scholarly journals Mulberry Fruit Extract Protects against Memory Impairment and Hippocampal Damage in Animal Model of Vascular Dementia

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Pratchaya Kaewkaen ◽  
Terdthai Tong-un ◽  
Jintanaporn Wattanathorn ◽  
Supaporn Muchimapura ◽  
Wiroje Kaewrueng ◽  
...  

Nowadays, the preventive strategy of vascular dementia, one of the challenge problems of elderly, has received attention due to the limitation of therapeutic efficacy. In this study, we aimed to determine the protective effect and possible mechanism of action of mulberry fruit extract on memory impairment and brain damage in animal model of vascular dementia. Male Wistar rats, weighing 300–350?g, were orally given mulberry extract at doses of 2, 10 and 50?mg/kg at a period of 7 days before and 21 days after the occlusion of right middle cerebral artery (Rt.MCAO). It was found that rats subjected to mulberry fruits plus Rt.MCAO showed the enhanced memory, the increased densities of neuron, cholinergic neuron, Bcl-2-immunopositive neuron together with the decreased oxidative stress in hippocampus. Taken all data together, the cognitive enhancing effect of mulberry fruit extract observed in this study might be partly associated with the increased cholinergic function and its neuroprotective effect in turn occurs partly via the decreased oxidative stress and apoptosis. Therefore, mulberry fruit is the potential natural cognitive enhancer and neuroprotectant. However, further researches are essential to elucidate the possible active ingredient.

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Chatchada Sutalangka ◽  
Jintanaporn Wattanathorn ◽  
Supaporn Muchimapura ◽  
Wipawee Thukham-mee

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.


2017 ◽  
Vol 2017 ◽  
pp. 1-13 ◽  
Author(s):  
Supannika Kawvised ◽  
Jintanaporn Wattanathorn ◽  
Wipawee Thukham-mee

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.


2019 ◽  
Vol 2019 ◽  
pp. 1-23 ◽  
Author(s):  
Jintanaporn Wattanathorn ◽  
Supannika Kawvised ◽  
Wipawee Thukham-mee

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.


2015 ◽  
Vol 8 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Nattaporn Phunchago ◽  
Jintanaporn Wattanathorn ◽  
Kowit Chaisiwamongkol ◽  
Supaporn Muchimapura ◽  
Wipawee Thukham-mee

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Lan Han ◽  
Zhaojie Ji ◽  
Weidong Chen ◽  
Dengke Yin ◽  
Fan Xu ◽  
...  

Tao-Hong-Si-Wu decoction (TSD) as a traditional chinese medicine (TCM) has been developed to treat thrombotic diseases for hundreds of years, and vascular dementia (VD) is a cognitive dysfunction syndrome caused by cerebral embolism. In this study, the protective effect of TSD on memory impairment and brain damage in rat model of VD induced by middle cerebral artery occlusion (MCAO) was investigated. The study showed that rats in MCAO treatment with TSD for 14 days significantly improved behavioral function, increased densities of neuron, and induced angiogenesis in the brain compared with model rats. TSD also adjusted the neurotransmitter levels, reduced the content of endothelin-1 (ET-1), and induced the activities of vascular endothelial growth factor (VEGF) in hippocampus. Moreover, the immunohistochemical staining and western blotting results also revealed that TSD decreased apoptosis via upregulated B-cell lymphoma-2 (Bcl-2)/Bcl-2 associated X protein (Bax) ratio. These results demonstrated TSD possesses neuroprotective and antidementia properties by preventing the loss of neural cells, adjusting brain neurotransmitter, promoting cerebral blood circulation, and decreasing apoptosis. These results suggested that TSD might be developed as an effective drug for the prevention of VD.


2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Jintanaporn Wattanathorn ◽  
Supaporn Muchimapura ◽  
Wipawee Thukham-Mee ◽  
Kornkanok Ingkaninan ◽  
Sakchai Wittaya-Areekul

To date, the effective preventive paradigm against mild cognitive impairment (MCI) is required. Therefore, we aimed to determine whetherMangifera indicafruit extract, a substance possessing antioxidant and cognitive enhancing effects, could improve memory impairment, cholinergic dysfunction, and oxidative stress damage in animal model of mild cognitive impairment. Male Wistar rats, weighing 180–200 g, were orally given the extract at doses of 12.5, 50, and 200 mg·kg−1BW for 2 weeks before and 1 week after the bilateral injection of AF64A (icv). At the end of study, spatial memory, cholinergic neurons density, MDA level, and the activities of SOD, CAT, and GSH-Px enzymes in hippocampus were determined. The results showed that all doses of extract could improve memory together with the decreased MDA level and the increased SOD and GSH-Px enzymes activities. The increased cholinergic neurons density in CA1 and CA3 of hippocampus was also observed in rats treated with the extract at doses of 50 and 200 mg·kg−1BW. Therefore, our results suggested thatM. indica, the potential protective agent against MCI, increased cholinergic function and the decreased oxidative stress which in turn enhanced memory. However, further researches are essential to elucidate the possible active ingredients and detail mechanism.


2016 ◽  
Vol 23 (5-6) ◽  
pp. 318-331 ◽  
Author(s):  
Dongfang Shen ◽  
Xiaoyan Tian ◽  
Wenxu Sang ◽  
Rongrong Song

2016 ◽  
Vol 74 (6) ◽  
pp. 482-488 ◽  
Author(s):  
Wenna Liang ◽  
Xiaoyang Zhao ◽  
Jinping Feng ◽  
Fenghua Song ◽  
Yunzhi Pan

ABSTRACT Objective Increasing evidence demonstrates that oxidative stress and inflammatory are involved in amyloid β (Aβ)-induced memory impairments. Ursolic acid (UA), a triterpenoid compound, has potent anti-inflammatory and antioxidant activities. However, it remains unclear whether UA attenuates Aβ-induced neurotoxicity. Method The aggregated Aβ25-35 was intracerebroventricularly administered to mice. Results We found that UA significantly reversed the Aβ25-35-induced learning and memory deficits. Our results indicated that one of the potential mechanisms of the neuroprotective effect was attenuating the Aβ25-35-induced accumulation of malondialdehyde (MDA) and depletion of glutathione (GSH) in the hippocampus. Furthermore, UA significantly suppressed the upregulation of IL-1β, IL-6, and tumor necrosis-α factor levels in the hippocampus of Aβ25-35-treated mice. Conclusion These findings suggest that UA prevents memory impairment through amelioration of oxidative stress, inflammatory response and may offer a novel therapeutic strategy for the treatment of Alzheimer’s disease.


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