to oral treatment of saline (0.25 ml), fluoxetine (10-20 mg/kg) or Phloridzin (10-20 mg/kg) for a period of 4 weeks. One hour after last dose, the immobility time of animals was evaluated in forced swim test (FST) and tail suspension test (TST). To further confirm the mechanisms involved in antidepressant effect of Phloridzin, biochemical parameters like brain derived neurotropic factor (BDNF), glutathione (GSH), extracellular signal-regulated kinase (ERK), tyrosine receptor kinase B (TrkB) and cAMP-response element binding protein (CREB) were estimated in the brain. Animals with T2D showed a significant increase in immobility as compared to control in FST and TST. However, 4 weeks administration of fluoxetine or Phloridzin attenuated this effect. A significant decline in GSH, BDNF, TrkB, CREB and ERK levels were noticed in the brain of mice with T2D. These changes were also attenuated by administration of Phloridzin. Phloridzin may ameliorates T2D-induced depression by mitigating the oxidative stress, and up-regulation of neurotrophins in the brain. Therefore, Phloridzin can be used as a therapeutic intervention for the management of depression co-morbid with T2D.
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Phloridzin ameliorates type 2 diabetes‐induced depression in mice by mitigating oxidative stress and modulating brain‐derived neurotrophic factor
Journal of Diabetes & Metabolic Disorders, 2021Co-Authors: Sandesh P. Kamdi, Amit Raval, Kartik T. NakhateAbstract:Purpose Type 2 diabetes (T2D) is linked with depression due to insulin resistance, oxidative stress and disruption of neurotrophic factors. We evaluated potential benefits of Phloridzin in ameliorating depressive symptoms in T2D. Methods Adult male Swiss-albino mice (25–30 g) on high-fat-diet (HFD) for 2 weeks were administered with streptozotocin (STZ; 35 mg/kg, intraperitoneal) to induce T2D. Seven days after STZ administration, diabetic mice on HFD were distributed into different groups. Animals were subjected daily to oral treatment of saline (0.25 ml), fluoxetine (10-20 mg/kg) or Phloridzin (10-20 mg/kg) for a period of 4 weeks. One hour after last dose, the immobility time of animals was evaluated in forced swim test (FST) and tail suspension test (TST). To further confirm the mechanisms involved in antidepressant effect of Phloridzin, biochemical parameters like brain derived neurotropic factor (BDNF), glutathione (GSH), extracellular signal-regulated kinase (ERK), tyrosine receptor kinase B (TrkB) and cAMP-response element binding protein (CREB) were estimated in the brain. Results Animals with T2D showed a significant increase in immobility as compared to control in FST and TST. However, 4 weeks administration of fluoxetine or Phloridzin attenuated this effect. A significant decline in GSH, BDNF, TrkB, CREB and ERK levels were noticed in the brain of mice with T2D. These changes were also attenuated by administration of Phloridzin. Conclusions Phloridzin may ameliorates T2D-induced depression by mitigating the oxidative stress, and up-regulation of neurotrophins in the brain. Therefore, Phloridzin can be used as a therapeutic intervention for the management of depression co-morbid with T2D.
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Phloridzin attenuates lipopolysaccharide-induced cognitive impairment via antioxidant, anti-inflammatory and neuromodulatory activities.
Cytokine, 2021Co-Authors: Sandesh P. Kamdi, Amit Raval, Kartik T. NakhateAbstract:Abstract Background Lipopolysaccharide (LPS) is known to produce neuroinflammation and memory impairment. Although Phloridzin (a phenolic phytoconstituent) shows antioxidant- and anti-inflammatory activities, its ameliorative potential in LPS-mediated neuroinflammation and memory dysfunction remains unexplored. Objectives To investigate the protective effect of Phloridzin against LPS-mediated memory impairment and neuroinflammation in mice. Methods Different groups of mice were treated with LPS (250 μg/kg) via intraperitoneal (ip) route to induce cognitive impairments. The animals were administered with Phloridzin (10–20 mg/kg, oral) or donepezil (1 mg/kg, intraperitoneal), and memory functions were evaluated by Morris water maze (MWM) and Y-maze. At the end of the behavioral experiments, the animals were sacrificed and different biochemical parameters like acetylcholinesterase (AChE), brain derived neurotropic factor (BDNF), tumor necrosis factor (TNF-α), interleukin-6 (IL-6), superoxide dismutase (SOD) and glutathione (GSH) concentration in the hippocampus and the cerebral cortex were estimated. Results While LPS administered animals showed significantly decreased memory retention in both MWM and Y maze, a significant reversal in all the parameters were observed following treatment with Phloridzin. LPS-treated animals showed significantly decreased level of antioxidants (SOD and GSH), neurotropic factor (BDNF) and cholinergic transmission (increased AChE) and increased levels of inflammatory/oxidative markers (TNF-α, IL-6 and MDA) in hippocampus and cortex. These changes were alleviated after the treatment with Phloridzin. Conclusions Phloridzin may have neuroprotective role against LPS-induced neuroinflammation and memory impairment by virtue of its antioxidant, anti-inflammatory, and enhanced cholinergic signalling activity in the hippocampus and cerebral cortex.
Amit Raval - One of the best experts on this subject based on the ideXlab platform.
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Phloridzin ameliorates type 2 diabetes‐induced depression in mice by mitigating oxidative stress and modulating brain‐derived neurotrophic factor
Journal of Diabetes & Metabolic Disorders, 2021Co-Authors: Sandesh P. Kamdi, Amit Raval, Kartik T. NakhateAbstract:Type 2 diabetes (T2D) is linked with depression due to insulin resistance, oxidative stress and disruption of neurotrophic factors. We evaluated potential benefits of Phloridzin in ameliorating depressive symptoms in T2D. Adult male Swiss-albino mice (25–30 g) on high-fat-diet (HFD) for 2 weeks were administered with streptozotocin (STZ; 35 mg/kg, intraperitoneal) to induce T2D. Seven days after STZ administration, diabetic mice on HFD were distributed into different groups. Animals were subjected daily to oral treatment of saline (0.25 ml), fluoxetine (10-20 mg/kg) or Phloridzin (10-20 mg/kg) for a period of 4 weeks. One hour after last dose, the immobility time of animals was evaluated in forced swim test (FST) and tail suspension test (TST). To further confirm the mechanisms involved in antidepressant effect of Phloridzin, biochemical parameters like brain derived neurotropic factor (BDNF), glutathione (GSH), extracellular signal-regulated kinase (ERK), tyrosine receptor kinase B (TrkB) and cAMP-response element binding protein (CREB) were estimated in the brain. Animals with T2D showed a significant increase in immobility as compared to control in FST and TST. However, 4 weeks administration of fluoxetine or Phloridzin attenuated this effect. A significant decline in GSH, BDNF, TrkB, CREB and ERK levels were noticed in the brain of mice with T2D. These changes were also attenuated by administration of Phloridzin. Phloridzin may ameliorates T2D-induced depression by mitigating the oxidative stress, and up-regulation of neurotrophins in the brain. Therefore, Phloridzin can be used as a therapeutic intervention for the management of depression co-morbid with T2D.
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Phloridzin ameliorates type 2 diabetes induced depression in mice by mitigating oxidative stress and modulating brain derived neurotrophic factor
Journal of diabetes and metabolic disorders, 2021Co-Authors: Sandesh P. Kamdi, Amit Raval, Kartik T. NakhateAbstract:Type 2 diabetes (T2D) is linked with depression due to insulin resistance, oxidative stress and disruption of neurotrophic factors. We evaluated potential benefits of Phloridzin in ameliorating depressive symptoms in T2D. Adult male Swiss-albino mice (25–30 g) on high-fat-diet (HFD) for 2 weeks were administered with streptozotocin (STZ; 35 mg/kg, intraperitoneal) to induce T2D. Seven days after STZ administration, diabetic mice on HFD were distributed into different groups. Animals were subjected daily to oral treatment of saline (0.25 ml), fluoxetine (10-20 mg/kg) or Phloridzin (10-20 mg/kg) for a period of 4 weeks. One hour after last dose, the immobility time of animals was evaluated in forced swim test (FST) and tail suspension test (TST). To further confirm the mechanisms involved in antidepressant effect of Phloridzin, biochemical parameters like brain derived neurotropic factor (BDNF), glutathione (GSH), extracellular signal-regulated kinase (ERK), tyrosine receptor kinase B (TrkB) and cAMP-response element binding protein (CREB) were estimated in the brain. Animals with T2D showed a significant increase in immobility as compared to control in FST and TST. However, 4 weeks administration of fluoxetine or Phloridzin attenuated this effect. A significant decline in GSH, BDNF, TrkB, CREB and ERK levels were noticed in the brain of mice with T2D. These changes were also attenuated by administration of Phloridzin. Phloridzin may ameliorates T2D-induced depression by mitigating the oxidative stress, and up-regulation of neurotrophins in the brain. Therefore, Phloridzin can be used as a therapeutic intervention for the management of depression co-morbid with T2D.
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Phloridzin ameliorates type 2 diabetes‐induced depression in mice by mitigating oxidative stress and modulating brain‐derived neurotrophic factor
Journal of Diabetes & Metabolic Disorders, 2021Co-Authors: Sandesh P. Kamdi, Amit Raval, Kartik T. NakhateAbstract:Purpose Type 2 diabetes (T2D) is linked with depression due to insulin resistance, oxidative stress and disruption of neurotrophic factors. We evaluated potential benefits of Phloridzin in ameliorating depressive symptoms in T2D. Methods Adult male Swiss-albino mice (25–30 g) on high-fat-diet (HFD) for 2 weeks were administered with streptozotocin (STZ; 35 mg/kg, intraperitoneal) to induce T2D. Seven days after STZ administration, diabetic mice on HFD were distributed into different groups. Animals were subjected daily to oral treatment of saline (0.25 ml), fluoxetine (10-20 mg/kg) or Phloridzin (10-20 mg/kg) for a period of 4 weeks. One hour after last dose, the immobility time of animals was evaluated in forced swim test (FST) and tail suspension test (TST). To further confirm the mechanisms involved in antidepressant effect of Phloridzin, biochemical parameters like brain derived neurotropic factor (BDNF), glutathione (GSH), extracellular signal-regulated kinase (ERK), tyrosine receptor kinase B (TrkB) and cAMP-response element binding protein (CREB) were estimated in the brain. Results Animals with T2D showed a significant increase in immobility as compared to control in FST and TST. However, 4 weeks administration of fluoxetine or Phloridzin attenuated this effect. A significant decline in GSH, BDNF, TrkB, CREB and ERK levels were noticed in the brain of mice with T2D. These changes were also attenuated by administration of Phloridzin. Conclusions Phloridzin may ameliorates T2D-induced depression by mitigating the oxidative stress, and up-regulation of neurotrophins in the brain. Therefore, Phloridzin can be used as a therapeutic intervention for the management of depression co-morbid with T2D.
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Phloridzin attenuates lipopolysaccharide-induced cognitive impairment via antioxidant, anti-inflammatory and neuromodulatory activities.
Cytokine, 2021Co-Authors: Sandesh P. Kamdi, Amit Raval, Kartik T. NakhateAbstract:Abstract Background Lipopolysaccharide (LPS) is known to produce neuroinflammation and memory impairment. Although Phloridzin (a phenolic phytoconstituent) shows antioxidant- and anti-inflammatory activities, its ameliorative potential in LPS-mediated neuroinflammation and memory dysfunction remains unexplored. Objectives To investigate the protective effect of Phloridzin against LPS-mediated memory impairment and neuroinflammation in mice. Methods Different groups of mice were treated with LPS (250 μg/kg) via intraperitoneal (ip) route to induce cognitive impairments. The animals were administered with Phloridzin (10–20 mg/kg, oral) or donepezil (1 mg/kg, intraperitoneal), and memory functions were evaluated by Morris water maze (MWM) and Y-maze. At the end of the behavioral experiments, the animals were sacrificed and different biochemical parameters like acetylcholinesterase (AChE), brain derived neurotropic factor (BDNF), tumor necrosis factor (TNF-α), interleukin-6 (IL-6), superoxide dismutase (SOD) and glutathione (GSH) concentration in the hippocampus and the cerebral cortex were estimated. Results While LPS administered animals showed significantly decreased memory retention in both MWM and Y maze, a significant reversal in all the parameters were observed following treatment with Phloridzin. LPS-treated animals showed significantly decreased level of antioxidants (SOD and GSH), neurotropic factor (BDNF) and cholinergic transmission (increased AChE) and increased levels of inflammatory/oxidative markers (TNF-α, IL-6 and MDA) in hippocampus and cortex. These changes were alleviated after the treatment with Phloridzin. Conclusions Phloridzin may have neuroprotective role against LPS-induced neuroinflammation and memory impairment by virtue of its antioxidant, anti-inflammatory, and enhanced cholinergic signalling activity in the hippocampus and cerebral cortex.
Eda Mehmeti - One of the best experts on this subject based on the ideXlab platform.
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highly selective electrochemical determination of phlorizin using square wave voltammetry at a boron doped diamond electrode
Food Analytical Methods, 2017Co-Authors: Eda Mehmeti, Dalibor M Stankovic, Astrid Ortner, Janez Zavasnik, Kurt KalcherAbstract:A boron-doped diamond electrode was used as an electrochemical sensor for the determination of phlorizin (aka Phloridzin, phlorrhizin) using square wave voltammetry (SWV). Phlorizin (Phl) exhibited a well-defined oxidation peak at +0.9 V (versus Ag/AgCl electrode 3 M KCl) in solutions with a pH value of 6.0. Parameters such as pH value and scan rate were optimized for cyclic voltammetry as well as amplitude and frequency for SWV. The sensor gave excellent response with a wide linear dynamic range for concentrations of phlorizin from 3 to 100 μM with a detection limit of 0.23 μM and a good repeatability (± 0.9%, n = 7 measurements, c = 10 μM). The effect of interferences by most common compounds was tested, and the method was successfully applied to the determination of the title compound in apple root extracts and urine samples with satisfactory recovery.