scholarly journals The Combined Extract of Black Sticky Rice and Dill Improves Poststroke Cognitive Impairment in Metabolic Syndrome Condition

2019 ◽  
Vol 2019 ◽  
pp. 1-19 ◽  
Author(s):  
Warin Ohnon ◽  
Jintanaporn Wattanathorn ◽  
Wipawee Thukham-mee ◽  
Supaporn Muchimapura ◽  
Panakaporn Wannanon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Experimental Period ◽  
Underlying Mechanism ◽  
Cognitive Enhancer ◽  
Anethum Graveolens ◽  
Neuroprotective Effects ◽  
Neuron Density ◽  
Oxidative Stress Status ◽  
Male Wistar Rats

Despite the increase in cognitive deficit following stroke in metabolic syndrome (MetS) condition, the therapeutic strategy is still limited. Since oxidative stress and neuroinflammation play the crucial roles on the pathophysiology of aforementioned conditions, the cognitive enhancing effect of the combined extract ofOryza sativaandAnethum graveolenswas considered based on their antioxidant, anti-inflammation, and neuroprotective effects together with the synergistic effect concept. Male Wistar rats weighing 180-220 g were induced metabolic syndrome-like condition by using a high-carbohydrate high-fat diet (HCHF diet). Then, reperfusion injury following cerebral ischemia was induced by the occlusion of right middle cerebral artery and treated with the combined extract ofO. sativaandA. graveolens(OA extract) at doses of 0.5, 5, and 50 mg/kg BW once daily for 21 days. Spatial memory was assessed every 7 days throughout the experimental period. At the end of the study, neuron and glial fibrillary acidic protein- (GFAP-) positive cell densities, the oxidative stress status, AChE, and the expression of proinflammatory cytokines (TNF-α, IL-6) in the hippocampus were determined. The results showed that OA extract at all doses used in this study significantly improved memory together with the reductions of MDA, TNF-α, IL-6, AChE, and density of GFAP-positive cell but increased neuron density in the hippocampus. Taken together, OA is the potential cognitive enhancer in memory impairment following stroke in MetS condition. The possible underlying mechanism may occur partly via the reductions of oxidative stress status, GFAP-positive cell density, and neuroinflammatory cytokines such as TNF-αand IL-6 together with the suppression of AChE activity in the hippocampus. This study suggests that OA is the potential functional ingredient to improve the cognitive enhancer. However, further clinical research is required.

scholarly journals Cerebroprotective Effect against Cerebral Ischemia of the Combined Extract of Oryza sativa and Anethum graveolens in Metabolic Syndrome Rats

2019 ◽  
Vol 2019 ◽  
pp. 1-19 ◽  
Author(s):  
Jintanaporn Wattanathorn ◽  
Warin Ohnon ◽  
Wipawee Thukhammee ◽  
Supaporn Muchmapura ◽  
Panakaporn Wannanon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Oryza Sativa ◽  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Cortical Area ◽  
Brain Infarction ◽  
Underlying Mechanism ◽  
Anethum Graveolens ◽  
Oxidative Stress Status

The novel strategy against ischemic stroke in metabolic syndrome (MetS) targeting at oxidative stress and inflammation has gained attention due to the limitation of the current therapy. Due to the antioxidant and anti-inflammation of the combined extract of Oryza sativa and Anethum graveolens, the cerebroprotective effect against cerebral ischemia in MetS condition has been focused. Since no data were available, this study was set up to determine the effects of the combined extract of Oryza sativa L. and Anethum graveolens Linn. against ischemic stroke in the animal model of metabolic syndrome. The possible underlying mechanism was also further investigated. Male Wistar rats (180-220 g) were fed with high-carbohydrate high-fat diet (HCHF diet) to induce metabolic syndrome-like condition. Then, MetS rats were subjected to reperfusion injury at the right middle cerebral artery. The combined extract of O. sativa and A. graveolens (OA extract) at doses of 0.5, 5, and 50 mg/kg BW was fed once daily for 21 days. Neurological assessment was performed every 7 days throughout the experimental period. At the end of study, brain infarction volume, neuron and glial fibrillary acidic protein- (GFAP-) positive cell density, the oxidative stress status, the expressions of proinflammatory cytokines (NF-κB, IL-6), and eNOS in the cortical area together with the expression of VCAM-1 and the histological changes of common carotid artery were determined. It was found that OA extract decreased brain infarction, neurological score, oxidative stress status, and inflammatory mediators but increased eNOS expression in the cortical area; the increased VCAM-1 and intima-media thickness together with the reduction of lumen diameter of common carotid artery of MetS eats with MCAO were also mitigated by OA extract. These data suggest the cerebroprotective effect of OA, and the underlying mechanism may occur partly via the improvement of oxidative stress status, inflammation, and brain blood supply.

scholarly journals Evaluation of Safety and Protective Effect of Combined Extract ofCissampelos pareiraandAnethum graveolens(PM52) against Age-Related Cognitive Impairment

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Wipawee Thukham-mee ◽  
Jintanaporn Wattanathorn
Keyword(s):  
Cognitive Impairment ◽  
Acute Toxicity ◽  
Protective Effect ◽  
Underlying Mechanism ◽  
Food Supplement ◽  
Anethum Graveolens ◽  
Neuron Density ◽  
Age Related ◽  
Male Wistar Rats ◽  
Oecd Guideline

The present study aimed to determine acute toxicity, the protective effect, and underlying mechanism of PM52, a combined extract ofCissampelos pareiraandAnethum graveolens,against age-related cognitive impairment in animal model of age-related cognitive impairment. PM52 was determined as acute toxicity according to OECD guideline. Male Wistar rats, weighing 180–220 g, were orally given PM52 at doses of 2, 10, and 50 mg/kg at a period of 14 days before and 7 days after the bilateral administration of AF64A via intracerebroventricular route. All animals were assessed according to spatial memory, neuron density, MDA level, the activities of SOD, CAT, GSH-Px, and AChEI effect in hippocampus. It was found that all doses of PM52 could attenuate memory impairment and neurodegeneration in hippocampus. The possible mechanisms might occur via the suppression of AChE and the decreased oxidative stress in hippocampus. Therefore, our data suggest that PM52 may serve as food supplement to protect against age-related cognitive impairment such as mild cognitive impairment (MCI) and early phase of Alzheimer’s disease. However, further researches are still essential.

scholarly journals Moringa oleiferaMitigates Memory Impairment and Neurodegeneration in Animal Model of Age-Related Dementia

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Chatchada Sutalangka ◽  
Jintanaporn Wattanathorn ◽  
Supaporn Muchimapura ◽  
Wipawee Thukham-mee
Keyword(s):  
Oxidative Stress ◽  
Animal Model ◽  
Spatial Memory ◽  
Moringa Oleifera ◽  
Underlying Mechanism ◽  
Preventive Strategy ◽  
Neuron Density ◽  
Age Related ◽  
Male Wistar Rats

To date, the preventive strategy against dementia is still essential due to the rapid growth of its prevalence and the limited therapeutic efficacy. Based on the crucial role of oxidative stress in age-related dementia and the antioxidant and nootropic activities ofMoringa oleifera, the enhancement of spatial memory and neuroprotection ofM. oleiferaleaves extract in animal model of age-related dementia was determined. The possible underlying mechanism was also investigated. Male Wistar rats, weighing 180–220 g, were orally givenM. oleiferaleaves extract at doses of 100, 200, and 400 mg/kg at a period of 7 days before and 7 days after the intracerebroventricular administration of AF64A bilaterally. Then, they were assessed memory, neuron density, MDA level, and the activities of SOD, CAT, GSH-Px, and AChE in hippocampus. The results showed that the extract improved spatial memory and neurodegeneration in CA1, CA2, CA3, and dentate gyrus of hippocampus together with the decreased MDA level and AChE activity but increased SOD and CAT activities. Therefore, our data suggest thatM. oleiferaleaves extract is the potential cognitive enhancer and neuroprotectant. The possible mechanism might occur partly via the decreased oxidative stress and the enhanced cholinergic function. However, further explorations concerning active ingredient(s) are still required.

scholarly journals Neuroprotective and Cognitive-Enhancing Effects of Microencapsulation of Mulberry Fruit Extract in Animal Model of Menopausal Women with Metabolic Syndrome

2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Supannika Kawvised ◽  
Jintanaporn Wattanathorn ◽  
Wipawee Thukham-mee
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Animal Model ◽  
Memory Impairment ◽  
Fruit Extract ◽  
Neuron Density ◽  
Erk Phosphorylation ◽  
Menopausal Women ◽  
Oxidative Stress Status ◽  
Memory Enhancing

Currently, the neuroprotectant and memory-enhancing agent for menopausal women with metabolic syndrome is required. Based on the advantages of polyphenolics on numerous changes observed in menopause with metabolic syndrome and the encapsulation method, we hypothesized that microencapsulated mulberry fruit extract (MME) could protect brain damage and improve memory impairment in an animal model of menopause with metabolic syndrome. To test this hypothesis, MME at doses of 10, 50, and 250 mg/kg was given to female Wistar rats which were induced experimental menopause with metabolic syndrome by bilateral ovariectomy (OVX) and fed with high-carbohydrate high-fat (HCHF) diet for 8 weeks. Spatial memory together with neuron density, oxidative stress status, acetylcholinesterase, and phosphorylation of Erk in the hippocampus was assessed at the end of the study. It was found that MME decreased memory impairment, oxidative stress status, and AChE activity but increased neuron density and Erk phosphorylation in the hippocampus. Therefore, the neuroprotective and memory-enhancing effects of MME might partly involve the enhanced cholinergic function and Erk phosphorylation but decreased oxidative stress status in hippocampus. Therefore, MME is the potential novel neuroprotectant and memory-enhancing agent for menopause with metabolic syndrome. However, further research especially clinical trial is still necessary.

scholarly journals Positive Modulation of PinkNelumbo nuciferaFlowers on Memory Impairment, Brain Damage, and Biochemical Profiles in Restraint Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Thawatchai Prabsattroo ◽  
Jintanaporn Wattanathorn ◽  
Pichet Somsapt ◽  
Opass Sritragool
Keyword(s):  
Oxidative Stress ◽  
Monoamine Oxidase ◽  
Spatial Memory ◽  
Brain Damage ◽  
Memory Deficit ◽  
Ki67 Expression ◽  
Mao B ◽  
Serum Corticosterone ◽  
Neuron Density ◽  
Oxidative Stress Status

Due to the crucial role of oxidative stress in the stress-induced memory deficit, the benefit of substance possessing antioxidant effect is focused. Since no data are available, we aimed to determine the effect ofNelumbo nuciferaflowers extract on spatial memory and hippocampal damage in stressed rats. Male Wistar rats, weighing 250–350 g, were orally givenN. nuciferaextract at doses of 10, 10, and 200 mg·kg−145 minutes before the exposure to 12-hour restraint stress. The spatial memory and serum corticosterone were assessed at 7 and 14 days of study period. At the end of study, acetylcholinesterase (AChE), monoamine oxidase type A and monoamine oxidase type B (MAO-A and MAO-B), oxidative stress status, neuron density, and Ki67 expression in hippocampus were also assessed. The results showed thatN. nuciferaextract decreased memory deficit and brain damage, serum corticosterone, oxidative stress status, AChE, and MAO-A and MAO-B activities but increased neuron density and Ki67 expression in hippocampus. These suggested that the improved oxidative stress status, adult neurogenesis, and cholinergic and monoaminergic functions might be responsible for the protective effect against stress-related brain damage and dysfunction of the extract. Therefore,N. nuciferaextract is the potential neuroprotective and memory enhancing agent. However, further researches are still required.

scholarly journals Encapsulated Mulberry Fruit Extract Alleviates Changes in an Animal Model of Menopause with Metabolic Syndrome

2019 ◽  
Vol 2019 ◽  
pp. 1-23 ◽  
Author(s):  
Jintanaporn Wattanathorn ◽  
Supannika Kawvised ◽  
Wipawee Thukham-mee
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Body Weight ◽  
Weight Gain ◽  
Protein Expression ◽  
Body Weight Gain ◽  
Atherogenic Index ◽  
Fruit Extract ◽  
Mulberry Fruit ◽  
Oxidative Stress Status

Currently, the therapeutic strategy against metabolic syndrome and its complications is required due to the increasing prevalence and its impact. Due to the benefits of both mulberry fruit extract and encapsulation technology, we hypothesized that encapsulated mulberry fruit extract (MME) could improve metabolic parameters and its complication risk in postmenopausal metabolic syndrome. To test this hypothesis, female Wistar rats were induced experimental menopause with metabolic syndrome by bilateral ovariectomy (OVX) and high-carbohydrate high-fat (HCHF) diet. Then, they were orally given MME at doses of 10, 50, and 250 mg/kg BW for 8 weeks and the parameters, such as percentage of body weight gain, total cholesterol, triglycerides, HDL-C, LDL-C, atherogenic index, fasting blood glucose, plasma glucose area under the curve, serum angiotensin-converting enzyme (ACE), oxidative stress status, histology, and protein expression of PPAR-γ, TNF-α, and NF-κB in adipose tissues were determined. MME improved body weight gain, adiposity index, glucose intolerance, lipid profiles, atherogenic index, ACE, oxidative stress status, and protein expression of TNF-αand NF-κB. Moreover, MME attenuated adipocyte hypertrophy and enhanced PPAR-γexpression. Taken altogether, MME decreased metabolic syndrome and its complication via the increased PPAR-γexpression. Therefore, MME is the potential candidate for improving metabolic syndrome and its related complications. However, further research in clinical trial is still necessary.

scholarly journals Memory-Enhancing Effect of a Phytosome Containing the Combined Extract of Mulberry Fruit and Ginger in an Animal Model of Ischemic Stroke with Metabolic Syndrome

2020 ◽  
Vol 2020 ◽  
pp. 1-19
Author(s):  
Jintanaporn Wattanathorn ◽  
Nut Palachai ◽  
Wipawee Thukham-mee ◽  
Supaporn Muchimapura
Keyword(s):  
Metabolic Syndrome ◽  
Ischemic Stroke ◽  
Erk Pathway ◽  
Enhancing Effect ◽  
Neuron Density ◽  
Mulberry Fruit ◽  
Extracellular Signal ◽  
Male Wistar Rats ◽  
Underlying Mechanisms ◽  
The Right

The prevalence of dementia following cerebral ischemia in metabolic syndrome (MetS) condition is increasing, and most of the cases are often severe. Unfortunately, no effective strategy for treating this condition is available. Based on the positive modulation effect of a polyphenol-rich substance on dementia and the improvement in bioavailability and stability of polyphenols induced by the phytosome technique together with the use of the synergistic concept, we hypothesized that a phytosome containing the combined extract of mulberry fruit and ginger (PMG) should mitigate dementia and memory impairment following ischemic stroke in MetS. MetS was induced in male Wistar rats weighing 180-200 g by exposure to a 16-week feeding period of high-carbohydrate high-fat (HCHF) diet. MetS rats were orally given PMG at doses of 50, 100, and 200 mg·kg-1 BW 21 days before and 21 days after the occlusion of the right middle cerebral artery (Rt. MCAO). Then, their spatial memory was determined and the possible underlying mechanisms explored via the alterations of acetylcholinesterase (AChE), neuron density, malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), interleukin-6 (IL-6), and signal transduction via extracellular signal-regulated kinase (ERK) pathway in both the cerebral cortex and the hippocampus. It was found that PMG significantly enhanced memory. It also decreased AChE, IL-6, and MDA but increased SOD, CAT, GSH-Px, neuron density, and phosphorylation of ERK. These data suggested the cognitive enhancing effect of PMG. The possible underlying mechanisms might occur partly via the improvement of cholinergic function via the ERK pathway together with the decrease in neurodegeneration induced by the reduction of oxidative stress and inflammation. However, a subchronic toxicity study is also required to assure the safety of PMG consumption before moving forward to a clinical trial study.

scholarly journals Electrospun Nanofibers Loaded with Quercetin Promote the Recovery of Focal Entrapment Neuropathy in a Rat Model of Streptozotocin-Induced Diabetes

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Chonlathip Thipkaew ◽  
Jintanaporn Wattanathorn ◽  
Supaporn Muchimapura
Keyword(s):  
Oxidative Stress ◽  
Functional Recovery ◽  
Electrospun Nanofibers ◽  
Diabetic Rats ◽  
Nerve Lesion ◽  
Electrospinning Technique ◽  
Oxidative Stress Status ◽  
Male Wistar Rats ◽  
Streptozotocin Induced Diabetes ◽  
The Right

In this study, quercetin-loaded zein-based nanofibers were developed using electrospinning technique. The therapeutic effect of these quercetin-loaded nanofibers on neuropathy in streptozotocin- (STZ-) induced diabetes in rats was assessed. Diabetic condition was induced in male Wistar rats by STZ, after which a crush injury of the right sciatic nerve was performed to induce mononeuropathy. Functional recovery was assessed using walking track analysis, measurements of foot withdrawal reflex, nerve conduction velocity, and morphological analysis. The oxidative stress status and the ratio of phosphorylated extracellular recognition kinase (pERK)/extracellular recognition kinase (ERK) expression in the nerve lesion were also assessed in order to elucidate the potential mechanisms involved. Results showed that quercetin-loaded zein-based nanofibers slightly enhanced functional recovery from neuropathy in STZ-diabetic rats. The potential mechanism might partially involve improvements in oxidative stress status and the ratio of pERK/ERK expression in the nerve lesion.

Sign in / Sign up

Export Citation Format

Share Document